Lessons from the Primal Health Research Data Bank
One of the oldest and most valuable studies in our database
was precisely about risk factors for obesity. It was published
as early as 1976 in an authoritative medical journal.(2) From
October 1944 to May 1945 an acute famine affected the western
Netherlands. The authors combined information about prenatal
and early postnatal status at the time of the famine with weight
and height at the age of 19 on examination of 300,000 men for
military service. The main conclusion was that deprivation during
the first half of pregnancy was related to significantly higher
obesity rates at age 19, while deprivation during the last trimester
of pregnancy and the first months after birth, was associated
with lower obesity rates.
This historical study opened the way to further research about
the long-term effects of being in the womb during the Dutch
famine. In one of these studies, published in 1999, the authors
measured the body size of 741 people born at term between November
1943 and February 1947 in Amsterdam. They compared people exposed
to famine in late, mid, or early gestation with those born before,
or conceived after, the famine period. It appeared in particular
that maternal malnutrition during early gestation was associated
with higher Body Mass Index and waist circumference in 50 year-old
women but not in men. Another study (published in 1998) looked
at the glucose tolerance of adults who had been exposed either
to the famine during fetal life, or who were born in the same
area the year before the famine, or who had been conceived after
the famine. Glucose tolerance – which is closely related
to the tendency to obesity – was significantly decreased
among adults who spent their intrauterine life during the period
of starvation. The siege of Leningrad also exposed the entire
population of a well-defined area to a severe famine. Among
those exposed to malnutrition the influence of obesity on blood
pressure was stronger.
Today the keyword ‘obesity’ (and the related keywords
‘insulin resistance’ and ‘diabetes type 2’)
leads to about 25 entries in our data bank (www.birthworks.org/primalhealth).
From an overview of all these studies we can easily draw the
conclusion that the risks of being obese in childhood and adulthood
are to a great extent already determined before the end of the
‘primal period’. Many studies researched the risks
for these diseases in relation to birth weight and confirmed
the results of the Dutch studies. Smoking in pregnancy was always
found to be a risk factor, as were the long-term effects of
drugs given to pregnant women. For example, it appears from
one study that betamethasone (a glucocorticosteroid) given to
a pregnant woman in order to prevent a respiratory distress
of her newborn baby might result in insulin resistance of that
child 30 years later.
There have been many studies evaluating the prevalence of obesity
in childhood, adolescence and adulthood in relation to infant
feeding. In general, it seems that breastfeeding has a protective
effect. However, the associations between breastfeeding, its
duration, and the risks of being overweight in childhood, adolescence
and adulthood have not been confirmed by large authoritative
studies extending to adulthood such as the 1958 British birth
cohort. It appears from several of these studies that the weight
of the mother is a stronger predictor of obesity than the mode
of infant feeding: a big mother will tend to produce a big baby.
Such data suggest that the metabolic profile of a pregnant woman
has more long-term influence than the kind of food consumed
by a baby.
Interestingly, from studies that focus in particular on the
first week following birth, we can conclude that the period
between birth and age 8 days is a critical window for nutritional
programming. One study looked at the weight gain during this
critical period of adults aged 20 and 32 who had been bottle-fed.
Another one examined the first week of extra uterine life of
children of diabetic mothers.
From this 2005 overview of the Primal Health Data Bank we can
conclude that the risks of being obese are to a great extent
determined by pre- and perinatal environmental factors.
When fat cells became endocrine glands.
Until recently adipose tissue was considered an inert energy
store. The turning point occurred in 1994 when leptin (from
the Greek word leptos, which means ‘thin’) was identified
as a hormone released by fat cells (adipocytes), the absence
of which resulted in morbid obesity in the ob/ob mouse.(3) Today
leptin may be regarded as one of the many ‘adipokines’—hormones
that signals changes in fatty tissue and energy status to control
fuel usage. (This new framework includes adiponactin, resistin,
plasminogen activator inhibitor-1, tumor necrosis factor-alpha,
visfatin, retinal binding protein 4). The relative roles of
all these hormones in modifying appetite and insulin resistance
are the subjects of intense research. While leptin is also secreted
by the placenta, the mammary gland, and the stomach, adiponectin
seems to be exclusively secreted by adipose tissue into the
bloodstream; its levels are inversely correlated with body mass
index. The word resistin was chosen because of the observed
insulin resistance after injections of this hormone. Visfatin
mimics the effects of insulin.
Hormones released by the fat cells are not the only signals
that communicate the state of energy balance in the body to
the brain. The recently -discovered gastric hormone ghrelin
increases hunger through its action on hypothalamic centers.
Blood ghrelin concentration increases during fasting. Humans
injected with ghrelin report sensations of intense hunger. A
gastric bypass operation tends to reduce the levels of this
hunger-inducing hormone.
In the current scientific context we are achieving a radically
new vision of energy homoeostasis. We used to visualize the
brain as being in control of the body. Today, we have to visualize
the continuous exchanges of signals between peripheral parts
of the body (fat cells, stomach) and the brain centers. The
concept of a ‘primal adaptive system’ is ever more
useful when referring to the basic adaptive systems involved
in what we commonly call health. Originally, I suggested this
term to avoid the artificial separations between the nervous,
immune, and endocrine systems. Today, as we are learning that
fat cells, the heart and the digestive tract are all endocrine
glands, the network we call the ‘primal adaptive system’
appears larger and much more complex than we could have imagined
twenty years ago. Our study of obesity is an opportunity to
formulate fundamental questions about when and how our basic
adaptive systems develop, adjust and regulate themselves.
It is probable that the recently discovered components of the
primal adaptive system also reach their set point levels during
critical phases of the primal period. This is suggested by animal
experiments which have detected a neonatal leptin surge following
intrauterine undernutrition that caused obesity in adulthood.(4)
Among humans it has been demonstrated that breastfed babies
have higher leptin values than bottle-fed babies in the first
four months of life.(5) Furthermore, breast milk of mothers
of small-for-gestational, large-for-gestational, and appropriate-for-gestational
babies has different amounts of leptin, especially during the
first month of postpartum life. More rapid growth and significantly-
reduced leptin levels are seen in the small-for-gestational
age group during the first postnatal 15 days, compared with
the others.(6) Although the details are complex, the point is
that important activity occurs during the critical perinatal
period.
Obesity and schizophrenia
There are many other fruitful ways to explore the ‘Primal
Health Research Data Bank’. One is to observe diseases
that share the same risk factors in the primal period. Where
obesity is concerned, this suggests possible links with schizophrenia
(visit www.birthworks.org/primalhealth and type the key word
‘schizophrenia’). It is now well established that
those who spent their prenatal life during the Dutch Hunger
Winter were also at increased risks of developing schizophrenia
later in life. This has been confirmed recently by an evaluation
of the rates of onset of adult schizophrenia following prenatal
exposure to the Chinese famine of 1959-1962, which involved
a population of 62 million in the Wuhu region of the Anhui province.
It is noteworthy that the well-known correlation between obesity
and schizophrenia predates the availability of modern antipsychotic
drugs.(7) It is also notable that the prevalence of glucose
intolerance and diabetes type 2 is high among schizophrenic
cohorts.(8) Today obesity, diabetes type 2, and schizophrenia
may be interpreted as the long-term consequences of developmental
defects during the pre- and perinatal periods of development.
We must also consider that certain brain structures (such as
the hippocampus) and the pancreas share the same basic nutritional
needs during their critical periods of development, for example
zinc. It is still premature to claim that obesity, different
expressions of insulin resistance, and schizophrenia are different
aspects of the same disease expressed in a great variety of
dominant symptoms, according to individual genetic predispositions.
But it is now time to claim that the concepts of ‘Primal
Adaptive System’ and ‘Primal Health Research’
are dissolving the conventional barriers between scientific
and medical disciplines.
Further research
The primal health research perspective suggests the sort of
research that can help explain the worldwide epidemic of obesity
(and diabetes type 2). We must compare the diet of modern mothers-to-be
with the diet of previous generations, whatever the geographical
context. For example soft drinks and trans-fatty acids are particularities
of modern diet. We must also look at how modern management of
the perinatal period deviates from the physiological model.
Today, among the unprecedented ways to interfere with the physiological
processes, the most common ones are the widespread practice
of labour induction, the increased rates of non-labour (elective)
caesarean, and the association of epidural anaesthesia with
synthetic oxytocin infusion. Bill Clinton has a lot on his plate
if, in his mind, ‘young people’ include—first
and foremost—mothers-to-be.
Michel Odent
References:
We mention the references that preceded the recent development
of Primal Health Research, and those that cannot be found in
the Primal Health Research Data Bank.
1 – Odent M. Primal Health. Century-Hutchinson. London
1986 (2nd edition. Clairview 2002)
2 - Ravelli GP, Stein ZA, Susser MW. Obesity in young men after
famine exposure in utero and early infancy. N Engl J Med. 1976
Aug 12;295(7):349-53
3 – Zhang Y, Proenca R, Maffei M, et al. Positional cloning
of the mouse obese gene and its human homologue. Nature 1994;
372:425-32
4 – Yura S, Itoh H, Sagawa N, et al. Role of premature
leptin surge in obesity resulting from intrauterine undernutrition.
Cell metabolism 2005; 1(6):371-78
5 – Savino F, Nanni GE, Maccario S, et al. Breast- infants
have higher leptin values than formula-fed infants in the first
month of life. J Pediatr Endocrinol Metab 2004; 17(11):1527-32
6 - Dundar NO, Anal O, Dundar B, et al. Longitudinal investigation
of the relationship between breast milk leptin levels and growth
in breast-fed infants. J Pediatr Endocrinol Metab. 2005 Feb;18(2):181-7
7 - Allison DB, Fontaine KR, Heo M, et al. The distribution
of body mass index among individuals with and without schizophrenia.
J Clin Psychiatry. 1999 Apr;60(4):215-20.
8 - Bushe C, Holt R. Prevalence of diabetes and impaired glucose
tolerance in patients with schizophrenia. Br J Psychiatry Suppl.
2004 Apr;47:S67-71.-
(Click here to go back to the top of the page)
