Introduction to Human Nutrition

152 Introduction to Human Nutrition

development, and the regulation of apoptosis and cell
survival.

Vitamin K defi ciency and requirements

Apart from deliberate experimental manipulation,
vitamin K defi ciency is unknown, and determination
of requirements is complicated by a lack of informa-
tion on the importance of menaquinones synthesized
by intestinal bacteria.
The classical way of determining vitamin K status,
and monitoring the effi cacy of anticoagulant therapy,
is by measuring the time required for the formation
of a fi brin clot in citrated blood plasma after the addi-
tion of calcium ions and thromboplastin: the pro-
thrombin time. A more sensitive index is provided by
direct measurement of preprothrombin in plasma,
most commonly by immunoassay using antisera
against preprothrombin that do not react with
prothrombin.
Based on determination of clotting time, and direct
measurement of prothrombin and preprothrombin,
an intake of 1 μg/kg body weight per day is consid-
ered adequate; this forms the basis of reference intakes
of between 65 and 80 μg/day for adults.
A small number of newborn infants have very low
reserves of vitamin K and are at risk of potentially
fatal hemorrhagic disease. It is therefore generally rec-
ommended that all neonates should be given a single
prophylactic dose of vitamin K.

Toxicity and drug interactions

There is no evidence that phylloquinone has any sig-
nifi cant toxicity. However, high intakes can overcome
the effects of warfarin and other anticoagulants. This
means that patients who are being treated with war-
farin could overcome the benefi cial effects of their
medication if they took supplements of vitamin K.
The danger is that if their dose of warfarin is increased
to counteract the effects of the vitamin supplements
and they then stop taking the supplements, they
would be receiving considerably too much warfarin
and would be at risk of hemorrhage.
It is unlikely that a normal diet could provide a
suffi cient excess of vitamin K to lead to problems, but
habitual consumption of especially rich sources could
result in intakes close to those that antagonize thera-
peutic warfarin. A diet containing relatively large
amounts of foods prepared with vitamin K-rich oils
may pose a risk.

8.6 Vitamin B 1 (thiamin)

Historically, thiamin defi ciency affecting the periph-

eral nervous system (beriberi) was a major public

health problem in south-east Asia following the intro-

duction of the steam-powered mill that made highly

polished (and therefore thiamin-depleted) rice widely

available. There are still sporadic outbreaks of defi -

ciency among people whose diet is rich in carbohy-

drate and poor in thiamin. More commonly, thiamin

defi ciency affecting the heart and central nervous

system is a problem in people with an excessive con-

sumption of alcohol, to the extent that there was a

serious suggestion in Australia at one time that

thiamin should be added to beer.

The structures of thiamin and the coenzyme

thiamin diphosphate are shown in Figure 8.8.

Thiamin is widely distributed in foods, with pork

being an especially rich source; potatoes, whole-grain

cereals, meat, and fi sh are the major sources in most

diets. Like other water-soluble vitamins, thiamin is

readily lost by leaching into cooking water; further-

more, it is unstable to light, and although bread and

fl our contain signifi cant amounts of thiamin, much

of this can be lost when baked goods are exposed to

sunlight in a shop window.

Thiamin is also destroyed by sulfi tes, and in potato

products that have been blanched by immersion in

sulfi te solution there is little or no thiamin remaining.

Polyphenols, including tannic acid in tea and betel

nuts, also destroy thiamin, and have been associated

with thiamin defi ciency.

N

H 3 C N NH 2

C

H 2

N

S

CH 3

CH 2 CH 2 OH

N

H 3 C N NH 2

C

H 2

N

S

CH 3

CH 2

H 2

C O P O P O-

O- O-

O O

Thiamin

Thiamin diphosphate

Figure 8.8 Thiamin (vitamin B 1 ) and the coenzyme thiamin

diphosphate.