Lecture 8- Thiamin Flashcards
food sources of thiamin
wholegrains,
pork (also other meats)
potatoes and their skin
what is enrichment
when you add in the nutrient to make up for some kind of processing that removed the nutrient
what is fortification
adding the nutrient to food that lots of people eat
3 examples of food related thiamin losses
1- refining grains
2- thiamin antagonists
3- thiaminases = enzymes that act on thiamin
how does refining grains result in thiamin losses
going from something like wholegrain down to brown down to white flour or bread etc
this removes thiamin, but improves shelf life as the embryo germ is removed
what are 3 thiamin antagonists and what are they found in
sulfites (preserve the colour of meat)
cyanogenic glycosides (in cassava)
tannins (tea, coffee, betel nuts)
how do tannins make thiamin less bioavailable
they will oxidise thiamin, making it less easy for your body to absorb
what are thiaminases
enzymes that act on thiamin
how can thiaminases cause thiamin losses
plants such as bracken fern
some kaimoana such as carp, mussels
some insects including African silk worm larvae
where is betel nut chewing an important practice
in South and South-East Asia, Asia Pacific
what is betel nut chewing considered
a stimulant drug, addictive
(one portion has the effect of about 6 cups of coffee)
what are the long term impacts of betel nut chewing
discolouration of teeth and gums, mouth ulcers and oral cancers
what is the chemical structure of thiamin
colourless organosulfur compound
is thiamin water soluble or water insoluble
water soluble
when is thiamin stable
when in acid solution and when frozen
when is thiamin unstable
unstable to heat, UV light and alkali
what are 3 of the 5 phosphorylated forms of thiamin (one of them has two names)
thiamin monophosphate (TMP)
thiamin diphosphate also known as thamin pyrophosphate (TPP)
thiamin triphosphate (TTP)
all forms of thiamin can be interconverted in tissues but what is the distribution of these usually
80% is TPP
5-10% is TTP
remainder TMP, free thiamin
how is thiamin converted to thiamin pyrophosphate
thiamin diphosphotransferase converted thiamin to its active form (TPP) via TMP
so converts it to thiamin monophosphate first and then thiamin pyrophosphate
where is thiamin absorbed
mainly in the jejunum and ileum
what are the two forms of thiamin absorption and when do they usually happen
active carried mediated process at low concentrations
passive diffusion at high concentrations (more at supplement level)
what is the bioavailability of thiamin
little information
absorption can be inhibited by alcohol consumption
absorption will increase when intakes are low
where is ~90% of the thiamin in your blood and why
in erythrocytes (red blood cells) in blood
because there is a TPP dependent enzyme that is on your red blood cells
where is thiamin found in the plasma
majority bound to proteins, mainly albumin
what is the average human storage of thiamin and how long does it take for this to be depleted
~25-30mg
can be depleted within 2-3 weeks
what are the highest tissue concentrations of thiamin
skeletal muscle
heart
brain
liver
kidneys
where is thiamin also present in the body
plasma / serum, milk, cerebrospinal fluid
what does thiamin have a critical role in
energy metabolism (key role in carbohydrate metabolism)
what enzymes is thiamin required for (4)
transketolase
a-ketoglutarate
dehydrogenase
pyruvate dehydrogenase
branched chain a-keto acid dehydrogenase
what is a good measure of thiamin status
transketolase
what kind of diets are risk factors for thiamin deficiency
monotonous diet with low thiamin staple
regular consumption of thiamin antagonists (e.g betel nut)
regular consumption of thiaminases (e,g raw fish)
what are other factors that are risk factors for thiamin deficiency
breastfed infants from thiamin deficient mothers
co-morbidities such as severe acute malnutrition with fever and shock, use of dextrose-based IV fluid
disease states with low thiamin intakes, absorption, thiamin utilisation (e.g alcohol dependancy, bariatric surgery)
what was the historical approach to Beriberi diagnosis
“wet” if it predominantly affects the cardiovascular system accompanied by oedema
“dry” is predominantly affects the peripheral nervous system
what was the historical symptoms that people then thought was Wernicke-Korsakoff encephalopathy
presents with neurological signs
classic syndrome of thiamin deficiency is Beriberi, what is it characterised by
oedema and cardiac enlargement due to intense vasodilation from
accumulation of pyruvate and lactate in tissues
bradycardia (bounding pulse)
cardiac failure
what is the response of Beriberi to thiamin treatment
prompt response to thiamin treatment > recovery could be 1-3 days
what does chronic Beriberi affect rather than the cardiovascular system
the peripheral nerves
what are symptoms of chronic Beriberi
foot drop
loss of sensation in feet
absent ankle reflexes
what are the non specific signs associated with infantile beriberi
irritability
refusal to breastfeed
vomiting
incessant “piercing” cry that may become a “silent” cry
what are the later signs of infantile beriberi
chronic heart failure
in low income countries what often happens with infantile beriberi
death before diagnosis
what is infantile beriberi often misdiagnosed as
viral infection, malaria, pneumonia
in older infants and children what is beriberi often misiagnosed as
meningitis
what are the more neurological symptoms associated with beriberi in older infants and children
loss of appetite, bulging frontanelle, loss of consciousness
what is the most common form of thiamin deficiency in older children and adults
Wernikes encephalopathy
what does Wernike’s encephalopathy affect in the brain and therefore what does this impact
cerebellum and brain stem = abnormal eye movement, gait ataxia, cognitive impairment
what is the most severe form of Wernike-Korsakoff encephalopathy and what does this cause
Korsakoffs psychosis = amnesia, confusion, confabulation , little or no working memory
who is Wernike-Korsakoff encephalopathy most common in and why
most common in people with alcohol dependancy
because decreased intestinal thiamin absorption and increased thiamin requirements for metabolism
what is possible if thiamin deficiency is corrected before development of significant brain damage in Wernike-Korsakoff encephalopathy
the neurological symptoms may be reversed
mild thiamin deficiency is non specific and easily overlooked, especially in older adults, what are the symptoms
sleeplessness, depression, weight loss, malaise, anorexia, fatigue
possible causes of mild thiamin deficiency
low intakes
lowered absorption
multiple medications
what is thiamin deficiency disorders an umbrella term for
describe the spectrum of overlap of clinical presentations attributable to thiamin deficiency across the life course
what are the 5 categories to the spectrum of thiamin deficiency disorders by the WHO
acute cardiologic form
aphonic form
pseudo meningitic form
encephalopathy
peripheral neuropathies
what is the acute cardiologic form of thiamin deficiency associated with
heart
what is the aphonic form of thiamin deficiency associated with
lack of sound - peak prevalence in 4-6 month old infants
initially hoarse cry until no sound is produced while crying
strategies to improve thiamin status
rice and wheat flour fortification programmes that include thiamin
what is the upper level for intake of thiamin
no upper level, just pee it all out
