M4-Lecture2 Flashcards
The microbiome in development and health
Acondition in which the gut bacteria become imbalanced.
Dysbiosis
Dysbiosis has been associated with diseases such asInflammatory Bowel Disease (IBD), Obesity, Diabetes, Autism, leaky gut syndrome, celiac disease, heart disease, dementia and certain gastrointestinal cancers.
True
There are many factors that can lead to dysbiosis:
the excessive or wrong use of antibiotics, excessive alcohol consumption, increased intake of sugar or protein, frequent use of antacids, exposure to pesticides, artificial sweeteners and chronic stress
Poor dental hygiene and anxiety can also lead to dysbiosis
True
See contributing factor but not cause
The bidirectional communication between the central nervous system and gut microbiota, referred to
Gut-brain axis
Through signaling from gut-microbiota to brain and from brain to gut-microbiota by means of
neural, endocrine, immune, and humoral links
Hormones, neurotransmitters and immunological factors released from the gut are known to send signals to the brain either directly or via autonomic neurons
True
Studies on Germ free animals have shown that bacterial colonization of the gut is central to development and maturation of both Enteric NS and Central NS
True
The absence of microbial colonization is associated to an altered expression and turnover of
Neurotransmitters in both nervous systems
Studies conduced on Germ free animals have also demonstrated that microbiota influences stress reactivity and anxiety-like behavior, and regulates the set point for HPA activity
True
Germ free animals, also have memory dysfunction probably to be ascribed to an altered expression of brain-derived neurotrophic factor (BDNF), one of the most important factors involved in memory
regulates internal organ functions such as digestion, heart rate, and respiratory rate, as well as vasomotor activity, and certain reflex actions, such as coughing, sneezing, swallowing, and vomiting.
The vagus nerve
Neurochemical and behavioral effects were not present in vagotomized mice, identifying the vagus as the major modulatory constitutive communication pathway between microbiota and the brain
Your gut and brain are also connected through chemicals
Neurotransmitters (control feelings and emotions)
Many of these neurotransmitters are also produced by your gut cells and the trillions of microbes living there
True
A large proportion produced in the gut:
neurotransmitter
Serotonin
Your gut microbes also produce a neurotransmitter called
Hint: which helps control feelings of fear and anxiety
gamma-aminobutyric acid (GABA)
Studies in mice have shown that certain probiotics (Lactobacillus and Bifidobacterium) can increase the production of GABA and reduce anxiety and depression-like behavior
Your gut microbes produce lots of
SCFA,such as butyrate, propionate and acetate by digesting fiber
SCFA affect brain function in a number of ways, such as reducing appetite. How?
Consuming propionate can reduce food intake and reduce the activity in the brain related to reward from high-energy food
Butyrate and the microbes that produce it are also important for forming the blood-brain barrier
True
Gut microbes also metabolize bile acids and amino acids to produce unconjugated and secondary bile acids that act as signalling molecules and metabolic regulators
is the main energy source for human colonocytes, can induce apoptosis of colon cancer cells, and can activate intestinal gluconeogenesis, having beneficial effects on glucose and energy homeostasis
Butyrate
is transferred to the liver, where it regulates gluconeogenesis and satiety signalling through interaction with the gut fatty acid receptors.
Propionate
the most abundant SCFA and an essential metabolite for the growth of other bacteria—reaches the peripheral tissues where it is used in cholesterol metabolism and lipogenesis, and may play a role in central appetite regulation
Acetate
See functions of SCFA
Your gut-brain axis is also connected through
The immune system
Gut and gut microbes play an important role in your immune system and inflammation by controlling
what is passed into the body and what is excreted
is an inflammatory toxin made by certain bacteria. It can cause inflammation if too much of it passes from the gut into the blood
LPS
Data from both human and rodent studies has linked an obese phenotype to elevated circulating levels of plasma LPS
This can happen when the gut barrier becomesleaky, which allows bacteria and LPS to cross over into the blood
Inflammation and high LPS in the blood have been associated with a number of brain disorders including severe depression, dementia and schizophrenia
In 2021, around29 percentof adults aged 18 years and older in Canada were obese, while 36 percent were overweight.(many factors contribute).
Just like other organs in the body, the microbiome can dynamically respond to a variety of internal and external physiological cues, such as food intake, energy requirements, and stress, in order to maintain a state of metabolic homeostasis
Germ-free mice had 42% less body fat than normal mice even though the normal mice ate 29% less food/day. When germ-free mice were colonized with bacteria they increased body fat by 57% even though they ate 27% less food (↓ in lean body mass).
In fat mice, the relative abundance of Bacteroidetes and Firmicutes was altered (↓ in Bacteroidetes).
is a major manipulator of gut microbiome; Ex., high-fat diet- (HFD-) feeding develops microbiome dysbiosis in parallel to systemic abnormalities into the host metabolism causing obesity and type 2 diabetes
Diet
The exact taxonomic composition that constitutes a “healthy” gut microbiota is still unclear
True
is an essential component to host health
Microbial diversity
Compared to their lean counterparts, obese individuals have a markedly lower bacterial diversity, and decreased fecal microbial gene richness
See diagram
True
The contribution of gut dysbiosis in obesity is well known
The mechanisms are not well defined
True
is a major manipulator of gut microbiome; Ex., high-fat diet- (HFD-) feeding develops microbiome dysbiosis in parallel to systemic abnormalities into the host metabolism causing obesity and type 2 diabetes
See diagram
Diet
The microbiota of people with obesity contains lower proportions ofBacteroidetesand higher proportions ofFirmicutesthan those from people without obesity as is also seen in pregnancy
Yes
Most studies of overweight and obese people show a dysbiosis characterized by a lower diversity
True
Germ-free mice that receive faecal microbes from obese humans gain more weight than mice that receive microbes from healthy weight humans.
True
Gut microbiota dysbiosis probably promotes diet induced obesity and metabolic complications by a variety of mechanisms including
(I) Immune dysregulation
(II) Altered energy production
(III) altered gut hormone regulation
(IV) pro-inflammatory (like LPS crossing endotoxins crossing gut barrier - to circulation
Randomized controlled trials have shown that higher production of SCFAs correlates with lower diet-induced obesityand with reduced insulin resistance
True
See diagram
Antibiotics kill both the good and the bad
True
Mice treated with antibiotics gained weight.
True
Antibiotics mixed with animal feed makes them grow quicker.
True
Children treated with antibiotics during the first 6 months have a 22% higher probability of being obese at 3 years.
True
Helicobacter pylori appears to lower risk of developing asthma and allergies.
True
It may have been a “normal” bacteria many years ago. Its loss may be associated with acid reflux
True
See digram
Why do some people have really poor outcomes and others are almost asymptomatic? What is different between these individuals?
Risk factors for poor outcome include age and metabolic disorders such as obesity and type 2 diabetes
The well-known comorbidities of COVID-19 are all associated with dysbiosis
True
1918 pandemic caused a cytokine storm in healthy individuals, while this one causes a cytokine storm in unhealthy individuals.
Yes
Infection with SARS-CoV2 can cause excessive inflammation with enhanced production of cytokines and interferons leading to severe disease with poor outcomes
True
COVID-19 may also cause epithelial barrier dysfunction enhancing damaging inflammatory responses
True
But healthy microbiota (variety and volume) can prevent the effects of COVID-19
Yes
microbes are beneficial microbes that directly act on the host immune system to prevent invasion and colonization of pathogenic microbes
Commensal microbes
Within one week of COVID-19 infection, they observed a reduction in alpha diversity in the gut microbiome
True
Gut microbiota dysbiosis after disease resolution could contribute to persistent symptoms
True
fecal bacteria transplantation (FMT), prebiotics, and probiotics may play a positive role in the treatment of COVID-19 and reduce the fatal consequences of the disease
True
Is traditionally divided into Crohn’s disease (CD) and ulcerative colitis (UC)
Inflammatory Bowel Disease (IBD)
is one of the most common gastrointestinal (GI) disorders and the bacterial role has been largely investigated
Irritable Bowel Syndrome (IBS)
Fecal and colonic mucosal biopsy samples from IBS patients and healthy controls demonstrated a significant reduction in the concentration of aerobic bacteria such as the Lactobacillus species in fecal samples from IBS patients compared to healthy controls
True
Increasing evidence shows that IBS patients are affected with higher levels of stress and a negative emotional well-being
Also, pre & post natal factors
diet
flora changes
prior infection
gut-brain axis
True
See diagram
Under normal circumstances, mucus epithelium barrier confines microbes to the epithelial surface or intestinal lumen where homeostatic immune responses are induced to maintain barrier integrity and tolerance among commensal microbes.
True
Once the barrier is breached by influx of inflammatory mediators, pathogens or any agents that provoke intense immune reactions, severe inflammation occurs and this will affect the intestinal environment, and changes the gut microbiota composition
True
Combination of low grade mucosal inflammation with visceral hypersensitivity and impaired bowel motility could be the underlying etiology for IBS pathogenesis
True
Reduction in the intake of foods that are high in fermentable oligosaccharides, disaccharides, and monosaccharides and polyols (FODMAP) reduces GI symptoms and improves disease-specific quality of life in patients with IBS. At least 86% of patients with IBS report symptomatic benefit
True
are short-chain carbohydrates that are easily fermentable by gut bacteria into methane and hydrogen gasses but are poorly absorbed
FODMAPs
Dysbiosis was found significantly greater in patients with CD than with UC, as shown by a more reduced diversity, a less stable microbial community and eight microbial groups were proposed as a specific microbial signature for CD
Yes
Although UC and CD share many epidemiologic, immunologic, therapeutic and clinical features, our results showed that they are two distinct subtypes of IBD at the microbiome level
True
See diagrams
Which hypothesis states that the lack of early microbial exposure may reduce tolerance of the adaptive immune response
Hygiene hypothesis
Factors at play for lack of early microbial exposure
cleaner living, urbanization and increased antibiotic use
Several studies demonstrated that gut microbiota composition is altered in patients suffering from T2D, but it is not clear whether these changes are a cause or simply a consequence of the disorder
True
See diagrams
have been shown to disrupt the balance and diversity of gut microbiota
Sucralose, aspartame, and saccharin
Food additives, such as emulsifiers, which are ubiquitous in processed foods, have also been shown to affect the gut microbiota in animals
True
Other areas of concern include the side effects of popular restrictive diets on gut health. These include
These include some strict vegan diets, raw food or “clean eating” diets, gluten-free diets, and low FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diets used to treat irritable bowel syndrome
See diagram
