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Roslin Institute has a diagram of its research logic in which the core is
molecular and developmental biology, relating to a number of applications
including genetics, growth, reproduction and even welfare. Within this view the
subject of nutrition has been thought sometimes to sit rather uneasily and the
Institute has had difficulty incorporating nutrition within its scientific
strategy. This may in part reflect a failure by those most closely involved in
nutrition to make a convincing case for the importance of nutritional research
and knowledge. So I have drawn up an alternative diagram in which I see
nutrition as a core subject, relating to and integrating the effects of a very wide
range of other disciplines, as shown in Figure 1.
Genetics
In my diagram, I have placed the interaction with genetics prominently
because nutrition starts with the bird and geneticists create the bird. It has
been stated, usually by geneticists, that the role of nutrition is to allow the bird
to express its genetic potential. This is in large part true, though with some
exceptions. Over the years geneticists have improved the production potential
of birds so greatly that it has been a challenge to nutritionists to maintain
optimum nutrient supply. Of course, the task of the nutritionist has been
assisted by the presence of models that allow the prediction of the needs
for some of the main nutrients, given knowledge of genetic potential.
This of course, is part of the Morris philosophy but there are many examples of
where knowledge has been incomplete.
Life would undoubtedly be simpler if geneticists
Had been able to create perfect birds but so far they have not, and nutritionists
have often been called upon to overcome or alleviate some of the genetic
flaws. Broilers have had a history of metabolic weak- nesses, generally thought
to have arisen as a result of heavy selection pressure on the main economic
traits of growth and food efficiency. Leg weakness, ascites and some fatal
syndromes are all conditions where fast growth seems to have put pressure on
a range of metabolic systems often with disastrous consequences. In some
cases nutritionists have been able to identify specific nutritional factors that
can alleviate the problem in part or in whole.
But, where specific solutions have not been identified, the nutritionist has
often been able to help solve the problem at a more general level by slowing
growth to take the pressure off these vulnerable metabolic systems. This
slowing of growth, particularly during the early growing stage, has been
achieved by qualitative or quantitative nutrient restriction and has put the
nutritionist in the position of trying to limit the gains in potential achieved by
geneticists. Geneticists are now trying to avoid this conflict between nutrition
and genetics by breeding birds that have altered growth profiles that more
closely match those achieved by nutritional management. Of
course, as
the specific characteristics of different strains evolve either in response to
selection for different components of growth or to selection for particularly
beneficial metabolic characteristics (to counter specific weak- nesses), it will
Some interesting interactions between nutrition and these subjects have been
discovered recently. Studies on bone biology have shown that tibial
dyschondro- plasia (TD) is a condition that can be influenced both by genetics
degeneration and was not a likely cause of death; for instance, the fat did not
cause rupture of the liver and fatal hemorrhage, as in Fatty Liver Hemorrhagic
Syndrome (FLHS) in laying hens. The pathology in FLKS was thus unique and
did not resemble any reported nutritional deficiency conditions. However, diet
was perhaps involve d, because changing the food sometimes altered the
course of an outbreak.
Industry was concerned and came to our Institute (then the Poultry Research
Centre). The veterinarians were baffled and so turned to the nutritionists. We
set up a team comprising 2 pathologists, Walter Siller and the late Peter
Wight, 2 biochemists, Don Bannister and Tony Evans, and nutritionists Bob
Blair and myself. So we set off on a hunt for the cause of FLKS, not knowing in
which direction it would take us. Note that this initiative was taken by the
scientists themselves, not at the behest of Institute management, in the
inefficient days when scientists were allowed to do what they thought best,
before the Rothschild Report had such a dramatic effect on UK agricultural
research administration and funding. So it predated the time when policy
groups deliberated research priorities and required fully coasted proposals with
detailed procedures and milestones.
The first research priority was to be able to reproduce the condition in
sufficiently high incidence to study the effects of possible factors and to
provide enough material from affected but alive birds to carry out
metabolic studies. Anecdotal and some experimental evidence suggested that
FLKS was often associated with diets with high wheat content and could be
alleviated by increasing dietary protein and fat. A diet was formulated to have
a high content of ME and wheat but relatively low proportions of protein and fat
(Whitehead and Blair, 1974). This diet gave instant success and after some
refinements we had our killer diet which could reliably reproduce mortalities of
20% to 40%. This mortality was sufficiently high to study the effects of varying
different factors and gave the biochemists plenty of material to work with.
The initial nutritional studies confirmed a strong effect of dietary energy-toprotein ratio on mortality (Whitehead and Blair, 1974). As energy decreased or
protein content increased, mortality fell to low levels. At this point we had to
resist management pressure to the effect that since FLKS could largely be
prevented by feeding high protein diets, the problem could be considered
solved and research should be transferred to something more useful. But we
carried on, ruling out lipotropic agents, finding that stress or short periods of
fasting precipitated mortality and that providing ME in the form of fat rather
than carbohydrate reduced mortality. Was fatty acid composition important?
The answer was no, there was little difference between fats of very different
fatty acid composition. Then, a breakthrough: very low mortality when the killer
diet was supplemented with large quantities of vitamins (Whitehead et al.,
1975). But which was the important vitamin, or perhaps combination of
vitamins?
Microbiology
Environment
The nutrition of birds is influenced greatly by the environment in which they are
kept. Thermoregulation depends upon the balance between heat production by
the bird and heat loss to the environment. Thus environmental temperature
and humidity in lance energy utilization and food intake. Mathematical
models are available to predict optimum diet composition under a range
of environmental conditions but when these conditions become sufficiently
severe to result in stress, nutrition becomes more problematical. There are
established dietary modifications to help the bird cope with heat stress and to
minimize depressions in productivity. Some nutrients, particularly vitamins,
have anti-stress roles. Vitamin C is one well known example.
Vitamin E is another nutrient that has been found to have a role in heat stress.
Dietary supplementation with vitamin E can prevent some of the loss in egg
production by hens exposed to heat stress (Bollinger-Lee et al., 1998, 1999). A
rather novel mechanism is involved, relating to vitellogenin supply. Vitellogenin
is synthesised in the liver, under the control of estrogen which is synthesised in
the ovary. Vitellogenin is transported in the blood to the developing oocyte
where it is taken up as the major yolk protein precursor. It has been found that
plasma vitellogenin concentration was drastically reduced in heat stress and it
was hypothesized that this lack of yolk precursor was a major reason for the
depression in egg production. Feeding extra vitamin E partially restored
vitellogenin, as it did egg production. The various factors involved in
vitellogenin production were studied, from estrogen through to the formation of
vitellogenin mRNA which was taken as an indicator of vitellogenin synthesis.
Hepatic synthesis of Vg was lower in heat stress, but vitamin E did not appear
to affect synthesis because it had no effect on estrogen or on the amount of
vitellogenin mRNA.
Although stress thus depresses vitellogenin synthesis, we found, to our
surprise, that there was actually a n increase in the liver vitellogenin
concentration in stressed birds (Whitehead et al.,
1998). This could be explained by a decrease in Vg secretion from the liver,
which resulted in an increase in liver Vg content and a greatly decreased
plasma- to-liver ratio of vitellogenin. Provision of extra vitamin E permitted
better vitellogenin secretion and restored the ratio to more normal values.
There was a very close relationship at an individual bird level between the ratio
of plasma to liver vitellogenin and egg output.
The problem thus involves an inhibition of transport of vitellogenin out of the
liver that leads to a build-up in the liver, even though synthesis has been
depressed by heat stress. The cellular role by which vitamin E exerts this may
be related to the traditional anti-oxidant role of vita min E in maintaining
the normal membrane structure. Alternatively, there may be a novel
mechanism involving a specific role for vitamin E in membrane transport. This
is a very recently discovered example of the interaction of nutrition with
environment. There is currently considerable interest in the influence of other
nutrients on stress resistance.
problem by breeding a bird that in its freely expressed adult state is totally
unfit for life. If it does not fall off its legs, it is liable to die suddenly and
will have had great difficulty in reproducing itself. Again, it is left to the
nutritionist to try to solve the genetic problems. Severe food restriction helps
partially solve the egg production problem but leads to other dilemmas over
welfare. Important work on the physiology y of the female broiler breeder
(Hocking et al., 1987 ) has demonstrated the effect of food and
bodyweight restriction on minimizing multiple ovulation and also the stresses
involved. The challenge now needs to be taken up by physiologists and
geneticists, to identify the mechanisms interrelating growth and reproduction
and to breed a bird that will grow quickly yet be able to sustain
reproduction without the need for severe food or bodyweight restriction.