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Printable Handouts
Navigable Slide Index
- Introduction
- Part I: background
- Adult BMI and CHD mortality
- Birth weight and CHD mortality
- How do both under\overnutrition elevate CVD risk
- How obesity leads to CVD
- How does prenatal undernutrition elevate CVD risk
- Developmental origins of health and disease (1)
- Birth weight and diabetes
- Visceral fat gain after SGA
- SGA, infant weight gain and fasting insulin
- Insulin resistance (guinea pig)
- Visceral adiposity (rat)
- Developmental origins of health and disease (2)
- Responses to undernutrition and CVD risk
- The "thrifty genotype" hypothesis
- Famine as a bottleneck
- Fetal undernutrition and obesity-related diseases
- A second type of bottleneck: developmental
- Outline: how much energy do our bodies have?
- Part II: the argument
- Metabolic scaling
- Fractal vasculature
- Fractal distribution
- Plant fractals
- Scaling of plant growth rate
- Constraints on energy
- Outline: how do humans partition their energy?
- Energy partitioning
- Growth rate vs. body mass
- Mammals vs. reptiles
- Humans have reptilian growth rate
- Human energy partioning: growth expenditure
- Use of 'saved' energy by the human body
- Brain size and energy needs
- Brain vs. body size in adult primates
- Neonatal brain size
- Percent of total RMR to brain in different animals
- Cerebral metabolism during infancy and childhood
- Percent of RMR to brain at different ages (human)
- Human energy partioning: brain expenditure
- Outline: developmental bottleneck
- Infant energy requirements
- Diarrhea (global estimate)
- Respiratory infections (Uruguay)
- Energy costs of infections
- Infection-malnutrition synergy
- Mortality rate by cause
- The developmental bottleneck
- Outline: metabolic adaptations
- How evolution equipped the infant's body to survive
- Baby fat
- Mammals: % fat at birth
- Fat percent by age
- Caloric deposition in fat
- Childhood infections as feast and famine
- The role of body fat
- Body fat and insulin resistance protect the brain
- Insulin resistance and fat gain
- Shunting glucose from muscle to fat
- Summary: adaptive role of insulin resistance
- Outline: early nutrition, evolution and health
- Fetal undernutrition and the metabolic syndrome
- Outline - SGA and metabolism: skeletal muscles
- SGA and insulin resistance
- Low birth weight and muscle insulin resistance
- Outline - SGA and metabolism: increased body fat
- Fat gain after SGA
- Outline - SGA and metabolism: fat deposition
- Visceral fat gain after SGA
- Outline - SGA and metabolism: fat mobilization
- SGA: hyperlipolytic response to stress
- Summary of hypothesis
- Part III: conclusion
- Review
- Summary of argument
- Developmental plasticity
- Modes of human adaptation
- Trends in dietary fat intake: Asian nations
- Low birth weight in Asian nations
- Thank you
- Further reading: baby fat, brains and evolution
- Further reading: DOHaD evidence
- Further reading: DOHaD evolutionary approaches
- Further reading: DOHaD public health implications
Topics Covered
- The Developmental Origins of Health and Disease
- The thrifty genotype hypothesis
- Metabolic scaling in mammals
- Energy partitioning in humans
- The developmental bottleneck of weaning
- Baby fat as a brain buffer
- How fat and insulin resistance protect the brain
- Why prenatal undernutrition induces the metabolic syndrome
- Implications for adaptation and global disease change
Links
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Talk Citation
Kuzawa, C. (2020, August 16). Early nutrition, development and health: evolutionary perspectives on the metabolic syndrome [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 3, 2024, from https://doi.org/10.69645/LNIJ4080.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Christopher Kuzawa has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Early nutrition, development and health: evolutionary perspectives on the metabolic syndrome
A selection of talks on Metabolism & Nutrition
Transcript
Please wait while the transcript is being prepared...
0:00
Welcome to Early Nutrition,
Development, and Health.
My name is Chris Kuzawa.
I'm a Biological Anthropologist
at Northwestern University.
In this talk, I'm going to
discuss some exciting new
research that's providing
insights into the causes
of some of the most common
sources of adult mortality,
including obesity, diabetes,
and cardiovascular disease,
and we've known for a long time
that these conditions have
both a hereditary component
tracing to the genes,
and a lifestyle component
tracing to factors like diet.
But during the past
15 years or so,
we've learned that
there's a third component
of risk for these conditions,
which traces to the plasticity
of developmental biology.
Biological systems
like energy metabolism
have the capacity to
modify their settings
in response to conditions
experienced early in life.
As we'll discuss,
this plasticity may have an
important adaptive function,
but also has an effect on
metabolism and physiology
that lingers into adulthood
to influence our risk of
developing metabolic and
cardiovascular disease.
Our goals in this lecture
will be to first review
the evidence for these effects
of development on later health,
but more importantly,
to use an evolutionary
framework to try
to illuminate why
the body responds
to early environments
in this way.
In the course of
addressing this problem,
we will cover a
broad terrain that
touches on everything from
the basic principles of
evolutionary biology,
fractals and nature, the
evolution of the human brain,
the function of baby fat,
and the causes and consequences
of infant mortality.
But before reviewing
this literature
and the evolutionary
forces that shape
this aspect of our
developmental biology,
let's first begin with a finding
that is likely quite familiar.
1:36
This graph shows
the relationship
between excess body weight,
as measured by the
body mass index,
and risk of suffering from a heart
attack or coronary heart disease.
If there's anything that we know
about cardiovascular diseases,
it's that gaining excess
weight is a sure way
to increase our risk
of suffering from one.
Now because this relationship
is so well known,
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