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Summary Nutrition and NCD: Cancer and Cardiometabolic Diseases (HNH20503)
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Nutrition and NCD: Cancer andCardiometabolic Diseases
HNH20503
Week 1
Week 2
Week 3
Week 1
Learning outcomes:
- Identify biological processes that contribute to the development and progression of
cancer
- Explain the role of diet, lifestyle and body composition in the development,
progression, and survival of cancer and how this translates into dietary guidelines
Video 1.1.c: Introduction to nutrition and cancer
Prevalence and incidence:
⅓ people in Western countries get cancer, and cancer causes ⅙ deaths worldwide. In many
parts of the world cancers cause even more deaths than CVD.
Cancer incidence in 2021 was 14 mil. people. It is expected that in 2030 this will be 22 mil.
It can partly be explained by increased weight and size of the population.
The most common types of cancer are: colorectal, breast, and prostate.
Non-modifiable risk factors:
- Age is the most important risk factor for cancer.
- 5-10% is familial cancer (inherited mutated gene).
Modifiable risk factors:
- smoking
- viruses
- occupational exposure
- nutrition: directly and indirectly
Video 1.1.d: Genes, lifestyle, or bad luck?
Scientific research has shown that cancer risk actually depends on a combination of genes
and exposures = 90%. Exposures known to increase cancer risk are:
- tobacco smoke
- hormones
- radiation
- medication
- chemicals
- infectious agents
- pollution
,Besides that: diet and exercise affect the risk of the most common types of cancer.
Furthermore, cancer is a multifactorial disease; all cancers are caused by more than 1
factor.
30-40% of cancers are preventable by a healthy lifestyle.
Video 1.1.e: The first evidence
Migration studies: large population moving to another place and adapting to their lifestyle.
Cancer occurrence among these migrant populations changes fast. Within one or two
generations the immigrants already develop the same types of cancer as the natives.
Example: 19th century Japanese people moving to the U.S. Colorectal cancer went up to the
same rates as the U.S. population within two generations, and stomach cancer went down.
Reading 1.2.a: The cancer process Basic concepts
Imbalances in nutrition can have an impact on many of the processes that are involved in
maintaining normal structure and function, and cancer is one consequence.
There is a wide variety of cells, tissues, and organs in the human body, and this arises from
just one fertilized egg which undergoes a highly regulated series of cell divisions.
Differentiation: cells get the capability to perform specialized functions. In mature, healthy
human cells, differentiation is irreversible, meaning a cell’s specialism is fixed.
As cells age, they become more likely to function abnormally. Apoptosis: a cell commits
suicide when it’s damaged because it’s programmed to.
The majority of mammalian cells contain the following:
- Plasma membrane: lipid bilayer with protein attached. It controls the entry and exit of
metabolites and nutrients and can sense its external and internal environment.
Functions of membrane proteins are:
- forming cell junctions
- enzymatic
- transport
- cell interactions
- receptors
- Cytoplasm: comprised everything that is within the plasma membrane apart from the
nucleus. Contains organelles like mitochondria.
- Nucleus: contains the genetic material of each cell, which are contained in stretches
of DNA. Nucleotides on DNA consist of three parts:
1. deoxyribose sugar and
2. phosphate group form the backbone, and
3. one of four possible bases (adenine, cytosine, thymine and guanosine)
These four bases cause the DNA to spiral through pairing: A-T and C-G.
The order of nucleotides makes up the genetic code. Individual genes are transcribed
to form mRNA → exported to cytoplasm → binds to organelles called ribosomes →
ribosomes translate mRNA amino acids into proteins.
Normal cell cycle: growth and maintenance of healthy tissue requires cells to create identical
copies of themselves as they mature and age. A cell's chromosomes must be replicated and
then separated into two daughter cells, each with its own complete set of chromosomes.
DNA replication is complex and vulnerable to errors. Furthermore, cells are constantly
exposed to factors that can damage DNA at any time. There are however several processes
,that can detect damage and repair it. But this is not perfect and cells with abnormal DNA
may be produced.
Mutations: permanent changes in DNA sequence. Evolution proves that this sometimes has
beneficial effects, but it can also be neutral or harmful. Accumulation of DNA alterations in
surviving daughter cells may result in genomic instability: more susceptible to accumulating
the genetic changes needed for a cancer cell.
Gene expression: process by which the information encoded in the DNA of a gene is
transcribed and translated to form a functional gene product, typically a protein. Several
mechanisms are known to influence whether any particular gene is switched on or off, and
this determines the cell's differentiation. The pattern of gene expression determines cells’
structure and function (phenotype).
Transcription factors: a set of proteins that form a mechanism that controls gene expression.
They bind to specific regions of genes and either promote or suppress gene expression.
Epigenetic changes: alterations in gene expression due to modifications in DNA and
chromatin structure. These are heritable but reversible.
- DNA methylation: an example of epigenetic regulation of gene expression. DNA
methyltransferases are enzymes responsible for a normal methylation pattern.
Cancer cells have abnormal DNA methylation patterns. Many genes can be
hypermethylated in cancer: regulation, repair, apoptosis and metastasis.
Hypomethylation can cause genomic instability, which also promotes cancer
development.
- Modifications of histone structure: also, an example of epigenetic regulation. The
structure of histones can be altered by methylation, but more commonly by
acetylation. This is mediated by enzymes histone acetyltransferase (HAT) and
histone deacetylase (HDAC)This modification creates a more open DNA structure,
facilitating gene transcription and expression.
- MicroRNAs: epigenetic modifications due to activity of non-coding RNA molecules.
MicroRNAs are small RNA molecules, which do not code for proteins and are
emerging as key regulators of gene expression. They bind protein encoding mRNA
and thereby affecting mRNA stability and translation. Involved in regulation of 50% of
gene expression. A single microRNA may alter the expression of 100’s of genes. The
human genome encodes for over 1000 microRNAs.
Ageing is characterized by a loss of reserve capacity and then by an actual loss of function,
and a greater likelihood of stress and loss of homeostasis in the face of external challenges,
such as infections. These whole-body effects reflect changes at a cellular or molecular level,
including telomere shortening.
Telomeres are located at the end of chromosomes and represent the biological clock. With
each cell division, telomeres shorten, until they become too short: the DNA strand becomes
unstable, and the cells become unviable. Other processes that contribute to telomere
shortening are smoking, stress obesity, low levels of physical activity (PA) and a poor diet.
Embryogenesis: period of development after fertilization. Many abnormal characteristics of
cancer cells are distorted versions of the cells during embryogenesis: distorted cell signaling,
rapid cell division, migration through tissues, invasion or neighboring tissue and
angiogenesis.
, Angiogenesis: the growth of new blood vessels. Which is normally not seen in mature
organisms. genes for this become inactive, or latent, in an adult organism, but they retain the
potential to be activated.
In many ways cancer can be seen as the inappropriate and abnormal resurrection of existing
primitive pathways necessary for normal development after fertilization.
Nutrition during development: if there is limitation in supply of energy or nutrients, this can
affect the process of cell division and differentiation, and therefore health. Adaptive
processes mediated through epigenetics are involved to maintain critical functions such as
brain development, but maybe at expense of other processes. This can influence
susceptibility to cancer or other diseases throughout life.
DNA damage and repair:
DNA is continuously exposed to products of normal intracellular metabolism, like: ROS,
hydroxy radicals, and oxygen peroxide; as well as to external environmental factors such as:
UV, cigarette smoke. All can damage DNA. The physiological responses to DNA change can
be modified by dietary factors and by hormones (which can depend on diet, PA and excess
body fatness). Defects in DNA repair leads to genomic instability: more rapid accumulation
of DNA mutations and predisposition to cancer (progression). Most cancers acquire genomic
instability.
Tumor-suppressor protein p53: protects cells against cancer, which is reflected by the
finding that TP53 (gene that encodes p53 protein) is the most commonly mutated gene in
human cancer. In response to a range of stresses, p53 causes cells to undergo cell-cycle
arrest or apoptosis. Without p53, cells with stresses proliferate and survive, promoting
cancer development.
Tumor suppressor genes and/or oncogenes: mutant genes associated with carcinogenesis.
- Tumor suppressor genes: encode proteins that slow cell proliferation, maintain
differentiation, and correct DNA damage. Inactivated, cancer risk goes up.
- Oncogenes: abnormally functioning versions of genes that are involved in activation
of growth, replication and survival signals. Unregulated proliferation and prolonged
survival.
Each normal cell has two copies of the same genes. A mutation in just one copy is enough
for activation of an oncogene to induce cancer behavior. Both copies must be damaged in
order for the tumor suppressor gene to have a carcinomic impact.
Hallmarks of cancer and that effects them:
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