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Supplements Flashcards

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1
Q

What are key functional insights related to Glucose?

A

🔹 Marker Description: Primary marker to get understanding of blood glucsoe / insulin reisstance / metabolism

Low glucose = glucagon released = blood glucose increase = insulin increase

Glucose utilisation in liver
Level of glucose in the blood is highly dependant on the liver through the breakdown of glycogen and via the adrenal glands which produce hormones that promote the gluconeogenesis (generation of glucose) from fats and proteins.

required by most cells for energy productin - brain and NS rely solely on glucose for energy

fasting glcose evaluate blood sugar regulation - insights into diabetes and insulin resistance

regulating blood sugar also reliased on hormonal function
Adrenaline, cortisol, thyroxine

🔻 Possible Low Reasons: reactive hypoglycemia (low blood sugar diet , fasting, strenous exericse) - often happens when excessive glcusoe consumed, then ‘delayed reollarcoaster’ = brings down blood glucos - but too low

OR possibly hyperinsulinism - chronic high blood sugar diet - chronic pancreatic overstimulation (reactive hypoglycemia) low level blood glucose - high insulin (Glut4 allows serum glucose to enter cell - low in blood)

Insulin resistance - might also see brown / red tint on shins

adrenal hypofunction
hypothyroidism - body might not be stim. as much gluconeogensis . check if low TS3/TS4 as well - could help improve thyroid.

Liver issues (cannot control blood sugar, glycogen storage issue)
- if see low glucose + high GGT, AST, high ALT - assess if it hypoglycemia is related to liver dysfunction [hypoglycemia = gluycogen storage issue ]

chronic stress: decerased cortisol - can see with chronic stress, lack of sleep, HPA axis dysregulation.
- adrenal hypofunction if chornic stress (addisons disease)
- tissue insentivity

medications (metformin, proranolol, tolbutamide)

low vit d.

tumours of pancetaic cells (beta cells - insulinomas)
- glycogen release issue (adrenal-foucsed treatment)
addisons disease

🔺 Possible High Reasons: Insulin resistance
Metabolic syndrome, Fatty liver, fasted NAFLD/MAFLD, diabetes
Acute/chronic stress!! - adrenal hyperfunction/cortisol resistance (stress hormones - cortisol,NE increases glucose - dyesregulated HPA axis (eg lack of sleep, anxiety etc))
Low insulin - Adrenal hypofunction- low secretion of cortisol from adrenal glands
Binging
Pancreatic issues!!! Severe renal disease.
PCOS
Medications - corticosteroids, thizaides, phenytoin, oestrogen
vit b1. deficiency
adrenal hyperfunction, hyperthryoidism, cushings disease

ALSO - could be due to stress - eg were they rushing that morning? was someone annoying them on the road? did they have an argument? etc

Cow’s milk proteins and some vaccines may trigger an immune response against pancreatic beta cells, increasing the risk of type 1 diabetes in genetically susceptible individuals.

📊 Patterns: Atherosclerosis: H Trig, H LDL, H URic Acid. L HDL.
Metabolic Syndrom: H Cholesterol, Trig, Insulin, Glucose, HBA1C. L HDL.

Pre-Diabetes: HBA1c 5.7-6.4%, Glucose 100-125 mg/dL
Diabetes: HBA1c >6.5%, Glucose >125 mg/dL

Reactive hypoglycemia: L Glucose, LDH, <3% HBA1C

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2
Q

What are key functional insights related to Insulin?

A

🔹 Marker Description: Insulin is a hormone secreted by the pancreatic beta cells in response to rising blood glucose levels.
It regulates glucose uptake and storage, playing a key role in metabolism and energy balance.

A fasting insulin test (after 12 hours of fasting) helps assess insulin sensitivity, resistance, or pancreatic function.
- v fast acting /to change (done after 12 hour fast - any more than 12 hours = insulin levels drop too mcuch
- Need to pay attention to insulin - but because it is such a small half life - pay more attention to HPM1C - can assume elevated insulin (and decreased AMPK)

In healthy individuals, insulin:
Regulated blood glucose and storage:
- Transports glucose into cells, making them more permeable to glucose and lowering blood sugar levels.
Instructs the liver to convert excess glucose into glycogen (short-term energy storage).
Promotes fat synthesis (long-term energy storage) when glycogen stores are full.

Also maintains Protein Function & Gut Integrity
- Insulin regulates proteins like zonulin, which is essential for maintaining intestinal barrier integrity.
- this is impaired in insulin resistance / hyperinsulinemia
- high insulin = downregulates AMPK = paracellular leakage (integrity breaks)

produced by pancreatic b cells -

🔻 Possible Low Reasons: fasting
diabetes (T1 ) - pncreatic cell dysfunction
pancreatic cancer, pancreatitis (low insulin + high blood glucose indicate damage to beta cells => can cause insulin-dependancy eg in T2D), beta cell damage, pancreatic islet b cells AI

macronutrient deficiencies (eg eating disorder) - (eg if see low insulin, low glucose, low Hb, low ferrtiin,low total protein)

🔺 Possible High Reasons: insulin resistance (prolonged exposure to insulin - receptors not sensitive - body keeps producing more insulin to compensate to try and get it to bind - pancrease has to make more and more)
- also inflammation in insulin resistance can also affect insulin - ecsp. if fertility issues (eg PCOS, hair loss - may want to look into adnrogen)

hypglycemia
obesity, high trans fat intake
cushings disease,
PCOS (as SBG is lower)
medications - corticosteroids, oral contraceptive pills, levodopa (AD)
h.pylori
paracellular permeability (>7 mU/L)

📊 Patterns: Low insulin, High Blood Glucose = pancreatic cell damage

Pay attention to HPA1C as T1/2 insulin low

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3
Q

What are key functional insights related to HBA1C?

A

🔹 Marker Description: Stickniness’ of RBCs
- glycated hemoglobin = measures the % of hemoglobin in red blood cells that has glucose attached to it.
- Reflects av. blood glucose levels over the past 2-3 months (120 days), giving a long-term picture of blood sugar control.
- Glucose combines with Hb to produce glyco-Hb indicates blood sugar levels over 120 days

2-3 month lag (120 days) - so good marker of change in diet
- eg if glucose and insulin have improved, but HB1AC still high - sign that diet has improved over past 2 months
- think of it like hunny - cells become stickier - measures blood glucose levels over RBC life span
- Glucose binds to hemoglobin, forming glycohemoglobin in a non-reversible reaction—meaning RBCs remain “sticky” for their lifespan (~120 days)

Used to assess diabetes risk, blood sugar regulation, and metabolic health trends.

Seasonal & Diurnal Variations:
- Higher in winter than summer—cold increases metabolic demand.
- Higher in the morning than afternoon due to overnight glucose dynamics.
- Suggests higher glucose efficiency is needed in colder environments.

🔻 Possible Low Reasons: hypoglycemia
blood loss, anemia, DONATING BLOOD
chronic renal disease
iron chelation
high dose vit c (less common)

Iron chelation or blood donation can artificially lower HbA1c by reducing older RBCs, HIDING THE MARKER (hiding high glucose levels).

🔺 Possible High Reasons: metabolic syndrom, pre-diabates, diabates
damage to kidneys, eyes , blood eslls, heart, nerves
increased CFH risk, fatty liver
lead toxicity

past overconsumption of carbs/calories - with recent improvement (if see H HBA1C, but normal isulin and glucose) - as there’s a lag (120 days)

📊 Patterns: Pre-Diabetes: HBA1c 5.7-6.4%, Glucose 100-125 mg/dL
Diabetes: HBA1c >6.5%, Glucose >125 mg/dL

Reactive hypoglycemia: L Glucose, LDH, <3% HBA1C

Iron chelation or blood donation can artificially lower HbA1c by reducing older RBCs, HIDING THE MARKER (hiding high glucose levels).

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4
Q

What are key functional insights related to Cortisol?

A

🔺 Possible High Reasons: stress - emptional, physical or chemical => incr. ACTH (bodyguards) => incr. cortisol

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5
Q

What are key functional insights related to TSH?

A

🔹 Marker Description: produced in anterioir prituitary gland - overall infication of thyroid function

TSH is like manager of work team - high levels - indicating thyroid is underperforming and thryoid ‘manager’ has to shout louder and louder

women are better with lower TSH than men

if elderly, or cardiovascualr risk - better to keep TSH in upper bracket of range (risk of fractues, and cardiovascualr risks with low TSH)

TSH >1.5 (F), >2(M) = strong chance TPO AB present

🔻 Possible Low Reasons: hyperthyroidism (manager slacking if T3/T4 busy and lots of them!)
graves disease, thryoiditis, thryotoxicosis
excess iodine,
pitutary dysfunction
medications
pregnancy (ecsp. 1st trimester)

liver toxicity

sleep deprivation (check time of testing)

🔺 Possible High Reasons: hypothyroidism, hashimotos thyroiditis (manager having to shout!!!)
thyroiditis, pituitary or hypothalamic dysfunctions
thyroidectimy, radiations (ioften treatment for hyperthyroidism)
iodine deficiency
low progresterone
adrenal fatigue (pituitary is attempting to compensate to so increase hormone output)

age - thyroid function declines with age - increased TSH to compensate

TSH >1.5 (F), >2(M) = strong chance TPO AB present

📊 Patterns: H TSH (2-4) - strong chance have TPO AB - check and mindful iodine
- TSH >1.5 (F), >2(M) = strong chance TPO AB present

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6
Q

What are key functional insights related to T4-Free?

A

🔹 Marker Description: T4 = Thyroxine

thyroid function naturally declines with age - age-adjusted range for thyroid - might be safer to have lower levels if wokring with older pop (eg over 65 yo) as high can have increased risk of CVD effects + thyroid functions decreased with age anyway

low T4 => low T3

🔻 Possible Low Reasons: hypothyroidism, hashimotos
pituitary or hypothalamus dysfunction

nutient deficiencies (iodine, tyrosine, zinc),
protein malabsorption

medications (methium, anti-thyroid drugs, amiodorione)
dysbiosis
low progesterone. adrenal fatigue.

🔺 Possible High Reasons: hyperthyroidism, graves, thyroiditis, progressed hashimotos,
excessive iodine intake, goiter
incorrect hormone replacement (elevate ciruclating levels)

liver toxicity (reduced ability to convert T4 into T3 - can occur due to deficnecies in any of cofcators required for conversion eg vit A, B vits, selenium, zinc, mag)

nut defiencies (A, B, mag, selenium, zinc)

📊 Patterns: H FT4 and L FT3 - look for selenium deficiency
- if have adequate selenium, low ALP - could be zinc deficiency

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7
Q

What are key functional insights related to T3-Free?

A

🔹 Marker Description: T3 (Triiodothyronine) - most active form and most biologically potent
- 3 iodines

Deioinsonation of T4 into T3 occurs in various body structures (liver, BAT, skeletal muscle, glial cels, placenta, kidneys). - dysnfunction in any of these tissues = abnormal T3 reading

Conversion of T4>T3 happens in liver - requires glucose, selenium, zinc, iron, progersterone
- any deficincies (ie in selenium, vit D, zinc, mag, iron = RT3 instead of FT3 is formed )
- IUD = low progesterone = prevents conversion

🔻 Possible Low Reasons: hypothyroidism, hashimotos, thyroiditis
nutrient deficicnes (selenium, zinc, iron, mag) also glucose,

malnutriion, dieting, low-cal diet
medications (lithium , interferon, ammidoerone, antithyroid drugs)
inflammation, ox stress
liver disease, kidney disease

IUD (low progersterone = impedes conversion)

🔺 Possible High Reasons: hyperthyroidism, graves, thyroiditis, progressed hashimotos,
excessive iodine intake, goiter
incorrect hormone replacement (elevate ciruclating levels)
trauma

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8
Q

What are key functional insights related to Reverse T3?

A

🔹 Marker Description: insig. marker in conventional medicine -
Reverse T3 (rT3) is an inactive form of triiodothyronine (T3). It is produced when the body converts thyroxine (T4) into rT3 instead of active T3.
- isomer of T3 -

can block T3 acting on receptors (rT3 competes with active T3 at cellular receptors but does not activate metabolism.)

if have deficiencies in selenium, vit D, zinc, mag, iron = RT3 instead of FT3 is formed

🔺 Possible High Reasons: Hypothyroidism (T3 cant do its job), hashimotos , thyroitis (High rT3 levels can cause functional hypothyroidism, where symptoms of low thyroid (fatigue, weight gain, brain fog) occur despite normal TSH and T4 levels. )

nut deficiencies (selenium, vit D, zinc, mag, iron)
low cal diets, low carb intake
liver / kidney issues - RT3 made instead of T3

📊 Patterns: Don’t take levothyroxine without assessing RT3

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9
Q

What are key functional insights related to TPO Antibody (Thyroid Peroxidase Ab)?

A

🔹 Marker Description: Thyroid Peroxidase (TPO) — an enzyme that makes T4 and T3
- Adds iodine to tyrosine residues
- essential enzyme for T. hormone production

TPO AB tags TPO and destroys it
- need to be v. careful if this AB is present - limit iodine
- high iodine can make self fulfilling proficy
- only 50% of patients will have electaed ABs in blood - essential to track symptoms (not just bloods)

Low TPO - want to ask if it is casued by destruction of thyroid OR by T4 not converting to T3?

🔺 Possible High Reasons: Graves, hashimotos,
dysbiosis
heavy metal toxicity
stress, environemntal factors
dysbiosis
RA, sjorgens disease, lupus
PCOS (27% of women with PCOS have either H TPO or Tg ABs = thyroid AI)
trauma - childhood sexual abuse = risk factor for thyroid ABs in women with post partum depression

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10
Q

What are key functional insights related to TBG Antibody (Thyroglobulin Ab)?

A

🔹 Marker Description: Thyroglobulin is a Large protein = scaffold for T4/ T3

B which ‘tags’ iodine
- need to be v careful if this AB is present - want to reduce iodine

Thyroglobuin is a protein made in thyroid = formation of T4 and T3 - requires TPO enzyme

🔺 Possible High Reasons: diseases - graves, hashimotos,
dysbiosis
heavy metal toxicity
PCOS (27% of women with PCOS have either H TPO or Tg ABs = thyroid AI)
trauma - childhood sexual abuse = risk factor for thyroid ABs in women with post partum depression

stress, enbironmental factors

📊 Patterns: check inflammation - CRP, ESR,

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11
Q

What are key functional insights related to RT3:T3 Ratio?

A

🔹 Marker Description: marker of thyroid function and metabolic efficiency/thyroid hormone conversion efficiency

This ratio is particularly useful in thyroid resistance and functional hypothyroidism cases where standard TSH and T4 levels appear normal but symptoms persist.

body converts T4 into rT3 instead of T3:
- insig. marker in conventional medicine - isomer of T3 - can block T3 acting on receptors

if have deficiencies in selenium, vit D, zinc, mag, iron = RT3 instead of FT3 is formed

🔻 Possible Low Reasons: <20 is optimal

🔺 Possible High Reasons: chronic stress, high cortisol
chronic illness
nutrient deficiencies
liver/kidney dysfunction

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12
Q

What are key functional insights related to Free T3/T4 Ratio?

A

🔻 Possible Low Reasons: Starvation, severe calorie restriction
hashimotos, T4 Monotherapy
acute/chronic disease, stress, CVD

🔺 Possible High Reasons: >0.3 Graves disease, <0.3 DESRTUCTIVE THYROTOXICOSIS

arterial stiffness, cardiomeabolic dysfunction
insulin resistance, metabolic syndrome
thyrotoxicosis, thyroiditis, hyperythroidism, pituitary resistance to thyroid hormones

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13
Q

What are key functional insights related to Sodium?

A

🔹 Marker Description: Sodium is the most abundant extracellular cation, playing a key role in fluid balance, nerve transmission, and pH regulation.
- Helps maintain osmotic pressure and proper hydration levels.

  • Works antagonistically with potassium (K) to regulate cellular transport, nerve function, and muscle contraction.
  • Sodium & potassium balance is crucial—imbalances can affect adrenal function, cardiovascular health, and neurological function.
  • Na + K work antagonistically - want to look at ratio. Sodium is extracellular, while K is intracellular

🔻 Possible Low Reasons: overhydration (dilutes sodium levels)
hypofunction adrenal glands / adrenal fatigue / addisons disease (if Na:K ratio < 30)

medications: ACE inhibitors, tricylic antidepressants, NSAIDs, vasopressin, Sulfonylureas

acid imabalance
chronic, emotional stress
low stomach acid
oedema
hypothyroid

🔺 Possible High Reasons: dehydration (or poor qual water) , diaarhoea, vomiting
hyperfunction adrenal glands (if Na high but K low - Na:K ratio > 35)

polyuria (increased urination)
diabates, cushing diseas
medications: steroids, aspirin, NSAIDs,
excessive intake calcium, liquirice (increases sodium retention)

adrenal stress

📊 Patterns: Conv: 135-145 mmol/L

NA:K ratio

Adrenal hyperfunction: H sodium. L potassium , cholesterol, trigs.
Adrenal hyperfunction: L sodium. H potassium , cholesterol, trigs.

Metabolic Acidosis:
H CO2 (>28-30), L Cl (<100), K+ L or normal

Metabolic alkalosis:
L CO2 (<25), H Cl (>106), Anion Gao (>12), K+

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14
Q

What are key functional insights related to Potassium?

A

🔹 Marker Description: Potassium is the main intracellular cation, playing a crucial role in cellular function, nerve conduction, muscle contractions, and pH balance.
- Only 2-5% of total body potassium is found in blood, with the majority stored inside cells. (primarily intracellular)
- Works closely with sodium (Na) and magnesium (Mg) for electrolyte balance and cellular metabolism.
- magnesium + pottasium related - supp both together

4.2 is ideal

Deficiency (hypokalemia) or excess (hyperkalemia) can lead to cardiovascular, kidney, and nervous system dysfunction.

🔻 Possible Low Reasons: dehyradtion, diaarhoea, vomiting , diuretics

low Magnesium (low GGT, low Vit D, low K = low mag) - if mmag is low - potassium wont be normalised until mag resolved
poor diet / malabsorption
cardiac dysfunction, High BP
kidney dysfunction, diurertics, stones (increased excretion Na)
stress, stroke
post-meonpasual osteoperosis ((bone resorption releases K).

🔺 Possible High Reasons: electrolyte imbalance (Na/K ratio disruption).
kidney disease ((reduced excretion of K).
insulin resistance, diabetes
adrenal fatigue, adrenal hypofucntion, addisons disease

high BP

Risks:
- CVD patients with high potassium = incr all cause mortality risk (issues with HR, brachycardia, hypotension)
- hyperkalemia
tissue destruction

📊 Patterns: Conv: 3.5-5.5 mmol/L

low Magnesium (low GGT, low Vit D, low K = low mag) - if mag is low - potassium wont be normalised until mag resolved

Adrenal hyperfunction: H sodium. L potassium , cholesterol, trigs Na/K ratio.
Adrenal hyperfunction: H potassium , cholesterol, trigs, Na/K ratio. L sodium.

Metabolic acidosis: H Chloride, Pottasium, Anion Gap.
Metabolic alkalosis: L Chloride, Potassium.

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15
Q

What are key functional insights related to Soidum/potassium ratio?

A

🔹 Marker Description: The Na:K ratio is a key marker for adrenal health, hydration, and cellular function.
- A low Na:K ratio (<30) may indicate adrenal insufficiency (e.g., Addison’s disease).
- A high Na:K ratio (>35) may indicate adrenal hyperfunction (e.g., Cushing’s disease).

🔻 Possible Low Reasons: hypofunction adrenal glands (if Na:K ratio < 30)

  • Possible adrenal insufficiency (low aldosterone).
  • Overhydration, chronic stress, or electrolyte imbalance.
  • May cause fatigue, hypotension, and poor stress tolerance.

🔺 Possible High Reasons: >35: hyperfunction adrenal glands (if Na high but K low - Na:K ratio > 35)

  • Possible adrenal hyperfunction (high aldosterone or cortisol dominance).
  • Dehydration, hypertension, and kidney dysfunction risk.
  • Often linked to high sodium intake, stress, and metabolic disorders.
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16
Q

What are key functional insights related to Chloride?

A

🔹 Marker Description: Chloride is the main extracellular anion (70% neg charged anions),
- working alongside sodium and potassium to regulate fluid balance, acid-base homeostasis, HCl production and nervous system function.

  • Chloride levels usually correlate with sodium levels (NaCl is common in food sources).
  • Has an inverse relationship with bicarbonate (HCO3-), affecting acid-base balance.

Required for GABA and glycine regulation, influencing nervous system function.

  • Regulates Fluid & Electrolyte Balance (Works with sodium to maintain hydration and blood pressure.)
  • Supports Acid-Base Balance & CO2 Transport (Chloride is required for dissolving CO2 in the form of bicarbonate. High chloride = low bicarbonate, which can cause metabolic acidosis.) = respiratory health + neurological function
  • Affects Digestion & Stomach Acid Production (Low chloride = low stomach acid (hypochlorhydria), leading to poor digestion.)

healthiest at 102 mol/L (for overall mortality)

  • want 6-12g / day

🔻 Possible Low Reasons: adrenal fatigue ((low sodium often correlates with low chloride ).
high aldosterone
low stomach acid (hypochloydia)
metabolic acidosis (disrupts acid-base balance.)
prolonged/recent vomiting / fluid loss /diarrhoea
dehydation / excess sweating (eg ssauna)

low sodium , strict low-salt diet , excessive fluid intake

chornic lung disease, emphysema , COPD (Affects CO2/bicarbonate exchange.)
kidney diseases
medications (steroids, laatives, theophylline)

(pH too high, not enough H+ ions)

🔺 Possible High Reasons: dehydration (Cross check with high albumin)
metabolic acidosis , hyperventilation, mouth breathing (low bicarbonate)
high sodium (excessive salt intake)

adrenal hyperfunction, parathyroid overactivity , cortisol dominance
kidney disease/dysfunction

medications (excess aspirin intake , NSAIDs)

(Low pH, metabolic acidosis)

📊 Patterns: Conv: 95-110 mmol/L

Metabolic Acidosis:
H CO2 (>28-30), L Cl (<100), K+ L or normal

Metabolic alkalosis:
L CO2 (<25), H Cl (>106), Anion Gao (>12), K+

Metabolic alkalosis with B1 Deficiency - might need to supplement):
L CO2, H Anion Gap, L HCT, L Hb, L LDH, H Glucose. Low energy. Really hungover from drinking.

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17
Q

What are key functional insights related to Bicarbonate / CO2?

A

🔹 Marker Description: Bicarbonate is a crucial buffer produced during cellular respiration, helping to neutralize acids (e.g., lactic acid, hydrochloric acid) and maintain blood pH balance.

Bicarb = CO2 = marker cellulalr metabolism

Key marker for kidney function and acid-base homeostasis.
- Imbalances often reflect electrolyte disturbances, kidney dysfunction, or respiratory issues
- maintains blood pH by neutralising acids like HCl and lactic acid

Optimal levels:
28 mmol/L – lowest disease prevalence.
<23 mmol/L – highest all-cause mortality risk.produced during cellulalr respiration - helps maintain blood pH by neutralizing acids (lactic, hyrochloric acid)

Maintains Acid-Base Balance (Blood pH Regulation) (Buffers excess acids in the blood to prevent metabolic acidosis.Works with the lungs and kidneys to regulate CO₂ and pH balance. )
Assesses Kidney & Lung Function
- Produced by the kidneys → reflects renal filtration & reabsorption.
- Lungs regulate CO₂ levels, which impact bicarbonate levels.

Plays a Role in Electrolyte Balance
Low bicarbonate is often linked to potassium imbalances, as seen in vomiting, diarrhea, or chronic stress.

🔻 Possible Low Reasons: metabolic acidosis

dehydration , electrolyte loss (vomiting, diarrhoea)
metabolic acidosis (e.g., diabetic ketoacidosis, lactic acidosis).
hyperventilation

adrenal hypofunction/insufficiency
acid stress, low vit b1 (affecting cellular metabolism)
diabates,
poor kidney function (reduced acid excretion)

medications (excess aspirin intake)

acidic neuritis

🔺 Possible High Reasons: (Metabolic Alkalosis) - other symptoms from this eg vomiting etc

pH reg. issues (failure to remove CO2,, respiratory issues
- respiratory issues: astham ephysema, chronic lung-related problems,
- shallow breathing (eg mold / mycotoxicity)

electrolyte imbalance (pottasium deficiency) - eg due to diarrhoea, vomiting, stress

adrenal hyperfunction

also could be:
alkalinity
low stomach acid
fever

📊 Patterns: Conv: 20-32 mmol/L

Metabolic Acidosis:
H CO2 (>28-30), L Cl (<100), K+ L or normal

Metabolic alkalosis:
L CO2 (<25), H Cl (>106), Anion Gao (>12), K+

Metabolic alkalosis with B1 Deficiency - might need to supplement):
L CO2, H Anion Gap, L HCT, L Hb, L LDH, H Glucose. Low energy. Really hungover from drinking.

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18
Q

What are key functional insights related to Anion Gap?

A

🔹 Marker Description: calculated value that represents unmeasured ions in the bloodstream

marker to assess electrolyte balance, metabolic function, and acid-base status.
often a marker overlooked.

(Sodium + Potassium) – (Bicarbonate + Chloride) -
- NB Due to the small quantity of potassium in blood, some labs exclude it from the calculation.

want in 7-12 range

🔻 Possible Low Reasons: A low anion gap may signal electrolyte depletion, adrenal fatigue, or hypochlorhydria (low stomach acid).

low sodium (verhydration or adrenal fatigue)
hypochlorydia / low stomach acid) – Can lead to poor digestion & nutrient absorption.
emotional stress & chronic fatigue – Affecting electrolyte balance.

🔺 Possible High Reasons: A high anion gap indicates excess acid production or poor clearance (e.g., kidney disease, mitochondrial dysfunction). = metabolic acidosis

Kidney dysfunction – Reduced acid excretion leads to metabolic acidosis.
Electrolyte imbalances (low calcium, low magnesium) - diaarhoea
Gut dysbiosis & leaky gut – Affecting nutrient absorption & metabolic health.
Mitochondrial dysfunction – Impaired cellular energy production.
Diet high in processed foods & sugar (Contributing to metabolic acidosis.)
Diabetes (ketoacidosis)

📊 Patterns: Metabolic Acidosis:
H CO2 (>28-30), L Cl (<100), K+ L or normal

Metabolic alkalosis:
L CO2 (<25), H Cl (>106), Anion Gao (>12), K+

Metabolic alkalosis with B1 Deficiency - might need to supplement):
L CO2, H Anion Gap, L HCT, L Hb, L LDH, H Glucose. Low energy. Really hungover from drinking.

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19
Q

What are key functional insights related to Kidney Function?

A

🔻 Possible Low Reasons: Kidney activates Vit D - converts D2 > D3 - kidney dysfunction / lack = Vit D def

📊 Patterns: If kidney issues - check:
- blood pressure (sufficient Mag, Na/K ratio)
- adequate water intake
- NSAID use?
- AI suspicions? lupus, graves, RA can damage kidney
- Infections
- Check gut health - any pathogens, issues that can be adding?
- Diabetes - increases blood viscocity = harder work for kidneys
- Toxic load - increases filtration work required by kidneys

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20
Q

What are key functional insights related to Urea (BUN - blood urea nitrogen)?

A

🔹 Marker Description: Tested to investigate kidney function and general non-specific illness

Measures amount of nitrogen in the blood that comes from urea
- Represents availability of AAs to the body
– urea is a byproduct of protein metabolism, formed in the liver and excreted by the kidneys.
- Commonly used to assess kidney function, and general non-specific illness

High levels BUN = high breakdown = suggest impaired kidney function OR increased production in the liver

Context matters:
- BUN increases when kidneys aren’t filtering properly or protein breakdown is excessive (e.g., catabolic states, high protein intake).
- BUN decreases with low protein intake, liver dysfunction, or poor digestion/absorption.

🔻 Possible Low Reasons: Low protein intake (malnutrition, vegetarian/vegan diet without adequate protein). low HCl.
Low sodium .

Adrenal fatigue, (poor regulation of electrolyte balance) Chronic stress (increased cortisol can alter protein metabolism).

Liver dysfunction (reduced ability to produce urea).

Hypochlorhydria (low stomach acid) → poor protein breakdown → less nitrogen for urea production.

Pregnancy (due to increased plasma volume, which dilutes BUN)

🔺 Possible High Reasons: Kidney dysfunction (poor filtration, obstructed urine flow, dehydration, decreased blood to kidneys).

Liver dysfunction (increased urea production due to excessive protein breakdown)/overconsumption protien.

Electrolyte imbalances (low calcium, low magnesium).

Gut dysbiosis / SIBO (constipation → increased ammonium production → urea) constipation = methane produced = ammonium production = increased urea

Mitochondrial dysfunction (inefficient ATP production increases nitrogen waste).

High sugar/processed food intake (affects liver and kidney clearance).

📊 Patterns: Conv: 2.5-7.8mmol/L / 2.4-6 mg/dL

H Urea + H ALT ~ chronic methane SIBO

Heavy metal toxicity: H BUN, uric, acid, bilirubin, globulin. L Platelets.

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21
Q

What are key functional insights related to Uric Acid [Male]?

A

🔹 Marker Description: A byproduct of purine metabolism
- (purines are found in RNA, DNA, and certain foods).

Kidney marker (gives us good overview of kidney function)
- normally uric acid is dissolved in blood and excreted : 70% excreted through the kidneys, 30% via the microbiome.

Purine marker – Can indicate tissue breakdown, oxidative stress, or inflammation.
-purine marker = could indicate tissue damage

  • In the U.S., 1 in 5 people have high uric acid levels (predominantly males).
  • Clinical cut-off: >6 mg/dL increases risk of comorbidities.

Clinical Associations:
- Gout (“King’s Disease”) – Uric acid crystallization in joints.
- Microtoxicity, fatty liver disease, gut permeability issues.
- BUT also has anti-oxidant effects - protection in certain neurological conditions eg stroke, Parksinsons,

High SUA levels associated with:
- Cardiovascular risk (can increase ILs linked to cardiovascular issues).
- Insulin resistance (dysregulated insulin secretion and response – careful with carbohydrate intake).
- Systemic inflammation.

🔻 Possible Low Reasons: molybdenum deficiency (cofactor in purine metabolism).

Protein malabsorption (low stomach acid, poor digestion).
Vitamin B9 (folate) & B12 deficiency.
Copper deficiency (affects enzyme function).

Poor detoxification capacity.

protective factore against hyperucemia (increasrd coffee and vit c consumption, low fat dairy products, weight changes (weught gain or weight loss, estrogen nd porgerseterone ccombination therapy)

🔺 Possible High Reasons: Diet:
- Purine-rich foods (shellfish, crab, red meat, organ meats).
- High fructose intake (processed foods, sugary drinks).
- Alcohol consumption (especially beer).

Metabolic issues:
- Gout, obesity, kidney disease, insulin resistance, HTN.
- Liver/gallbladder dysfunction (reduced detoxification).
- Inflammation, oxidative stress, gut permeability issues (leaky gut)
- HTN, cardiovascular disease (CVD), circulatory disorders

Environmental & Toxin Load:
- Candida overgrowth, mold toxicity (often seen with high eosinophils, basophils, monocytes).
- Medications (aspirin, caffeine, diuretics).

Very high Vitamin D levels – Requires testing of active form (1,25-OH D), not just standard Vitamin D.

Other Risk Factors:
- Male, African American ethnicity,
sleep apnea,
renal failure, low water (dehydration), excessive exercise
high BMI, hypercholesterolemia, hypertriglyceridemia.
myerlorproliferative neoplassms)

📊 Patterns: Conv: 210-430 umol/L / 3.4-7 mg/dL

Molybdenum deficiency - L Uric Acid

Heavy metal toxicity: H BUN, uric, acid, bilirubin, globulin. L Platelets.

Renal disease: H creatinine, uric acid, phos., LDH , AST

Paracellular leaky gut: Primary patterns: H monocytes, H uric acid, H ALP, H ferritin
(secondary H insulin, basophils, eosinophils, CRP.
Tertiary: L GGT, AST (L or H), ALT (L or H).

Transcellular: H monocytes, H uric acid, L or H ALP, L ferritin, H CRP, H ESR
(secondary: H basophils, eosinophils, homocysteine, L total protein
tertiary: L GGT, L or H AST, L or H ALT)

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22
Q

What are key functional insights related to Uric Acid [Female]?

A

🔹 Marker Description: A byproduct of purine metabolism
- (purines are found in RNA, DNA, and certain foods).

Kidney marker (gives us good overview of kidney function)
- normally uric acid is dissolved in blood and excreted : 70% excreted through the kidneys, 30% via the microbiome.

Purine marker – Can indicate tissue breakdown, oxidative stress, or inflammation.
-purine marker = could indicate tissue damage

  • In the U.S., 1 in 5 people have high uric acid levels (predominantly males).
  • Clinical cut-off: >6 mg/dL increases risk of comorbidities.

Clinical Associations:
- Gout (“King’s Disease”) – Uric acid crystallization in joints.
- Microtoxicity, fatty liver disease, gut permeability issues.
- BUT also has anti-oxidant effects - protection in certain neurological conditions eg stroke, Parksinsons,

High SUA levels associated with:
- Cardiovascular risk (can increase ILs linked to cardiovascular issues).
- Insulin resistance (dysregulated insulin secretion and response – careful with carbohydrate intake).
- Systemic inflammation.

🔻 Possible Low Reasons: molybdenum deficiency (cofactor in purine metabolism).

Protein malabsorption (low stomach acid, poor digestion).
Vitamin B9 (folate) & B12 deficiency.
Copper deficiency (affects enzyme function).

Poor detoxification capacity.

protective factore against hyperucemia (increasrd coffee and vit c consumption, low fat dairy products, weight changes (weught gain or weight loss, estrogen nd porgerseterone ccombination therapy)

🔺 Possible High Reasons: Diet:
- Purine-rich foods (shellfish, crab, red meat, organ meats).
- High fructose intake (processed foods, sugary drinks).
- Alcohol consumption (especially beer).

Metabolic issues:
- Gout, obesity, kidney disease, insulin resistance, HTN.
- Liver/gallbladder dysfunction (reduced detoxification).
- Inflammation, oxidative stress, gut permeability issues (leaky gut)
- HTN, cardiovascular disease (CVD), circulatory disorders

Environmental & Toxin Load:
- Candida overgrowth, mold toxicity (often seen with high eosinophils, basophils, monocytes).
- Medications (aspirin, caffeine, diuretics).

Very high Vitamin D levels – Requires testing of active form (1,25-OH D), not just standard Vitamin D.

Other Risk Factors:
- Male, African American ethnicity,
sleep apnea,
renal failure, low water (dehydration), excessive exercise
high BMI, hypercholesterolemia, hypertriglyceridemia.
myerlorproliferative neoplassms)

📊 Patterns: Conv: 150-350 umol/L / 2.4-6 mg/dL

Molybdenum deficiency - L Uric Acid

Heavy metal toxicity: H BUN, uric, acid, bilirubin, globulin. L Platelets.

Renal disease: H creatinine, uric acid, phos., LDH , AST

Transcellular: H monocytes, H uric acid, L or H ALP, L ferritin, H CRP, H ESR
(secondary: H basophils, eosinophils, homocysteine, L total protein
tertiary: L GGT, L or H AST, L or H ALT)

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23
Q

What are key functional insights related to Creatinine [Male]?

A

🔹 Marker Description: Kidney filtration test / measure
- not a big hitting marker for kidney function - but look in combination

Creatinine is a waste product of muscle metabolism, excreted by the kidneys.
Produced by breakdown creatinine phsophate in muscles.

muscle mass must be taken into account -
Higher muscle mass = naturally higher creatinine (men typically > women).

24-hour urine collection is a more accurate assessment of kidney function than serum creatinine alone.

higher creatinine, higher Hb and higher Creatinine-Cystatin C ratio = decr risk mortality, cancer,

🔻 Possible Low Reasons: Diet:
- Malnutrition, low-protein intake, plant-based diets.
Caloric restriction,
- Vitamin D deficiency (affecting muscle & kidney health).

Impaired digestion (low stomach acid, malabsorption issues).

Muscle
- muscle wasting, sarcopenia.
- low muscle mass - eg - Under-exercising (muscle loss reduces creatinine levels).

check lean muscle mass - eg if elderly woman - might not be something to worry about
- overhydration?
- medications?

🔺 Possible High Reasons: Kidney dysfunction (reduced clearance leads to accumulation). = renal insuffienciency, urinary tract congestion, dehydration
Dehydration (affects kidney filtration).
Overexercising (muscle breakdown increases creatinine production).
Excess protein intake or creatine supplementation (supp can remain in bloods for 2-3 weeks post supp - might see in bloods still!)

Benign prostatic hyperplasia (BPH) (growth of prostate) – urinary congestion.

Take into account their muscle mass!!

📊 Patterns: Conv: 64-104 umol/L / 0.74-1.35 mg/dL

  • anemia? if kidney markers out of range and low RBC (due to low EPO)

Renal disease: H creatinine, uric acid, phos., LDH , AST

  • lower levels seen with higher WBC
  • higher creatinine, higher Hb, higher creatinine-Cystastin-C ratio = lower cancer risk, lower overall mortality
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24
Q

What are key functional insights related to Creatinine [Female]?

A

🔹 Marker Description: muscle mass must be taken into account - higher the muscle mass = higher the baseline level of creatinine . men typically have higher creatinine than women.
- also need diff level if athletes (high mucle)

24 hour urine collection can give a more accurate assesment of kidney function

🔻 Possible Low Reasons: Diet:
- Malnutrition, low-protein intake, plant-based diets.
Caloric restriction,
- Vitamin D deficiency (affecting muscle & kidney health).

Impaired digestion (low stomach acid, malabsorption issues).

Muscle
- muscle wasting, sarcopenia.
- Under-exercising (muscle loss reduces creatinine levels).

check lean muscle mass - eg if elderly woman - might not be something to worry about
- overhydration?
- medications?

🔺 Possible High Reasons: Kidney dysfunction (reduced clearance leads to accumulation). = renal insuffienciency, urinary tract congestion, kidney stones
Dehydration (affects kidney filtration).
Overexercising (muscle breakdown increases creatinine production, recent exertion eg just ran marathon).
Excess protein intake or creatine supplementation.

Medications - eg NSAIDs, antibiotics
Diabetes (incr. blood viscotiy/vol = kidneys have to work harder)

Take into account their muscle mass!!

📊 Patterns: Conv: 49-90 umol/L / 0.59-1.04 mg/dL

anemia? if kidney markers out of range and low RBC (due to low EPO)

Renal disease: H creatinine, uric acid, phos., LDH , AST

  • lower levels seen with higher WBC
  • higher creatinine, higher Hb, higher creatinine-Cystastin-C ratio = lower cancer risk, lower overall mortality
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25
What are key functional insights related to Creatine Kinase (CPK)?
🔹 Marker Description: Enzyme found in muscle cells, released into the blood when muscle tissue is damaged. Not specific for one area - but indicates tissue / muscle damage Important for energy production – catalyzes conversion of creatine into creatine phosphate (energy storage in muscle cells). - Levels naturally rise after training – peak around 24-72 hours post-exercise (important to consider when testing). - Athletes typically have 2x higher levels due to increased muscle turnover. - super important to consider recency of training (will be high after) - 3 days after training high levels - indicate muscle damage/diseases (MI/heart attack, muscular dystrohpy,trauma, rabdo) , Extreme exercise or overtraining /recent training Dr might order isoenzyme test - identifies areas of body with tissue damage (high CPK) - CPK1 - brain, CPK2 GI, CPK3 - muscles 🔻 Possible Low Reasons: Muscle atrophy / loss of muscle mass (e.g., aging, chronic illness, severe malnutrition). Low physical activity / sedentary lifestyle. Hyperthyroidism (increased metabolism, breakdown of muscle enzymes). 🔺 Possible High Reasons: - Recent training (<3 days prior to test - in 30% people 3 days training not enough to rest) - Athletes (naturally higher baseline). Muscle trauma or injury, stress fractures etc Severe infections or inflammatory conditions. Heart attack./ MI / Stroke Hypothyroidism. Concussion Medication side effects (e.g., statins, also B Blockers, Antivirals) Pathogens, viruses Coeliac cocaine - within 2 weeks might still incr. CPK Dr might order isoenzyme test - identifies areas of body with tissue damage (high CPK) - CPK1 - brain, CPK2 GI, CPK3 - muscles 📊 Patterns: other markers for tissue damage - ESR, CRP - AST, ALT - liver damage? - Antibodies
26
What are key functional insights related to eGFR?
🔹 Marker Description: Estimated Glomerular Filtration Rate . Ccalculation to estimates kidney function – how well kidneys filter small particles (Eg creatinine) from the blood. - Not highly accurate, as it’s calculated based on age, gender, and creatinine levels. also drastic differnces in diets (equation not as reflective), Black individuals tend to have higher eGFR than white individuals due to muscle mass differences, etc. - 90% of the time, it’s within 30% accuracy – but 10% of cases can be completely off! - More accurate alternative: 24-hour urine creatinine clearance test (still some limitations). Clinical Significance: eGFR <60 mL/min → Impaired kidney function. 🔻 Possible Low Reasons: Kidney dysfunction/disease (reduced filtration ability). Dehydration (affects blood volume & filtration rate). Vitamin D & magnesium deficiency (affecting kidney metabolism). Adrenal hypofunction (low aldosterone & cortisol levels). Mycotoxin exposure (e.g., mold) – slows kidney clearance rates. correlation with high ocrotoxin (ext. slow clearance rate in kidneys ) 📊 Patterns: Conv: >90 ml.min / >60 ml/min/1.73m
27
What are key functional insights related to Bilirubin (Total)?
🔹 Marker Description: A yellow pigment formed from RBC breakdown Processed in the liver and supports antioxidant and methylation pathways. Tissue protector, antixodiant and antiinflammatory agent High = impaired bile flow or RBC fragility OR liver ability to remove bilirubin is imparied Symptoms like dry skin, red bumps on elbow, tiny bumps on upper arm may indicate fatty acid deficinecy - may reflect bile/lipid digestion issues. Functional range prefers upper end (~2 mg/dL). cytoprotector 🔻 Possible Low Reasons: low levels RBC breakdown/underproduction cardiac pathology (eg angina, CAD , atheroscleoris, inflammation) spleen insuffiency high levels vit C (neg foodback loop stops bilirubin forming approrpiately) 🔺 Possible High Reasons: jaundice - eg new born babies biliary stasis (thickening of bile) , bilary tract obstruction ox. stress thymus dysfunction, high eostrogen liver dysnfunction, gilbert syndrome (P450 enzymes issues - cant convert bilirubin to direct), impared phase 2 liver detoxification (imparied glucaronidation / overload of sulfating glycination) carb resrticting, fasting extreme physical exertion insulin resistance def in B3, B6, mag, iron red blood cel fragility (eg anemia) methylation newborn babies 📊 Patterns: Conv:3-17umol/L / 0.1-1,2 mg/dL
28
What are key functional insights related to Bilirubin (Direct)?
🔹 Marker Description: A yellow pigment formed from RBC breakdown Processed in the liver and supports antioxidant and methylation pathways. Tissue protector, antixodiant and antiinflammatory agent High = impaired bile flow or RBC fragility OR liver ability to remove bilirubin is imparied Symptoms like dry skin, red bumps on elbow, tiny bumps on upper arm may indicate fatty acid deficinecy - may reflect bile/lipid digestion issues. Functional range prefers upper end (~2 mg/dL). cytoprotector 🔻 Possible Low Reasons: spleen insufficiency cardiac pathology (CAD, angina, atherosclerosis) h pylori (infected patients 49% more likely to have low direct bilirubin AND higher LDL) 🔺 Possible High Reasons: biliary stress. obstruction, liver dysfunction gilberts - disruption to ? gene - bilirubin naturally high impaired glucoronidation (gilberts) metabolic syndrom, obesity , BMI, high triglcerides, IR, dyslepediama, metabolic syndrome, ox stress thymus dysfunction vit deficiencies - B3, B6, mag, iron 📊 Patterns: L HDL and H LDL often seen in H Pylori
29
What are key functional insights related to Bilirubin (Indirect)?
🔹 Marker Description: A yellow pigment formed from RBC breakdown Processed in the liver and supports antioxidant and methylation pathways. Tissue protector, antixodiant and antiinflammatory agent High = impaired bile flow or RBC fragility OR liver ability to remove bilirubin is imparied Symptoms like dry skin, red bumps on elbow, tiny bumps on upper arm may indicate fatty acid deficinecy - may reflect bile/lipid digestion issues. Functional range prefers upper end (~2 mg/dL). cytoprotector 🔻 Possible Low Reasons: spleen insufficiency cardiac pathology (CAD, angina, atherosclerosis) h pylori (infected patients 49% more likely to have low direct bilirubin AND higher LDL) 🔺 Possible High Reasons: biliary stress. obstruction, liver dysfunction gilberts - disruption to ? gene - bilirubin naturally high impaired glucoronidation (gilberts) metabolic syndrom, obesity , BMI, high triglcerides, IR, dyslepediama, metabolic syndrome, ox stress thymus dysfunction vit deficiencies - B3, B6, mag, iron
30
What are key functional insights related to Alk Phosphatase (ALP)?
🔹 Marker Description: removes phosphate from a range of molecules - present in all tissues in body - but largets conc. in liver , bile ducts... Phosphatase = chop compounds and put on phospahtes . Zinc-dependant An enzyme with multiple isoenzymes, acting as a "family" with different functions: ALP1 – Liver. ALP2 – Bile ducts, kidneys, bones. ALP3 – Intestines. (real short T1/2 - needs to protect) ALP4 – Placenta (in pregnancy). responds best in alkaline environemnt ALP activated by mag and zinc - low zinc/ mag might actually see slight rise ALP after supplementation produced during periods of rapid cellular proliferation and repair - typically seen in response to liver disease, normal bone growth, low vit Vit D , leaky gut Roles and Functions: - Dephosphorylation of lipopolysaccharides (LPS) – helps regulate immune responses and prevents systemic toxicity = protective. - Needs a high turnover for it to work correctly and regulate LPS = prevent body going into systemic / toxic shock - Essential for bone turnover and growth – involved in calcium and phosphate metabolism. - Supports gut integrity – modulates tight junction proteins (occludin, ZO-1).= help reduce gut permeability (leaky gut) and systemic inflammation. low ALP - impair gut lining. Required for epithelial cell health = low ALP = weakened cells = not as resiliant against ox stress/chronic inflammation. - Systemic inflammation (deactives LPS) - liver and bilary function - high ALP inidctae liver / gallbladder diease Fasting recommended for testing – ALP can be temporarily elevated post-meal. > 80 not good for health outcomes - at this range will probably start to see other markers start to flag up = Elevated ALP may indicate liver disease, bone turnover (fracture healing, Paget’s disease), low vitamin D, or gut permeability. - Low ALP is often linked to zinc deficiency, hypothyroidism, or poor liver function. 🔻 Possible Low Reasons: Zinc deficiency - first thing you will think! (zinc dependant enzyme) - want to look wgy low zinc? (look at stomach acid. pattern: low total prottein, low WBC and low ALP = zinc def.) also check LH/testosterone?) B6 (pattern - low ALT, low AST, Low MCV, high prolactin) magnesium deficiency, low stomach acid, mental health (low b6 could mean low NTs eg dopamin), low immunity (bc low zinc + stomach acid), poor immunity transcellular permeability (<40U/L) oral contraceptive pill (causes zinc deficiency) wilsons disease 🔺 Possible High Reasons: paracellular permability (>80, plus high monocytes, uric acid, ferritin) bile issues - eg blocked, inflamed bile guts, gallstones, copper, boron, vit D deficiency pregancy (ISO enzyme for involved with placenta) liver disease (if both ALP AND GGT high - likley liver ) bone growth, elevated osteoblast activity (eg teenagers - diff range for teens) tumours (liver or bone cancer) HSV (herpes) falesy elevated from eating / not fasted 📊 Patterns: Conv:30-130 U/L if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Leaky gut: H (>80) ALP and H Monocytes (also H Uric Acid, ferritin) ~ Paracellular leaky gut: Primary patterns: H monocytes, H uric acid, H ALP, H ferritin (secondary H insulin, basophils, eosinophils, CRP. Tertiary: L GGT, AST (L or H), ALT (L or H). Transcellular: H monocytes, H uric acid, L or H ALP, L ferritin, H CRP, H ESR (secondary: H basophils, eosinophils, homocysteine, L total protein tertiary: L GGT, L or H AST, L or H ALT) Vit C deficiency: L Albumin, L Hematocrit, L Hb, L MCH, L MCHC, L Iron, H MCV, H ALP, H Fibrinogen (>350) Zinc deficiency: if ALP <40 - check for zinc deficiency. Also might see L ALP, L WBC. B6 deficiency: L ALT, AST, MCV. H prolactin. biliary stasis/insufficiency: H ALP, Cholesterol Intra--hepatic bilary obstruction: H GGT, ALP, LDH, BILIRUBIN Extra-hepatic bilary obstruction: H ALP, LDH, >85 GGT Liver dysfunction,: H ALT, AST, ALP, Bilirubin, LDH, ferritin, iron. L Cholesterol, Trigs, BUN, urate, albumin. Stress - check for L ALP, LH
31
What are key functional insights related to ALT (SGPT) [Male]?
🔹 Marker Description: ALT = LIVER can sometimes be referred to as SGPT (american bloodwork) , alanine transaminase Transaminase = take amine groups and put on/off vit B6-dependant enzyme - key involved in krebs cycle + AA metabolism (Aerobic) - breakdiwn of alanine into alpha-ketoglutarate (aerobic energy production) Primarily found in liver cells but also present in muscle and kidney tissue. marker of cellular damage and membrane breakdown , dont want this outside of single digits - best 13-17. (17-20??) Naturally a bit lower than AST Marker of Liver Function & Cellular Damage: - Marks cellular / membrane breakdown, disrupted gut-live axis Detoxification & Ammonia Regulation: - excess ammonia can elevate ALT levels. - Impaired ALT function may contribute to toxic metabolite accumulation, impacting energy production and neurological function. - ammonia detoxification - high ammonium = high ALT - helps shuttle nitrogen from muscle to liver for conversion into urea - high levels of ammonia might also see smelling of urine, sweat T1/2 17 hours (ALT 47 hours) - levels fall faster than ALT Production of glutamate (excitatory NT) if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Key Considerations: - Slight elevations (<40 U/L) may be benign, but persistent increases warrant further investigation. - Significant ALT elevation (>100 U/L) suggests more severe liver dysfunction. - Assess alongside AST, GGT, ALP, bilirubin, and ammonia levels for a full picture. ALT has a much bigger 1/2 life than AST - 47-57 days. AST should be slightly lower than ALT. 🔻 Possible Low Reasons: vit B6 defieicny (PLP - active form og B6) krebs cycle issues UTI , fatty liver - early stages gall bladder / bilary issues, medications, alcohol, NAFLD, chrones, endotoxins, GN bacteria (can look to see if they are stressed, eating sulphate-rich foods, low gluthathione? low stomach acid?) low ALT lead indicator of PSP deficiency risk of dementia (incr. B amyloid) 🔺 Possible High Reasons: excessive muscle breakdown + training dysfunctions in liver, fatty liver, cirrhosis (only in late stages - normally drop at start) bilary tract obstruction, alcohol , obesity if ALT > 31 - investigate fatty liver disesase transcellular permeability (>25 U/L), IBD, celiac, chroncs, UC, endotoxemia heavy metals (lead) diabetes, medication (aspirin, antibiotics, statins, antipsychotics) viral infections (herpes, ononucleosis) choline deficiency age - increases ALT excess ammonia* (animal studies) - 📊 Patterns: conv: 5-40 (EU) / 7-56 U/L (US) if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Vit B6 deficiency: L ALT, AST, GGT, MCV, MCH, MCHC. H Homocysteine.
32
What are key functional insights related to ALT (SGPT) [Female]?
🔹 Marker Description: ALT = LIVER (Alanine Transaminase) can sometimes be referred to as SGPT (american bloodwork) vit B6-dependant enzyme - involved in krebs cycle + AA metabolism Primarily found in liver cells but also present in muscle and kidney tissue. marker of cellular damage and membrane breakdown , dont want this outside of single digits - best 13-17. Naturally a bit lower than AST Marker of Liver Function & Cellular Damage: - Marks cellular / membrane breakdown, disrupted gut-live axis Detoxification & Ammonia Regulation: - excess ammonia can elevate ALT levels. - Impaired ALT function may contribute to toxic metabolite accumulation, impacting energy production and neurological function. - ammonia detoxification - high ammonium = high ALT - helps shuttle nitrogen from muscle to liver for conversion into urea - high levels of ammonia might also see smelling of urine, sweat T1/2 17 hours (ALT 47 hours) - levels fall faster than ALT Production of glutamate (excitatory NT) if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Key Considerations: - Slight elevations (<40 U/L) may be benign, but persistent increases warrant further investigation. - Significant ALT elevation (>100 U/L) suggests more severe liver dysfunction. - Assess alongside AST, GGT, ALP, bilirubin, and ammonia levels for a full picture. ALT has a much bigger 1/2 life than AST - 47-57 days. AST should be slightly lower than ALT. 🔻 Possible Low Reasons: malabsorption, chronc inflammation - low albumin = Seriously compromised absorptive state low stomach acid transcellular permeability acute infection impared protein syntheiss , vit C deficiency kidney dusfunction , liver dysfunction 🔺 Possible High Reasons: dysfunctions in liver, fatty liver, cirrhosis (only in late stages - normally drop at start) bilary tract obstruction, alcohol transcellular permeability (>25 U/L) heavy metals (lead) coeliac, chronic, colitis, diabetes, obesity medication (aspirin, antibiotics, statins, antipsychotics) viral infections (herpes, ononucleosis) choline deficiency age - increases ALT - menopause if ALT > 31 - investigate fatty liver disesase metabolic syndrom - 60% more likely when ALT 16-21, 2.6x more likely when 22-31 📊 Patterns: conv: 5-40 (EU) / 7-56 U/L (US) if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Vit B6 deficiency: L ALT, AST, GGT, MCV, MCH, MCHC. H Homocysteine.
33
What are key functional insights related to AST (SGOT) [Male]?
🔹 Marker Description: sometimes referred to as SGOT (america) - Aspartate Transaminase outSide liver (still has implications in liver - but also outside eg biliary tree, cardivascular etc) not speciifc to liver - rises in response to gerneral tissue damage (still implicated in liver - but also have implications with cardiobascualr, cardia health, etc) dont want this outside of single digits - best 16-26. (20-26??) Naturally want a bit higher than ALT. similar to ALT - but not speicifc to liver - also B6 dependnant enzyme involved in krebs cycle - key for biosyntheis and breakdown of AAs s(alpha-ketogluterate into glutamate and oxaloacetate) - if def. = lower energy/fatigue T1/2 17 hours (ALT 47 hours) - levels fall faster than ALT. AST should be higher than ALT. . if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas 🔻 Possible Low Reasons: B6 defiicnecy (pattern - low ALT, low AST, Low MCV, high prolactin) 🔺 Possible High Reasons: check for dehydration / recent training dysfunctions outside of liver / bilary tree , as well as liver cell damage, liver dynsfunction, alchol CHD , CAD celiac, chrons, colitis pregancy herbal medicines (echinacera, velerian) viral infection (HSV1,2, EBV etc) medications - aspirin, ABs (sign of endotoxemia if jumps up super high when take ABs), statins,antipscyhotics 📊 Patterns: conv: 5-40 (EU) / 7-56 US if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Vit B6 deficiency: L ALT, AST, GGT, MCV, MCH, MCHC. H Homocysteine. Renal disease: H creatinine, uric acid, phos., LDH , AST
34
What are key functional insights related to AST (SGOT) [Female]?
🔹 Marker Description: sometimes referred to as SGOT (america) outSide liver (still has implications in liver - but also outside eg biliary tree, cardivascular etc) not speciifc to liver - rises in response to gerneral tissue damage (still implicated in liver - but also have implications with cardiobascualr, cardia health, etc) dont want this outside of single digits - best 16-26. (20-26??) Naturally want a bit higher than ALT. similar to ALT - but not speicifc to liver - also B6 dependnant enzyme involved in krebs cycle - key for biosyntheis and breakdown of AAs s(alpha-ketogluterate into glutamate and oxaloacetate) - if def. = lower energy/fatigue T1/2 17 hours (ALT 47 hours) - levels fall faster than ALT. AST should be higher than ALT. if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas 🔻 Possible Low Reasons: Low B vits - ecsp. B6 defiicnecy (pattern - low ALT, low AST, Low MCV, high prolactin) 🔺 Possible High Reasons: check for dehydration / recent training dysfunctions outside of liver / bilary tree , as well as liver cell damage, liver dynsfunction, alchol CHD , CAD celiac, chrons, colitis pregancy herbal medicines (echinacera, velerian) viral infection (HSV1,2, EBV etc) medications - aspirin, ABs (sign of endotoxemia if jumps up super high when take ABs), statins,antipscyhotics 📊 Patterns: conv: 5-40 (EU) / 7-56 US if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Vit B6 deficiency: L ALT, AST, GGT, MCV, MCH, MCHC. H Homocysteine. Renal disease: H creatinine, uric acid, phos., LDH , AST
35
What are key functional insights related to AST:ALT (AAR)?
🔹 Marker Description: T1/2 17 hours (ALT 47 hours) - levels fall faster than ALT - so if someone trained 2 days prior - ALT may be higher as AST levels fall quicker 🔺 Possible High Reasons: alcholoic hepatitis, cirrhosis (>2 ratio in 70% patients with A.H and cirrhosis) alcholoic liver disease (>3 highly suggestive of alcholoic liver disease ) low ALT lead indicator of PSP deficiency 📊 Patterns: if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas
36
What are key functional insights related to GGT (GGPT)?
🔹 Marker Description: gamma-glutamyl transferase enzyme required for the synthesis and degradation (recylcing, production ) of glutathione, the body’s master antioxidant. = surrogate marker for oxidative stress and membrane dysfunction. - most abundant in luminar surfaces of cells - where secretions happen. this is where theres high likelihood for ox stress - a lot resides within mitochondria - if see high - look / mindful of mitochondria less of a standalone marker of liver function that AST and ALT - reflective of inflammation - but not hyper acute Oxidative Stress & Glutathione Balance / Membrane dysfunction Indicative of oxidative stress, higher need for glutathione, poor cellular membrane health Indicates weakened transcellular pathways Liver & Detoxification Function: - can indicate issues with liver - but not good as diagnostic marker just by itself (look at patterns) - GGT is elevated in liver disease, but it is not specific – it should be interpreted with other markers (ALT, AST, ALP). Cardiovascular & Metabolic Implications: - Elevated GGT is linked to increased cardiovascular disease risk, metabolic syndrome, and insulin resistance. - Plays a role in fat metabolism and cholesterol transport. if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas - GGT alone is not diagnostic but provides insight into oxidative stress and liver function. - Ideal levels are <30 U/L in men and <20 U/L in women. - Should be interpreted alongside ALT, AST, and liver ultrasound if needed. 🔻 Possible Low Reasons: gluthathione issue mag (low GGT, low Vit D, low K = low mag) deficiency vit B6 deficiney (or also Vit A, zinc) impaired protein utilisation impared liver detoxification 🔺 Possible High Reasons: indicates oxidative stress (higher need for glutathione) liver cell damage, bilary obstruction . stasis, alcohol bile obstruction / stasis , gallstones pancreaitis transcellular permeability (>28 U/L) imapierd gluthathione synthesis excess iron, mercury toxicity viral infection (EBV, HSE??.....) medical conditions (incld. brain tumours, pancreatitis, kidney, prostatic, cardiac diseases) - high GGT = incr. risk sudden cardiac death heart issues medications - eg parkinsons medication (levodopa) - if GGT is vvvv high- - stroke / parkinsons meditcation / polypharmacy can cause elevation - see drastic increase when they start taking if GGT jump 📊 Patterns: conv: 9-48 U/L if AST > ALT and GGT - area of involvement outside liver/bilary tree (eg heart, kidney , lungs) . Should be slightly higher than ALT. if ALT > AST and ALT - area of involvement may be in liver if GGT> ALT and AST - area of involvement may be in bilary tree / pancreas Vit B6 deficiency: L ALT, AST, GGT, MCV, MCH, MCHC. H Homocysteine. Mag deficiency: L Uric Acid
37
What are key functional insights related to Protein (Total)?
🔹 Marker Description: rough sum = albunin + globulin = total protein total of albumin and globulin absorbed from diet AND formed in body (from AAs) - Gen overview of kidney and liver function, nutrional status 2 proteins that make up total protein : Cluster of globulins (1/2 life 7-23 days) Albumin (½ life 20 days) essential for detox (AAs derived from protein) also primary ingrediant of immune cells 🔻 Possible Low Reasons: protein factors: Poor protein intake / malabsorb., raw food diet, malnutrion, low stomach acid transcellular permeability (ecsp. if low albumin) chronc inflammation zinc deficiency (required for stomach acid) liver disease estensive burns connective tissue breakdown 🔺 Possible High Reasons: dehydration (check against albumin) - high Albumin + high protein liver issue adrenal fatigue chronic inflammatin, chronic infection (infection increases globulin(s) = incr. protein) liver / gallbladder dysnfunction RA, diabetes 📊 Patterns: Conv: 60-80 g/L / 6.3-8.2 g/dL Zinc def: L total protein, low WBC and low ALP. Also look at stomach HCl
38
What are key functional insights related to Albumin?
🔹 Marker Description: synthesised in liver plays important role in moving small mols through the blood (eg bilirubin, calc, medications) + prevents fluid leaking into tissues (maintains osmotic presssure / homeostasis) - water soluble =makes lipids solvent in blood/fluids = indictaes potential of body to transport nutrients, mols, fat etc around body antioxidant - major buffer against metabolic acidosis - trap for ROS represents amount of leeway body has against disease - major buffer against acidosis binding!! binds to almost all drugs/mols - eg FAs, thyroxine, almost all known drugs bind helps bind and transport mols around body part of super family - lndicates bodies ability to transport mols in body - includes VDP low albumin - indicates chronic inflammation + malabsorption = seriously compromised absorptive state Protein leakage through damage membranes Reduced liver production Increased inflammation Malabsorption mainly lost from intravscaulr space by - produce a lot - but also lose a lot!! need to be super careful of glycation - eg if someone has increased glycation (eg HBA1C) and have high albumin can have risk factors eg epilepsy etc etc - blood tissue barriers - parenchyma - post traumatic eplipelsy (if someone has neurodegenerative disease - want to be super careful of glucgation end prooducts - eg increase polyphenols etc toa ctively reduce advanced glycation end products) (one of first identified proteins - noted bubbled in urine with liver issues - due to albumin) anatomical structure - in shape of heart! <3 🔻 Possible Low Reasons: malabsorption, chronc inflammation - low albumin = Seriously compromised absorptive state low stomach acid transcellular permeability acute infection impared protein syntheiss , vit C deficiency kidney dusfunction , liver dysfunction ox stress malabsoprtion eg chrons, ceoliac, IBD 🔺 Possible High Reasons: dehydration anabolic steroids, insulin, growth hormone 📊 Patterns: Conv:33-50g/L Vit C deficiency: L Albumin, L Hematocrit, L Hb, L MCH, L MCHC, L Iron, H MCV, H ALP, H Fibrinogen (>350)
39
What are key functional insights related to Globulin?
🔹 Marker Description: Globulin = generic term used to describe set of 60 proteins Glovulins are ABs (=fight infections) - low = immunocompramised state - term used to desribe set of 60 proteins synthesised in response to inflam, toxins, infection and required for AB Production 🔻 Possible Low Reasons: immunocompramised , immune insufficiency are they sick? digestive dysfunction / inflammation eg IBD 🔺 Possible High Reasons: low stomach acid ox stress, chronic inflammation/ infection liver cell damage heavy metal toxicity possibly even autoimmune disease 📊 Patterns: Conv: 20-35 g/L / 6.3-8.2 g/dL Heavy metal toxicity: H BUN, uric, acid, bilirubin, globulin. L Platelets.
40
What are key functional insights related to A/G Ratio?
🔹 Marker Description: marker of liver function, immune activity, and overall protein balance - 🔻 Possible Low Reasons: immune or inflammatory response (<1.5 - immune activation) chronic inflammation /chronic infections - increased globulin levels liver disease (less albumin production) kidney disease (albumin loss) 🔺 Possible High Reasons: dehydration or high protein intake (overproduction of albumin) Immune suppresion (low globulin levels)
41
What are key functional insights related to LDH?
🔹 Marker Description: intracellular enzyme releaed during cell injury - suggests epithelial cells are compormised invollved in conversion of pyruvate to lactate found in almost all cells v good marker for tumour growth - assoicated with 48 diseases 🔻 Possible Low Reasons: hypoglcemia/not eating a lot / issues with blood sugar deficiency B3, 📊 Patterns: Conv: 120-250 U/L (EU) / 140-280 U/L (US)
42
What are key functional insights related to Cholesterol?
🔹 Marker Description: Roles of cholesterol: 1. Precursor to steroid hormone production 2. Precursor to endogenous vit D production (activated by UVB radiation on skin) 3. Present in structure of cel membranes 4. Requirement for bile production ~70-90% hcolesterol is due to endogenous production, only 10-30% from diertary sources - produced in liver - product of glucose metabolism (HMG-CoA reductase pathway) -HMG CoA reductase upregulated in presence of high blood sugar - moderated by insulin and glucagon <5 actually shows greater risk of all-cause mortality (north korea study) 🔻 Possible Low Reasons: liver/ bilary dysfunction malnutrition, low fat diet, managase deficiency adrenal hyperfucntion, hyperthyroidism, ox stress, hevay metal toxicity , autoimme disorders schizophrenia 🔺 Possible High Reasons: inflammation, metabolic sydnrom (diabtes) insulin resistance fatty liver / bilary stasis, poor metabolism fats hypothyroidism cardiovascualr disease, atherocloserosis, (likely see elev. homocysteine) chronic infection h/pylori , chronic vacterial and viral infections, MS vit d deficiency familial hypercholesterolemia 📊 Patterns: Conv: <5 mmol/L / 125-200 mg/dL - lower all cause mortality when cholesterol above conv. range - even more so for women. Better range: 5-6 M /5-6.5 F Atherosclerosis: H Trig, H LDL, H URic Acid. L HDL. Metabolic Syndrom: H Cholesterol, Trig, Insulin, Glucose, HBA1C. L HDL. Adrenal hyperfunction: H sodium. L potassium , cholesterol, trigs. Adrenal hyperfunction: L sodium. H potassium , cholesterol, trigs.
43
What are key functional insights related to Triglycerides?
🔹 Marker Description: Type of fat in blood that serve as major energy storage - involved in livers conversion of fat - blood and vice versa when body becomes more efficient and starts to burn fat - tricglycerides can often increase in short time (in overweight indiviudals losing weight) - as trigs are released from fat cells 🔻 Possible Low Reasons: malabsorption, low cal /fat diet diet fat absorption, low bile (gallbladder issues?), liver, bilary dusfunction hyperthyroidism, adrenal hyperfunction autoimmune disorders medications (statins, metformin, high dose niacin) 🔺 Possible High Reasons: obesity, early stage hyperglycemia, metabolic syndrome, fatty liver, T2D, IR, CVD, atherosclerosis, stroke h pylori hypothyroidism hyper caloric diet, smoking, alcohol medications: corticosteroids, beta blickers, HIV medications, oestrogen and bile acid sequestrants 📊 Patterns: Conv: <1.7 mmol/L / <150 mg/dL Adrenal hyperfunction: H sodium. L potassium , cholesterol, trigs. Adrenal hyperfunction: L sodium. H potassium , cholesterol, trigs.
44
What are key functional insights related to HDL Cholesterol?
🔹 Marker Description: only lioprotein involved in removal of fat from cells (incl. artery walls) - remove LDL cholesterol and triglycerides via liver and -also used by body for production of prostoglandins (protective) -distribute fat sol vits, and antixodiants - support prostaglandin production (end products of omegas/antiinflam markers -PGE1/3 anti , PGE2 - rel inflam) ideally HDL should be >40% of total cholesterol 🔻 Possible Low Reasons: Obesity, fatty liver, metabolic sundrome, CVD, atherosclerosis raw food diet high trans fat acid consumption ox stress, heavy metals, high andorgens hyperthyroidism h pylori lack of exercise <1 -possible autoimmunity 🔺 Possible High Reasons: autoimmune disorders heavy metal toxicity (along with low platelet count, high mean platelet vol, Chol/HDL ratio<3) normal-high: -god detoxiifcation protential low carb, high-protein diet. intense physical activity. 📊 Patterns: Conv: M: >1 mmol/L / >40 mg/dL, F: >1.2 mmol/L / >50 mg/dL <1 -possible autoimmunity heavy metal toxicity (along with low platelet count, high mean platelet vol, Chol/HDL ratio<3)
45
What are key functional insights related to LDL Cholesterol?
🔹 Marker Description: LDL delivers cholesterol to cells, make and repair cell membranes, synthesis steroid hormones, convert sunlight into vit D Can accumulate in artery walls = atherosclerosis - good indicator of atheroclerosis further assess LDL by measuring actual cholesterol particle size (apo-A and apo-B results) -size of particles mroe closely assoicated with risk of CVD larger LDL particle size = more protective. LDL size can be increased by diet and exercise. 🔻 Possible Low Reasons: higher susceptability to infections, (less endotoxin-neutrilising capacity of LDL - normally bind to endotoxins of gram neg bacteria) - candida inflammation, depression, cancer, anxiety, memory impariment low LDL in preg often assoicated with premature birth and low birth weight impact on testosterone levels 🔺 Possible High Reasons: metabolic syndrome, ox stress impaired glucose metabolism associated with higher risk: CVD, atherosclerosis, hyperlipidemia, hypothyroidism h . pylori, mycotoxins, endotoxins liver dysfunction 📊 Patterns: Conv: <3 mmol/L / <100 mg/dL Hihger LDL had lower risks hypercholesteroemia than statins! Candida/infection - if LDL high - more acute/recent candida, if LDL low - more chronic candida
46
What are key functional insights related to VLDL Cholesterol?
🔹 Marker Description: transports trigs from liver to tissues - mainly assoictaed with trig transport - can temp increase LDL as mobilises from arteries 🔻 Possible Low Reasons: increased physical activity hyperthyroidism , chronic stress severe calorie resrtiction,malabsorption deficiencies omega 3, b6, b9, b12, magensium, imbalanced omega 3:6 ratio antioxidant deficinecy 🔺 Possible High Reasons: insulin resistance, metabolic syndrome, obesity, chronic inflammation, poor glycemic control elevate triglycerides liver / kidney dysfunction 📊 Patterns: Conv: 1.2-1.7 mmol/L / 2-30 mg/dL
47
What are key functional insights related to Triglycerides/HDL Ratio?
🔹 Marker Description: good marker of insulin resistance + predictor of heart disease should be < 2:1, preferably around 1:1
48
What are key functional insights related to Total Cholesterol/HDL Ratio?
🔹 Marker Description: predictor of heart disease risk should be >0.24 ideally >40%
49
What are key functional insights related to Lipase?
🔹 Marker Description: digestive enzyme primarily produced by the pancreas, but also by the mouth and stomach. It is secreted into the duodenum (first section of the small intestine) to help digest dietary fats. Often measured in blood tests to assess pancreatic function and detect issues like pancreatitis or exocrine pancreatic insufficiency (EPI). Essential for fat breakdown and absorption of fatty acids. - Works with bile (from the liver/gallbladder) to break down triglycerides into free fatty acids and glycerol, which can be absorbed and used for energy. - Crucial for absorbing fat-soluble vitamins (A, D, E, K). 🔻 Possible Low Reasons: diabates, metabolic syndroms (high BP, high cholesterol, diff loosing weight , varicose veins ) pancreatic insufficiency poor fat digestion bile dysfunction (gallbladder, liver disease) ceoliac, chrons disease rasacea medicatiosn - codeine, indomerthaic, morphine 🔺 Possible High Reasons: v.high: acute pancreatitis (2-5x normal range - massively high), pancreatic cancer gallbladder dysfunction kidney disease salivary gland inflammation (saliva stim. release lipase) [check if bubbles under tongue] peptic ulcer blocked gallbladder
50
What blood marker patterns are indicative of Diabetes?
Diabetes: HbA1c >6.5%, Glucose >125 mg/dL Pre-Diabetes: HbA1c 5.7-6.4%, Glucose 100-125 mg/dL
51
What blood pattern is typical of Atherosclerosis?
H Triglycerides, H LDL, H Uric Acid, L HDL
52
What blood markers suggest Metabolic Syndrome?
H Cholesterol, Triglycerides, Insulin, Glucose, HbA1c; L HDL
53
What lab pattern might suggest Reactive Hypoglycemia?
L Glucose, L LDH, HbA1c <3%
54
How does pancreatic cell damage appear in bloodwork?
L Insulin, H Glucose, possible high HbA1c
55
What patterns suggest Hashimoto's or autoimmune thyroiditis?
TSH >2.5 (esp. >1.5 in females), check TPO antibodies, low ALP
56
What patterns might indicate adrenal hyperfunction?
H Sodium, L Potassium, H Cholesterol, H Triglycerides (or the reverse if hypo)
57
What markers are involved in identifying metabolic acidosis?
H CO2 (>28-30), L Chloride (<100), K+ low or normal
58
What markers are involved in identifying metabolic alkalosis?
L CO2 (<25), H Chloride (>106), H Anion Gap, K+ disturbances
59
What pattern would suggest metabolic alkalosis with B1 deficiency?
L CO2, H Anion Gap, L HCT, L Hb, L LDH, H Glucose
60
What lab markers suggest paracellular leaky gut?
H Monocytes, H Uric Acid, H ALP, H Ferritin; L GGT, variable AST/ALT
61
What pattern would suggest heavy metal toxicity?
H BUN, Uric Acid, Bilirubin, Globulin; L Platelets
62
What labs support a diagnosis of renal disease?
H Creatinine, Uric Acid, Phosphate, LDH, AST
63
What labs would indicate possible mold exposure?
Uric Acid >5.5, Eosinophils >3%, Basophils >1%
64
What is the bloodwork pattern for zinc deficiency?
L ALP (<40), L WBC, L Total Protein
65
What markers indicate Vit B6 deficiency?
L ALT, AST, GGT, MCV, MCH, MCHC; H Homocysteine
66
What pattern suggests Vitamin C deficiency?
L Albumin, Hb, HCT, Iron; H MCV, H ALP, H Fibrinogen
67
What is the lab pattern for PCOS?
H LH, L FSH (LH:FSH > 2:1), H Androgens, L SHBG, L Progesterone
68
What pattern supports macrocytic anemia?
H MCV (>90), H MCH, H RDW, L Hb, L RBC
69
What blood markers indicate dehydration?
H Albumin, H Hb, H RBC, possible H BUN
70
Why might glucose be low?
Possible Low Reasons: reactive hypoglycemia (low blood sugar diet , fasting, strenous exericse) - often happens when excessive glcusoe consumed, then 'delayed reollarcoaster' = brings down blood glucos - but too low OR possibly hyperinsulinism - chronic high blood sugar diet - chronic pancreatic overstimulation (reactive hypoglycemia) low level blood glucose - high insulin (Glut4 allows serum glucose to enter cell - low in blood) Insulin resistance - might also see brown / red tint on shins adrenal hypofunction hypothyroidism - body might not be stim. as much gluconeogensis . check if low TS3/TS4 as well - could help improve thyroid. Liver issues (cannot control blood sugar, glycogen storage issue) - if see low glucose + high GGT, AST, high ALT - assess if it hypoglycemia is related to liver dysfunction [hypoglycemia = gluycogen storage issue ] chronic stress: decerased cortisol - can see with chronic stress, lack of sleep, HPA axis dysregulation. - adrenal hypofunction if chornic stress (addisons disease) - tissue insentivity medications (metformin, proranolol, tolbutamide) low vit d. tumours of pancetaic cells (beta cells - insulinomas) - glycogen release issue (adrenal-foucsed treatment) addisons disease
71
why might glucose be high?
Possible Low Reasons: reactive hypoglycemia (low blood sugar diet , fasting, strenous exericse) - often happens when excessive glcusoe consumed, then 'delayed reollarcoaster' = brings down blood glucos - but too low OR possibly hyperinsulinism - chronic high blood sugar diet - chronic pancreatic overstimulation (reactive hypoglycemia) low level blood glucose - high insulin (Glut4 allows serum glucose to enter cell - low in blood) Insulin resistance - might also see brown / red tint on shins adrenal hypofunction hypothyroidism - body might not be stim. as much gluconeogensis . check if low TS3/TS4 as well - could help improve thyroid. Liver issues (cannot control blood sugar, glycogen storage issue) - if see low glucose + high GGT, AST, high ALT - assess if it hypoglycemia is related to liver dysfunction [hypoglycemia = gluycogen storage issue ] chronic stress: decerased cortisol - can see with chronic stress, lack of sleep, HPA axis dysregulation. - adrenal hypofunction if chornic stress (addisons disease) - tissue insentivity medications (metformin, proranolol, tolbutamide) low vit d. tumours of pancetaic cells (beta cells - insulinomas) - glycogen release issue (adrenal-foucsed treatment) addisons disease
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