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College aantekeningen HNH34106 Nutrition and the ageing body (HNH34106)
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Nutrition and ageing bodyLecture 1 & 2
- Life-expectancy increased with 5.7 years between 2000 and 2019
- 21% of Europeans are >65 years
- Projection for 2050:
o 30% of Europeans >65 years
o 150 million
- Despite increase in average life expectancy, no increase in max lifespan
- Health span = years of life spend in good health
- Controversy → unhealthy/disease
- In real life → health is on a spectrum, not black and white
- We want to get older in a healthy situation
- Gap with lifespan is increasing
- Main reasons for health gap: CVD, diabetes mellitus, cancer, AD, dementia
- Health gap variation:
o 7-year gap in lifespan between Dutch people with a low income (practical
education) and high income (theoretical education)
o 15-year gap in healthspan between these two groups
- Prevention given health care
- National prevention agreement:
o Smoking
o Obesity
o Alcohol abuse
- Advise council for public health and society:
o Sugar levy (tax), lower tax on fruits and vegs, ban commercials for unhealthy
foods
o Less fast-food shops in certain areas, such as around high-schools
- Influence Covid-19 on:
o Maximum lifespan; possibly, but not per se
o Average lifespan; -1.13 years in US
o Health-span; post-IC syndrome, clear decline in health
o Socio-economic gap in health-span; yes, it is unequally hitting low social
economic classes
- What is more important for longevity? → lifestyle and environment
- Blue zones → high ages → Loma Linda, Sardinia, Okinawa etc. What do these people
do?
o Loma linda: healthy social circle, nut consumption, whole grains, culturally
isolated, high soy consumption, no alcohol, faith, family, no smoking, semi-
vegetarian, constant moderate physical activity, social engagement, legumes.
o Okinawa: No time urgency, likeability, turmeric intake, empowered women,
sunshine, gardening, family, no smoking, semi-vegetarian, constant moderate
physical activity, social engagement, legumes.
o Sardinia: fava beans, high polyphenol wine consumption, high soy
consumption, no alcohol, faith, family, no smoking, semi-vegetarian, constant
moderate physical activity, social engagement, legumes, whole grains,
culturally isolated, empowered women, sunshine, gardening.
,- Effect of lifestyle on lifespan: large multi-cohort study in high-income countries.
o Smoking: ca. -4.8 years
o Physical inactivity: ca. -2.4 years
o Alcohol abuse: ca. -0.5 years
Impact of diet was not assessed, but intermediates:
o Diabetes: -3.9 years
o BMI: -0.7 years
o Hypertension: -1.6 years
- If you have a sibling of >100 years old, you have a 4-8x higher chance to reach 100
years yourself.
- Genetics vs lifestyle:
o Long-lived sibling increases change to reach high age
o Parents and offspring of long-lived persons also reach higher ages
o However, also spouses of long-lived persons reach higher ages
o Spouses are not genetically similar but share: traits, behavior, environment
o Longevity families: combination of genetics, environment and cultural factors
- Twin studies are used to unravel the true genetics determinants from environmental
determinants. Compare monozygotic vs dizygotic twins. Estimation of true heredity
of lifespan:
o max. 25%
o most recent estimates around 12%
12-25% is based upon genes. The rest is lifestyle, environment, bad luck.
- Genes may play a role in longevity:
o Many studies have explored associations between variations in the genome
and longevity
o Only two gene location (loci) have been identified:
▪ APOE (E2 = protective, E4 = deleterious) → apolipoprotein E: a
cholesterol carrier in peripheral tissues and the brain. Associated with
susceptibility to CVD and AD.
o FOXO3A
▪ Trigger for apoptosis (programmed cell-death)
- Evolution of ageing: why does ageing exist? Is there an evolutionary benefit? Human
species experience ageing mainly after reproductive fitness
- Essential Life Span (ELS) = the period of survival of the body until reproduction, for
which evolutionary forces and natural selection have resulted maintenance
mechanisms protecting structural and functional designs of the organism.
- ELS: 45-50 years, to menopause (losing fertility), similar for men (45 years). Bone
density deteriorates more in women, but they become older.
- Average lifespan: 80 years
- Maximum lifespan: 122 years
- No evolutionary advantage of ageing and limited lifespan. Under natural conditions:
death will occur before old age (Accidents, diseases, predation). No mechanisms
were ever needed to ‘make room for newborns’, death is not programmed in our
genes. Absence of natural selection pressures. After you have reproduced, there are
no evolutionary pressures selecting genes that promote lifespan and health at later
age.
- Lifestyle and environment (75%) are more important for longevity than genes (25%).
,Lecture 3
- Evolutionary reason for menopause, 2 possibilities:
o Adaptive: selective advantage of female reproductive cessation. More energy
used for helping existing children instead of having more children.
o Non-adaptive theory: artifact of the dramatic increase in human life
expectancy. Nonexistent in other mammals (in wildlife you will already die
before encountering menopause).
- Grandmother hypothesis = you help raising your grandchildren. Without a
grandmother, sisters had different amounts of children (lower amount of children of
the sister, when the grandmother was dead already). There is no evolutionary benefit
of ageing (absence of survival pressure). There might be evolutionary benefit of
longevity.
- Male menopause → is it different with females? Testosterone production/levels
decrease gradually beginning around age 30 (but is not even a decrease of half).
Sperm production does not stop.
- Sarcopenia = muscle loss (muscle atrophy) that occurs with aging and/or mobility.
- Ageing = the process during which structural and functional changes accumulate in
an organism as a result of the passage of time. The changes manifest as a decline
from the organism’s peak fertility and physiological functions until death.
- When does ageing start?
o Brain volume: peak around 15.2 years of age. White matter: peak around
around 28.7 years of age.
o Muscle strength: males peak around late 30s, female peak around 30 years
also.
o Bone mineral density: males and females peak around 30, females have a
steeper decline in bone mineral density, males have a gradually decline.
- Ageing is accumulation of damage → is partly inevitable, from the inside. Due to
metabolism, DNA replication damage, genetic predispositions (APOE allele). Outside
damage is preventable, from the outside, due to exposure to toxins, sunlight, alcohol,
smoking, radioactivity and diet.
- Hallmarks of ageing:
o Genomic instability
o Loss of proteostasis
o Altered intracellular communication
o Etc.
- Hallmarks of ageing should fulfill 3 criteria:
o Should manifest during normal ageing (without syndromes/diseases)
o Its experimental aggravation should accelerate ageing (fast forward ageing in
mouse model)
o Its experimental amelioration should retard the ageing process and thus
increase healthy lifespan (slowed down ageing in mouse)
- Loss of proteostasis (protein misfolding)
o Oxidative stress, heat shock, ER stress → can lead to misfolded proteins →
unfolded protein → 3 options:
▪ Get rid of it via autophagy
▪ Protein degradation
, ▪ Or it is refolded in the right folding or it is aggregated/accumulated
leading to ageing.
- Stress causes protein to unfold. Unfolded proteins should refold/be disposed, if not:
aggregation. Nutrients spermidine and omega-6 fatty acids activate autophagy in
mice and nematodes and thereby increase lifespan.
- Loss of proteostasis can lead to Alzheimer’s Disease, Parkinson’s Disease,
Huntington’s disease, ALS and Cataract (Staar).
- Genomic instability:
o Ageing = accumulation of genetic damage throughout life
o Increased DNA damage accumulation can cause Werner syndrome (lack of
proofreading)
- Werner syndrome = premature ageing syndrome. Early hair greying, hair loss,
wrinkling. Early death (around 54 years), often due to CVD or cancer.
- Genomic instability caused by:
o Endogenous induced damage: metabolism and replication
o Exogenous damage: air pollution, toxins
- Endogenous DNA damage, by metabolism:
o Mitochondria → where metabolism takes place. Oxidative phosphorylation
pathway → reactive oxygen species (ROS) → can cause damage to cells and
DNA. They also have positive functions (signaling). ROS are superoxide anion,
peroxide, hydroxyl radical, hydroxyl ion, they have free radicals and become
unstable. 3 anti-oxidants:
▪ SOD (superoxide dismutase): attacks destructive oxygen free radicals
like superoxide.
▪ Catalase detoxifies peroxide.
▪ GPx: glutathione peroxidase.
Other oxidative molecules from nutrition: vitamin C.
o ROS-induced damage: mitochondria damage, lipid peroxidation (cell
membrane), DNA damage and mutation and protein damage.
- Endogenous DNA damage, by replication:
o DNA replication by DNA polymerase (build building blocks and proof reads,
checking the letters).
o 1 cell contains 6x10^9 base pairs of DNA
o Spontaneous errors occur in every 10^9 BP.
o You have 10^14 cells in your body, that divide >1 per year: 6x10^14 mistakes
per year
o Due to Proofreading of DNA polymerase is: 1 error per 10^14 BP of DNA
copied.
o But still many replication errors occur causing replication induced damage.
- Telomere attrition: telomeres are protective caps at the end of chromosomes.
Telomeres shorten per reproduction cycles until they reach replicative senescence
(Hayfick limit). Telomerase increases telomere length, but telomerase is not
expressed in many cells.
- Telomeres are the gap of the end of your shoe laces. It protects the chromosome
from damage. The telomere shortens every certain multiple replication. Telomere at
senescence. Telomerase adds more telomeres to the ends of DNA, however it is not
expressed in every cell.
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