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Soc 663
October 9th
The decline of mortality
Note: All figures and tables and the PP presentation for this lecture are in the FTP same
directory where you find this file. They are in the form of *.GIF files, *.BMP files or *.PPT
files. You can actually download them to your directory and place them all in a single
WORD or WP document if you prefer.
1. General considerations
-Paradoxically, just as Malthus was revising his first edition, several monumental changes were
beginning to take place. First, the secular mortality decline that took place starting perhaps as
early as during the last quarter of the 18th century and with all certainty , after 1825. This change
would be continuous, irreversible (in most places) and would be completed in several stages.
Second, a revolution in the production of energy that marks the onset of an increasing control of
nature by man through technological innovations.
Third, a revolution in aspirations and the separation between sex and reproduction that would
lead to increasing cost of children and a complete collapse of the old regime of natural fertility.
-The demographic changes that occur during this period take place in several stages. The
following is an arbitrary grouping of this stages that will be useful for us:
Mortality:
1750-1940------first stage of mortality decline (not dominated by medical innovations)
1940-2000------second stage of mortality transition(dominated by medical innovations)
Fertility:
1850-1950-----------first stage of fertility decline(mostly in developed countries)
1950-2000-----------second stage of mortality decline (mostly in developing countries)
As far as Europe is concerned, it is thought that the period that begins with the mortality decline
marks the beginning of the so-called demographic transition which culminates with the collapse
of the old fertility regime
After 1750 (perhaps somewhat earlier in England and other Northern European countries as
well) the values of natural increase (r) gradually go up. In 1950, as the mortality decline reaches
developing countries, r explodes to average values as large as .025. This is the period that leads
to the population bomb scare.
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2. The mortality transition: lots of facts
2.1.The following is a very stylized set of stages in the mortality decline for North America and
Europe:
life expectancy between
A
A
A
30-40 by 1830
45-50 by 1920
50-65 by 1970
65-80 by 2000 (lower values in republics from former USSR)
Relatively speaking these changes are concentrated: for 150,000 years life expectancy hover
around 30; in about 170 years it shoots up to about 80: 50 years of gains or about .80 years every
3 years!
2.2. In developing areas things are somewhat different:
life expectancy by
A
A
A
1900 about 35-40
1945 about 38-40
1975 about 65
2000 about 70-75
Notice how much more concentrated in time are the gains in life expectancy in developing
countries.
Remark: despite differences across countries and years, the decline is precipitous, virtually
irreversible , universal and massive:
2.3 The changes in Western Europe and North America are somewhat sudden and spread over a
(relatively) short period (in evolutionary time). The stages and periodization above are useful
since the factors that explain the decline are different in each of them.
Remark: a slow and gradual improvement was occurring over long periods of time even before
the onset of the modern decline
Remark: from here on out I will use CDR and life expectancy to assess changes in mortality.
Remember that their values are inversely related.
2.4. In Figure 1 we display life expectancy in E&W and Sweden for a periods of about 300
Years. Note two features: (a) cessation of fluctuations and (b) rapid increase in a short period of
time
2.5 In Figure No 2 we plot values of life expectancy in England and Wales and for the
aristocracy. Note that a general increase starts in 1750 but that it is only after 1825 or so when
the increase becomes continuous. The graph shows that aristocracy mortality declines quite a bit
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earlier than in the general population. But also that it was quite a bit lower before 1700 or
so...Why would this be?
2.6 Figure No 1 shows life expectancies for Sweden and E and W; whereas Figures 3a and 3b
shows death rates in France, England, Sweden, Norway and Finland over a stretch of 200 years
There are important similarities in the process but differences in initial levels. Figure 3c displays
the CDR for a few other countries until 1920.
2.7. To give you an idea of how mortality proceeds in the XXth century, examine Figure 4 for
several countries in the Western and Eastern hemisphere: everywhere there is a decline, even
though the initial levels of mortality are quite heterogeneous. The pace of mortality decline is
very similar everywhere.
2.8. Disappearance of mortality crises:
An important characteristic of the transition to a new regime is the disappearance or attenuation
of mortality crises. Figure 5 shows the coefficient of variation (standard deviation/mean) of the
crude death rate between 1750 until 1900.
The coefficient of variation is a measure of “average relative dispersion” and the graph clearly
shows that this is attenuated as we move closer to 1900.
Remark:
At this juncture one question that emerges right away is the following: did the disappearance of
crises account for the mortality decline? That is, if the overall (secular) trend had not declined, as
it really did, but crises had disappeared (oscillations had gone away), would one have observed
gains in survival?
The answer seems to be no. The most important reason is that every period with higher than
normal mortality (a crisis) was followed by a compensating period of lower than normal
mortality. The reduction of the net excess mortality associated with crises amounts to only a few
percent points of the total decline in mortality
2.9 An example from NY (figure 6): the CDR fro NY between 1800 and 1970 displays the role
of crisis and of other factors that played an important role in the decline.
note the attenuation of crises mortality (epidemics)
note that despite clear role of purification of water pasteurization etc...something
was already happening before because mortality was declining and fluctuations
were pretty much gone...what was happening?
2.10. Why did mortality crises disappear? There are several explanations.
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=The end of cyclical weather fluctuations associated to long term trends in temperature (the
interval 1500-1800) included a long stretch of very cold weather.
=The end of frequent visits by the plague, probably due to improvements in routes of
transportation or to a lessening of the virulence of the organisms.
=A third explanation invokes improvements in technology for producing, storing and
transporting goods that led to attenuation of periodic famines and starvation periods. Indeed, the
disappearance of crises coincides with the attenuation of price fluctuations.
Can this be taken as evidence that economic progress led to the elimination of mortality crises?
=Finally, a fourth explanation (probably not independent of some of the others) assigns a crucial
role to the emergence of the state and central administration as efficient mechanisms to
(a) manage epidemics through warning signals, isolation, organizing inflow and outflow of
people (b) extend protection to high risk groups (c) negotiate offsetting mechanisms (distribution
of food, subsides etc...)
Summary: the evidence we have suggest that the frequency of crises declined after 17001750. It is also known that the proportionated contribution of NET excess mortality
associated with the decline or outright disappearance of crises, is not more than 15 to 20%.
Thus, something else must explain the secular mortality decline.
3. A framework to understand the secular mortality decline
-One can think of a mortality rate at age y due to cause z, M(z,y) (number of deaths at age y due
to cause z in a year divided by midyear population aged y) as a product of three quantities:
E(z,y)* Re(z,y) * Rec(z,y)
where E(z,y) refers to the fraction of people in the age group who are exposed to condition or
illness z; Re(z,y) is the fraction of all those people who are exposed to disease z and who
contract it; Rec(z,y) is the fraction of all those who contract the disease who die of it. The latter
is usually known as the lethality rate.
-Thus a reduction in mortality can originate in one of three sources: a reduction in exposure, a
reduction in the lack of resistance and a reduction in the lethality rate.
Mortality due to certain causes is more amenable to control via manipulation of exposure (for
example bacterial diarrhea); other diseases are more amenable to control via increased resistance
(through vaccination or through natural increase in the immune capacity).
Finally, others are more likely to be reduced if one reduces the lethality rate.
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-Examples:
Respiratory TB responds well to streptomycin (recovery); BCG is a vaccination strategy that
works well also (resistance)
Plague disappeared from Europe as a result of ability to break down the chain of transmission
(exposure to vectors, rodents) and perhaps also to increased immunity (resistance or,
alternatively reduction in virulence)
Ebola is a pulsating illness because we are able to cordon it off and disconnect the transmission
chain; we thus control exposure very well but are unable to do much else about it
The only known way to wipe out HIV is through changes in sexual behavior (exposure)
Cancer mortality is lower due to ability to increase survival of cancer patients (lethality); for a
few cancers we know how to manipulate exposure (lung)
-Factors that may affects exposure, resistance and recovery:
Table 1 is a coarse classification of factors according to level of aggregation (at what level can
the factor operate?) And according to whether their main influence is on exposure, resistance or
recovery
Table # 1
-Let us combine resistance and recovery in one category (RR) and treat it as a single one. Let us
treat exposure separately(E). In theory we could think that a society’s level of mortality is the
result of a level of exposure and a level of resistance/recovery. A way of formalizing this is to
use the idea of production function.
Our ‘output’ is a level of mortality, our ‘inputs’ are: exposure and resistance and recovery.
life expectancy = E a * R b
We could actually draw a ‘iso-mortality curve’ such as that in Figure 7. A single curve represents
points created by a combination of E and RR that lead to the SAME mortality level. Curves that
are higher represent LOWER mortality (higher life expectancy) and those lower represent
HIGHER mortality.
Figure 7 on Life expectancies achieved with different
Combinations of exposure and resistance/recovery
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Any mortality decline can be mapped in this figure. In particular, progress against most diseases
can be represented by displacements along the axis of the figure. The overall trajectory of
mortality in a society will simply be the weighted average of the trajectories associated with each
cause of death.
How did the secular mortality decline occur? Did it move societies downwards across the
horizontal direction or across a vertical direction or a combination of both?
4 Why did mortality decline in XVIII-XX?
4.1. Important reminders
-Remember we need to identify factors that affect either exposure, resistance or recovery.
-Examine the classification of factors (see table 1) and their potential importance during
different periods of time and for different age groups. For example, nutritional status is less
likely to be of importance during the first year of life in societies where there is full
breastfeeding. In those instances, nutritional status is more likely to affects ages 5-14 with more
force but also adult ages.
(See Table 1)
4.2. Introduction to Thomas McKeown’s work
4.2.1 Background
McKeown initiated work in this area with a view to resolving the following controversy: did the
population growth spur during the XVIII century and thereafter owe anything to mortality or was
it simply a result of increases in fertility? Habbakkuk, an economic historian, argued strongly for
the latter and recent estimates of fertility from Wrigley-Schofield confirm that increases in
marriage (and subsequent increases in overall fertility) explain the bulk of population increase.
But, it is also true that mortality had been declining though subjected to a somewhat erratic
trend: there was a decline from 1600 or so on, a halt during the period 1830-1860 and the a
renewed impetus to the mortality decline. McKeown worked with information that only revealed
the part of the decline that took place after registration systems are established, 1838.
Figure 8 About mortality dcline in E&W and France
4.2.2. McKeown’s main paradigm:
a. Classification of factors that alter mortality rates, Mx
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exposure
resistance
recovery
b. Classification of diseases
airborne
water-food-borne
vector-borne
other
There is an association between types of disease and mode of control;
For example, exposure is probably less controllable for airborne diseases (though crowding,
population density, coordinated and efficient quarantine measures as well as past prevalence of
the disease may be influential factors), but it is more for water-food and vector borne diseases.
It is also known that nutritional status (resistance) is more relevant for some airborne but not for
vector or water-food borne
So we have these approximate associations:
airborne more susceptible to control via nutritional enhancement of immune system
water borne more susceptible to controls via exposure (individual contact)
vector born more susceptible to control via exposure
c. Methodological strategy
McKeown uses the method of exclusion: argues for the impossibility or implausibility of a set of
factors to explain the decline and then, by default, what’s left is what must explain the
phenomenon.
He identifies FACTORS that may have induced the mortality decline. Each factor is associated
with exposure, resistance and recovery
The factors are as follows:
evolutionary adaptation
medical knowledge and techniques
public health interventions
nutrition
The alternative explanations are as follows:
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i. autonomous decline due to changes in virulence of microorganism
This affects resistance (acquired immunity) and, if the diseases agent population declined,
exposure to it.
ii. Medical knowledge and techniques
direct intervention such as vaccination (resistance), chemotherapy (resistance, recovery), surgery
(recovery), knowledge of germs (exposure)
iii. Public health
Mostly through infrastructure (exposure) and widespread knowledge of hygiene (exposure)
but also through work on prevention and isolation
iv. Nutrition
Mostly through increased resistance and recovery
Here is the main strategy used by McKeown:
-examine total decline in mortality from 1838 or so onward
-assign contribution to causes of death; single out the most important cause of death
-proceed to review whether any one of the factors in (i) and (iv) could be assigned
responsibility
-in the end, after systematic elimination, what’s left as a possibility? What is the most
likely factor to be responsible?
4.2.3. Presentation of main evidence using McKeown’s graphs
a. What does the mortality decline observed and focused on by McKeown look like?
Figure 9 with standardized death rates
Mortality appears to have been declining for a while, even before 1841 though only slightly
Figure 7 (above) from Fogel in E&W and France does indeed reveal a decline
prior to the period on which McKeown is focusing
If one compares with the new estimates of life expectancy by Wrigley and Schofield we get a
different picture: mortality was declining up until 1820, then the decline stalls for nearly half a
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century and resumes in 1880.
McKeown pays little notice to this lack of gradual pace in the fall of mortality. But this is an
important for the integrity of his thesis. It is important to also remember (see PP presentation
with figures on real wages and life expectancy) that during this period (1820-1880) wages were
increasing and that they begin to dip after 1891.
Figure 9 on Real wages and life expectancy for England
But McKeown focuses on the picture you see, namely the sharp decline that probably begins
after 1871.
b. What are the most important causes of death explaining the decline?
Tables 2 and 3
Note the importance of TB but also note the importance and awkward trend of IPB. What are we
to make of this? McKeown does not explain the issue at all.
c. What are the most important age groups affected by these trends up until 1900 approximately?
If you examine several tables fromMcKeown one will see that the most favored age groups are:
1-14 and 15-35 mostly
In some cases more males than females (for example in TB)...this is important for it may help to
weaken the case for some factors (for example nutritional status)
It was only in a second stage, between 1900 and 1960 that mortality in infancy begins a serious
decline. And in a third stage, after 1960, mortality decline affects the older age groups.
In figure 4 we display the percentage decline in mortality by age groups in Sweden from 1900 to
1980 and then from 1960 to 1996.
Figure 10
Remark: A decline in mortality brings with it a shift in the age distribution of deaths; the secular
mortality decline means a complete shift of the age distribution as displayed in figure 10
4.2.4. A review of the “adaptation” explanation
Very important: in most cases (except scarlet fever and smallpox) one does not see the
prior increase in death rates that one should find to speak of increased acquired immunity
through selection. In fact, lack of exposure may lead to increased susceptibility (less
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selection).
According to this explanation the organism(s) generating the diseases would have become milder
and turned the disease into one of reduced lethality
AIR BORNE
Certainly not applicable to TB. TB is as virulent today as it used to be.
Possibly applicable to scarlet fever but this is not as salient a cause of death
Perhaps measles and, much less so, smallpox are examples of this mechanism
Not applicable to IPB
WATER BORNE
None of the water-food borne diseases, dyphteria, cholera, dysentery and diarrhea
VECTOR BORNE
Possible plague but plague had waned before the period under scrutiny
Not Typhus which simply vanished
4.2. 5. The medical explanation
Two important set of dates and names
PASTEUR
KOCH
1860-70
1880-90
Distinction medical knowledge and medical treatment. Medical knowledge does not
always leads to treatment. The germ or contagion theory did not lead to important interventions
for a long time. Although knowledge about germs was available back in 1880, a complete germ
theory was an affair not completed until early 1900. But even if such knowledge had been
available before, it did not translate into effective practices until later. This is particularly true of
surgery but also of chemotherapy and vaccination. However, knowledge and information about
transmission can be a powerful tool to reduce exposure.
The main medical treatment we refer to here are
chemotherapy
vaccination
recovery treatment
preventative
surgery
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Let me suggest an answer: medical treatment had precious little to do with the morality decline
in almost all cases:
Table 4 from McKinlay and McKinlay
Figure 11 from McKeown about TB
What about the other diseases?
Figure 126 McKeown, p.94 IPB
Figure 13 McKeown. 96, Whooping cough, measles
Figure 14 McKeown p.96, Scarlet Fever,
4.2.6. The case of the US and the rest of Europe.
i. McKinlay and McKinlay have studied the case for the US. First mortality rates were declining
before 1900 and continued declining from about 10 to about 2 in the course of the 1900-1970
interval.
Figure 15: McKinlay and McKinlay in p. 413
Table 4: McKinlay and McKinlay in p.418
As in the case of England, all medical interventions occur well after the bulk of the decline in the
diseases that contributed the most had already taken place
Figure 16 in p.423 with timing of various interventions
Figure 17 in p.415 shows no relation between medical expenditures and CDR
Read McKinlay and McKinlay’s conclusions: they, as McKeown a few years earlier, see no
evidence to support the idea that medical intervention had anything to do with most of the
mortality decline. It is not just that interventions failed to come into the picture until well after
rge entire decline was almost finished but that governmental expenditures in health began to
increase well after the initial decline (1880-1940) was finished.
ii. . Vallin makes the SAME case forcefully for Western and Eastern Europe
(figures not shown)
figure 2, p. 4
figure 3, p.5
figure 4, p. 6
figure 5, p 7
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figure 6, p. 8
4.2.7. Improvement of hygiene
There are two dimensions to this: personal hygiene (boiling water and milk, washing hands,
proper clothing, avoidance of contact, clealiness in general), on the one hand, and institutional
services, infrastructure and outlays, on the other (water supply, sewage, storage, food sanitation)
or community efforts at isolation .
Personal hygiene requires some acceptance of medical knowledge: the theory that some diseases
at least are produced by infectious organisms. Thus this could have been in place early in 1880,
when the germ theory of disease gained some acceptance in the medical community. But
diffusion of these ideas to the population is another matter...
With the exception of airborne diseases that are amenable to control via isolation, ‘cordon
sanitaires’ and quarantine, the diseases most affected by sanitation are water-food borne diseases
and vector borne diseases. The role of contaminated milk is very important (typhoid, non
respiratory TB, diphteria)
McKeown argues that techniques of food sterilization (Pasteurization) are introduced late in the
XIXth century and that they are unlikely to have contributed much until then. As for sanitation,
he argues that they are probably more important for water-food borne and vector diseases, not
airborne diseases. And that even in the case of those water food borne diseases, improvements
took place long after the diseases themselves had begun to decline. Witness the cholera epidemic
in London in 1865 or the one in Hamburg for that matter, in 1892.
McKeown claims that personal hygiene not important until mid XIXth century. Efficient water
purification systems and sewage management has a mixed record in England because of relative
deterioration during the early stages of industrialization (1850-1900). In fact, the conditions of
cities and large towns may have led to a deterioration of sanitation.
It is much more difficult to support the idea for the case of airborne diseases. McKeown pays no
attention to the increased ability of states and local governments to cordon off areas struck by an
epidemic and, in general, to any political and social measure that leads to a reduction of
transmission. Perhaps improvements in the environment due to lower prevalence of a disease
contributed some but it behooves us to explain the initial decline.
4.2.8. The nutrition explanation
After rejecting that the main factors behind mortality decline could be related to
(a) adaptation and evolution
(b)medical treatment and medical knowledge
(c) public health interventions
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we are left only with the residual explanation: nutritional status
i. Before going on to explain this why nutrition may have been behind the fall of mortality, it is
necessary to make a distinction: chronic malnutrition and deficiencies that lead to associated
conditions such as pellagra, scorbuto, marasmus, rickets, beriberi, kwashokior, etc..and marginal
malnutrition that may induce other effects that are not as severe (in principle at least). We will be
talking mostly about the latter, not the former.
ii. Nutritional status vs diet: diet refers to nutritional intake whereas nutritional status refers to
net nutrition after we allow for calories spent in metabolism (BMR), ingestion and digestion and
work and other activities
ii. Mechanism producing connection with nutrition
Remember the distinction between cell mediated and blood mediated immune mechanisms
Nutrition affects immunological status as well as tissue integrity
The immune system can react at various points:
obstruction of initial entrance (membrane porosity)
effects on agent preventing it from latching on to tissues (reproduction of organism)
(These are direct effects on cell mediated immune system)
effects on secondary infections
more efficient and accelerated recovery
iii. What are the most important diseases related to nutritional status?
Table 5 shows classification of diseases according to their sensitivity to
nutritional status
iv. Reasons for suspecting increase in nutritional status...............
In McKeown’s rendition this is all an issue of increases in nutritional intake, namely, diet.
improvements in production (redeployment of old technology0
Crop rotation
Winter feeding
Transportation and marketing: lessening distribution bottlenecks
Storage
new staples
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Evidence used by McKeown: read text pp 129
Evidence from wages: from Wrigley’s time series (see Figure on wages and life expectancy for
E&W) as well as from other studies (see Figure 18 from Lindert and Williamson) we see that
wages are decreasing from 1750 until 1800, then they begin to increase until 1850 and then they
begin a decrease until 1900.
Evidence from GDP per capita from Floud and Harris in book by Steckel and Floud
Remarks:
-there is still a controversy about what happened to real wages after 1880. This apparently is now
settled (read from Height, Health and History, pp291l; refer to Feinstein’s findigns cited in
Floud’s paper pp25 and to text by Steckel and Floud p. 117)
-What does this tell us about nutritional status?
It does tell us about nutritional intake but real wages do not tell us much about nutritional status
It does also suggest that ability to purchase food was changing as one would think it did
according to McKeown. But unless we have better figure on labor force participation one is hard
pressed to use real wages as evidence to support McKeown’s hypothesis.
4.3. Objections to McKeown
4.3.1 . The issue of laissez faire: McKeown’s position implies that economic development is to
waited for before we can have improvements. Although he did not explicitly say it, the
implication is that all one needs for life expectancy increase is a good, solid economic growth
record. He was to be proven incorrect on this score.
4.3.2. Smallpox (Razzel) Minimizes the importance of smallpox and its multiplying effects as
people afflicted with small pox and also experienced other diseases of the respiratory system.
4.3.3. Short term fluctuation of mortality relative to wages were weak to say the least (elasticity
of .10-.15 at most). If real wages reflect nutritional intake, why wouldn’t this be reflected in short
run fluctuations?
4.3.4. The aristocracy (Razzell) Why would life expectancy in the aristocracy be so close to
overall life expectancy if they, among all other groups, should have had a better nutritional
record? And why should it be the case that their mortality conditions also improved and some
time before the conditions for the rest of the population?
McKeown argues that for them it was the decrease in other diseases and less exposure to TB not
so much nutritional intake. Thus, in explaining the “exception” McKeown moves away from a
purely nutrition hypothesis and must invoke exogenous influences regarding the impact of other
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diseases or by arguing that it was exposure and not resistance to TB that made the case for the
aristocracy.
4.3.5. Sanitation and Public Health
A. Advances in national but specially communal and municipal levels in England were
neglected by McKeown (Szreter). Of particular importance: the ability to resolve conflicts that
lead to local government paralysis (example of cholera in Hamburg (see Death in Hamburg)) and
to apply knowledge to increase supply of hygienic “goods and services” There is strong evidence
suggesting that in towns with improved sanitation systems (water and sewage), cohort mortality
improved and there was a noticeable decline in mortaltiy due to water borne diseases. The best
studied case is in France in 1850 (Preston and Van de Walle)
B. But the most important objection comes from both Szreter and Fogel and requires to
understand the concepts of nutritional intake and nutritional status. Nut Int refers to Kilocalories
consumed and nutritional status refers to the net value of calories once we discount the claims
made against by all energetic needs not included by basal metabolic requirements. An individual
of a given height and weight living in a particular environment (temperature, humidity and
altitude) requires a certain number of kilocalories to function. This is called Basal Metabolic
Rate (BMR). Add to that now the energy required to ingest and digest food and the amount of
energy required to produce the food (work) as well as associated leisure). That will determine
total energy requirements above the BMR. compare that individual with another in exactly the
same conditions but exposed to diarrheal illnesses. The energy requirements of the latter are
higher than that of the former. If nutritional intake remains the same, the latter individual may
experience nutritional deficiencies and his/her body may adjust by reducing weight or partially
stunting (if individual has not yet reached maturity).
synergisms: nutritional status gets worse with infections as Basal Metabolism Rate increase and
ability to absorb nutrients decreases. Thus, if a person contracts an infection his/her food intake
(in terms of kilo-calories per day per person) must increase or else the risk of deficiencies
develops.
Now consider that water borne diseases are highly taxing on individuals who contract them. The
elimination or reduction of one of them can thus increase nutritional status even if there is not
increase in nutritional intake. Thus, there are multiplying effects: reduction in a water food
borne disease may lead to better nutritional status and this may lead to reduction in the lethality
of some airborne disease. So imagine the following scenario:
At time T1 there are interventions to reduce exposure to cholera
Even though cholera is not a principal cause of death, its prevalence is extensive
At time T2 individuals’ nutritional status improves thus increasing their ability
to fight off respiratory TB
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The lethality of respiratory TB declines and so does its death rate
At time T3 there are improvements in nutritional status due to decline in respiratory TB
5. Robert Fogel and the revisionist case.: more and better evidence to support McKeown
Fogel’s attempts to revise and reintroduce McKeown’s hypotheses but in a more elaborated
form. He starts from some basic premises:
5.1. Nutritional status is a function of nutritional intake and claims against it, including work and
exposure to and resistance of diseases
5.2. Basic Metabolic Rate is between 1350 and 2000Kcalories per day per individual of average
size and moderate temperatures. In addition, there is an extra 25% needed for ingestion
digestion. This represents the minimum needed to survive. Finally, if work and other activities
occur, then extra calories will be needed. Finally, exposure to diseases must be factored in and
this increases the caloric requirement.
Tables from Fogel:
Figure 19: progress in calories consumed ( calories per year)
Table 6: Calories in French and English diets
5.3. What is calories intake fall below what is demanded? Individuals and population can adjust
in one of three ways:
Reducing body size( height and weight)
Decreasing activities (labor force participation and effort)
Increased mortality.
5.4. When claims on nutritional intake increase unaccompanied by increases in nutritional intake
the organisms adapts in one of two ways (before death can occur): if the excess demand occurs
before maturity (the age of maturity itself varies with nutritional status but is roughly put at 1522) and particularly during infancy and early childhood, stunting occurs. When the excess
demand occurs after, there can be wasting. The first type of reaction leads to individuals who
small, low stature. The second leads to individuals whose weight for height (Body Mass Index)
is low (BMI=weight/(height)^2, weight divided by the square of height).
5.5. Mortality risks and indeed the risk of a number of chronic conditions are associated with
height and weight in complicated ways. But two mechanisms are salient;
marginal nutrition is early childhood is reflected in height and affects a number
of conditions including those experienced as adults (chronic)
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Continued marginal nutrition or excess demands is reflected i n loss of weight and also
leads to experience of higher risk of infections as well as chronic conditions
Thus, there should be clear relations:
between body height and mortality
between BMI and mortality
between height and BMI and chronic conditions
Figure 20 from Fogel pp 375 Nobel address
Figure 21 from Fogel pp 376 Nobel address
Figure 22 from Fogel pp 378 Nobel address
Figure 23 from Costa and Steckel pp54: Norwegian and Union Army
The relations can be summarized in the so called but can be summarized using Waaler’s
surfaces.
Figure 24 shows relation between BMI and mortality risks
From this point on Fogel’s uses historical data on heights, on mortality and on health status that
lead him to an interpretation of the mortality decline in Europe and North America that is similar
to but much more flexible than McKeown’s. For starters, he must accept Szreter’s idea that
improvements in exposure to water borne diseases may have had a lot to do with mortality
decline. That is, he is more receptive and more open to the idea that nutritional intake is only part
of the story.
Table 7 containing of average heights in Europe, p. 11
(Note: One could object that gains in height only appear very late. However, notice that even
small improvements in heights may lead to sharp declines in mortality risks. See Waaler surface.
Also, remember that the height of a cohort and its mortality reflect conditions during early
childhood mostly. Thus, mortality and height at time T must be related to conditions at time T-20
if cohorts are aged 20 at time T)
Secondly, his analysis lead him to support the idea that improvements in nutritional status
preceded improvements in life expectancy and that, in general, the evolution of mortality and
prevalence of chronic conditions traverses the Waaler surface in a predictable way.
Figure 25 on relation between army recruits height and life expectancy over a
long period of time from Floud et al in England (use also figure 7.3 pp 293 and
Figure 4.1. in pp 136)
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Figure 26 on the trajectory of French mortality on a Waaler surface.
(See also Figure 27 on trajectory of US from contemporaneous data)
Thirdly, his analyses also leads to the following inference: at low levels of nutritional
status, societies must have been constrained to low levels of productivity. As soon as nutritional
status improves, productivity will tend to raise. Consequently, economic development owes a lot
to health and mortality improvements.
Note: Figure 28 is included (life expectancy in EW from 1700 so that you can visualize it
together with trends in heights displayed in Figure 25
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THIS IS FIGURE 1
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THIS IS FIGURE 2
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THIS IS TABLE 1
F
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THIS IS FIGURE 8
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THIS IS FIGURE 9
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F
THIS IS FIGURE 10
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THIS IS TABLE 2
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THIS IS TABLE 3
THIS IS TABLE 3
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THIS IS FIGURE 11
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THIS IS FIGURE 12
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THIS IS FIGURE 13
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THIS IS FIGURE 14
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THIS IS FIGURE 15
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THIS IS FIGURE 16
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THIS IS TABLE 4
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THIS IS TABLE 5
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THIS IS FIGURE 17
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THIS IS FIGURE 18
THIS IS FIGURE 19
THIS IS FIGURE 18
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THIS IS FIGURE 19
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THIS IS FIGURE 20
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THIS IS TABLE 6
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THIS IS FIGURE 21
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THIS IS FIGURE 22
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THIS IS FIGURE 23
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THIS IS FIGURE 24
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THIS IS FIGURE 25
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THIS IS FIGURE 26
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THIS IS FIGURE 28
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THIS IS FIGURE 29