FFN Midterm 3

breathe. you can literally do this.

T/F: a single study can be enough to change nutrition recommendations

FALSE: a single study (generally) isn’t enough evidence to change nutrition recommendations

T/F: the pyramid of hierarchy of evidence build from bottom to top

TRUE: all the evidence builds on top each other, gives info to go higher up the pyramid

Why is there so much nutrition misinformation? (3)

* food labels, social media, and marketing are main sources of nutrition education for consumers
* Health Canada has strict FFN labelling regulations, but **compliance oversight is lacking -** companies can bend rules, work in grey zone
* **poor regulation of many nutrition providers** (eg blogs, product promotion, clinical counselling); evidence is cherry-picked

name the marketing considerations of FFN

(6)

* **health benefit**, communicate positive messages
* taste
* simplicity
* images that convey good taste, health (eg sun rays coming out of brain, conveys brain health with no actual claim)
* frequency of use and dosage
* target market regulation

What are the differences between a registered dietitian and a nutritionist in Ontario?

__Nutritionist__

* not a **legally protected** title (anyone can call themselves this)
* **no regulatory monitoring/compliance** - no regulatory college to go file a complain to

__Dietitian/Registered Dietitian__

* **legally protected** title
* **education/certifications:**
* 4-year undergrad in nutrition/dietics
* competitive internship (\~1 year)
* licensing exam
* jurisprudence exam (test of ethics and regulations) every 5 years
* **ongoing regulatory monitoring/compliance**

T/F: most Ontarions truly understand the difference between a dietician and nutritionist

FALSE: most public does percieve a difference, but when asked to name actual differences/prove it, \~73% cannot

from Justine’s study, what term was a standardized definition proposed for, and what was the definition?

**Medical nutrition therapy:** the **provision of nutrition information/advice** (dietary or supplemental) for the assessment/reassessment, diagnosis, intervention or monitoring of a disease or condition, to treat or manage **symptoms and/or medical conditions**

What is the current legislation around medical nutrition therapy (MNT) and what is the proposed legislative amendment (from Justine’s study)?

Currently: anyone in Canada can practice MNT regardless of skills, education, training etc

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Proposed Legislative Amendment: MNT is protected as a controlled act for regulated health professionals (RDs, medical doctors, nurses, optometrists, pharmacists, midwives etc) - ONLY within their own scope (eg dentists focus on teeth)

What are the media red flags when it comes to FFN therapies? (6)

1. promises a miracle cure/quick fix
2. testimonials as evidence
3. supporting research is single study, animal studies, or cherry-picked evidence
4. not supported by a credible source
5. sounds too good to be true
6. conflicts of interest (eg media getting commisions)

specific to weight management, what are the media red flags to look for? (8)

* miracle cure (‘lose weight fast!’)
* recommends very low kcal diet (anything < 1200-1500 kcals)
* lots of dependency on $$$ products
* lack of education on general healthy lifestyle factors
* salespeople acting as ‘conselors’ with no credible training/education
* pressure to sign up immediately for sales
* no potetential risks specified
* is it sustainable?

What is PEN?

Practice-Based Evidence; a resource to look for credible info; grades based on evidence

What are the steps to responding to nutrition misinformation

1. **Assess the impact** - what is the population health and safety issues; are there any risks (decreased quality of life, economic hardship etc)
2. **Collect the facts** - what does evidence suggest? what misinformation un/intentional? systems or policy issue? who was involved, who funded it?
3. **Consider your Role** - do I have the expertise to address this? will I be alone, do I have support? what is the solution I can give? what are consequences of taking/not taking action?
4. **Take action** - provide timely, concise feedback; choose format most appropriate to situation, identify resources
5. **Reflect** - what worked well? what were the barriers? changes for next time?

what does the environment (greenhouse gas production, plastics and pharmaceuticals in the coeans) have to do with bacteria and probiotics?

diseases in humans emerge from many factors, such as

* genetic and biological factors
* **physical environmental factors**
* **ecological factors**
* social, political and economic factors

T/F: *Lactobacillus rhamnosus* is a probiotic. Explain

FALSE: genetic research shows it isn’t (?)

Define probiotic

Live microorganisms that when administered in adequate amounts confer a health benefit on the host

define prebiotic

A substrate that is selectively utilized by host microorganisms conferring a health

define synbiotic

a mixture, comprising live microorganisms and substate(s) selectively utilized by host microorganisms, that confers a health benefit on the host

define postbiotic

a preparation of inanimate microorganisms and/or their components that confers a health benefit on the host

define fermented food

foods made through desired microbial growth and enzymatic conversions of food components

T/F: the higher the viable count and number of strains, the better the probiotic

FALSE: the type of strain is what matters, industry can try to trick by acting like how many strains you have and its count is important

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* fake nutritionists, celebrity health care providers, ‘experts’ are always giving advice

T/F: probiotics are produced by the body and come through the diet

FALSE: the only probiotics insisde us come when we consume them

Name some example of non-food probiotic products that exist

probiotic mattress pad, aftershave lotion,

Is there a link between obesity and probiotics/gut microbia? Why or why not?

original study done was on mice! 18 years after that study there have been no other studies that prove bacteria causes/reduces obesity

what is the gut-brain axis? does this concept have any validity?

the concept that the brain and gut ‘communicate’ through the central and enteric nervous system ; it has not been validated (I think) by studies;

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there are many connections of vagus nerve from the brain to different body parts; why not a brain-eyes connection, brain-kidneys, why just brain-gut

T/F: human studies exist suggesting brain effects with probiotic strains. Explain

TRUE: RDBPC study of 44 adults with IBS, diarrhea etc and mild-moderate anxiety and/or depression were studied; 14/22 patients in experimental group had depression reduced by 2 points, where only 7/22 of placebo did

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probiotic had no effect on anxiety, IBS symptoms

Can taking probiotics effect amounts of heavy metals adsorbed by the human body?

15% of Canadian women of reproductive age have enough mercury (0.3 microgram/g) to cause neurological damage to the fetus

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study in Tanzania showed that daily intake of Lactobacillus rhamnosus GR-1 supplemented yogurt for 3+ months resulted in 36% less mercury and 75% less arsenic adsorbed

what is the link between trauma patients and probiotics?

a study showed that trauma patients given probiotics combined with fermentable fibers for 15 days had significant reductions in number of death, sever sepsis, chest infections, central life infections and ventilation days

Administration of probiotics by mouth to **women** can prevent ____________________; it this proven?

urinary tract infection reccurance in post-menopause

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study showed that group of women who got probiotics on top of a drug TMP/SMX went from 6.8 UTI to 3.1 after one year

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note: the drug TMP/SMX went from 7 to 2.8

is there evidence to prove a link between probiotics and general colds/immunity?

supplementation of a probiotic for 3 weeks reduced winter infection duration by 20%, days with fever were also lower

name the 8 imprtant effects that the human microbiome has on the human body

1. affect your mental health, thoughts, and behaviours
2. help enforce skin’s protective barrier
3. play important role in cardiovascular health
4. they digest some of the food you eat
5. affect insulin production
6. affect health + functioning of your liver
7. regulate your immune system
8. affect density + strength of your bones

what quality of bacteria makes it more difficult to commercially develop them as a probiotic?

many bacteria in the oral and intestinal microbiotas are obligate anaerobes and are killed by oxygen

how do we get microbes when we are born

a lot come from the brith canal - babies who are born via C-section are exposed to less/different microbes

What is nectrotizing enterocolitis? what’s it’s link to probiotics?

commonest GI emergency of unknown cause, happens a lot in pediatric ICU; altered microbiota results in immature intestinal barrier = inflammation and tissue injury = intestinal necrosis

* 6% of preemies

if you want to choose or recommend a probiotic, what is a good website/resource

www.probioticchart.ca

www.usprobioticguide.com

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gives probiotic strains in products you eat + their applications to different diseases, dosage forms, CFU/dose

define fecal microbiota transplantation

the process of transplanting fecal matter, containing bacteria, viruses, metabolites, intestinal epithelial cells, undigested fiber, fat, protein and inorganic matter, from a healthy individual into a recipient; could be the future of microbiology

T/F: the types of microbes in your stool determine how healthy you are

FALSE: everyone’s stool microbes are different, nobody knows what composition is healthy or not

Give one example of fecal microbiota transplant being used to reduced a disease/symptom of a disease

cancer upregulates a transmembrane protein (PD-L1) that functions as a key regulator of T cells; this inhibits T cell attacks; antibodies bind to PD-1, block that interaction allowing T cells to attack BUT this causes damage to gut cells causing more inflammation - FMT is being used to recued the inflammation

what is the future of FMT?

we will be able to identify the organisms in the donor stool suitable for a specific application

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match post-transplant diet to encourage certain organisms to proliferate

What is the one study of his that Dr. Gregor Reid showed us?

A novel millet-based probiotic fermented food for the developing world

what are most common sources of caffeine, and how much caffeine do they contain? what are some additional sources?

coffee - 80-200 mg

tea - 15-50 mg

coke - 35-50 mg

chocolate - 10-30 mg

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other sources: energy drinks, caffeine energy gum, alcohol infused with caffeine

are energy drinks regulated as food or NHPs?

until 2011, were NHPs, now as foods

what are the new labelling requirements for energy drinks?

* nutrition facts panel
* total caffeine listed in mg, and cannot exceeed 180 mg / single serving container
* mandatory statements: high source of caffeine, not to be mixed with alcohol, not recommended for children, pregnant/breastfeeding, those sensitive to caffeine ETC

explain the mechanism of action of caffeine

caffeine is an antagonist to adenosine receptors; it is structually similar to adenosine to can bind to its receptors without activating them - acts as a competitive inhibitor

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adenosine receptors not being activated =

adenylate cyclase activated =

ATP convert to cAMP (aka increase in cAMP concentration) =

proteinkinase A is activated=

**broncodilation, neutrophil degranulation, mental excitation, tachycardia**

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comes from anti-oxidant content of coffee

T/F: caffeine = coffee. Explain

FALSE: coffee contains 100s of other biologically active compounds

T/F: a study found that acute ingestion of caffeine increased insuling sensitivity

FALSE: it decreased insuling sensitivity, which is not good - acute consumption of caffeinated coffee showed similar results

T/F: regular coffee drinking is protective against T2D in a dose-dependent manner

TRUE: study showed people who drank coffee regularly had dose-dependent response in lowering risk; dose-dependence gives us confidence

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control group of decaf coffee showed no pattern in risk reduction

when thinking of T2D, why does caffeine consumption vs coffee consumption show two different results?

the health benefits of coffee may come from compounds other than caffeine

what are some bioactive compounds in coffee other than caffeine?

**chlorogenic acid (CGA)**, potassium, niacin, magnesium Vit B3 precursor trigonelline, phenols, quinides

what is chlorogenic acid, and what is it’s potential mechanisms of action

the main source of anti-oxidant in coffee; 60+% of dietary antioxidant comes from coffee!

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CGAs are hydrolyzed by colonic microorganisms, then abosrbed in the large intestine - individual variability may come from people’s diverse microbiota

CGA may slow glucose absorption in the gut

when consuming caffeine pills vs decaf coffee, what do study results show?

caffeine pill - more glucose and insulin, less insulin sensitivity = negative effects

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decaf coffee = reduced glucose, higher insulin sensitivity = some positive effects

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this shows that other bioactibes than caffeine in coffee may result in good results

explain the study with cereal and coffee

* 10 healthy subjects
* 2 cereals: Crispix (high GI) or all-bran (low GI)
* 1 hr before cereal” caffeinated coffee or decaffeinated coffee
* caffeinated coffee increased glucose response to a high-GI cereal
* caffeinated coffee increased glucose response to a low-GI cereal
* looking at all 4 combos, high GI cereal with decaf had increased glucose response than low GI with caff… nothing can be concluded because of small sample size

in relation to T2D risk, caffeine ___________ and coffee _________

* caffeine may acutely decrease insulin sensitivity
* chronic consumption of coffee has been associated with reduced risk of T2D

T/F: patients at risk for T2D may benefit from decaffeinated coffee

TRUE: they could get all the benefits of chronic coffee consumption with detrimental effect of acute caffeine consumption

caffeinated beverages _______________ blood pressure

acutely increase

do caffeine containing beverages increased CVD risk or risk of heart failure?

no - but a lot of research has gone into answering this question for CVD

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for heart disease, long-term cohort study found no increase of risk

are there any studies linked coffee consumption, T2D, and CVD?

yes -cohort study in Finland found resthat CVD mortality decreased in T2D population - **coffee MAY decrease risk of CVD in T2D population**

what is nutritional genomics?

the concept that depending on someone’s genotype, exposure to a nutrient that have a different health or performance response

what is the link between nutritional genomics and caffeine?

a gene called CYP1A2 codes for a liver enzyme that metabolizes caffeine; accounts for 95% of caffeine metabolism

2 polymorphisms (variants) of the gene: CYP1A2\***1A/*1A** = fast metabolizer and CYP1A2\***1F*1A/1A or *1F/*1F** = slow metabolizers

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the **hypothesis** is that slow metabolizers of caffeine may be more at risk for the detrimental effects of caffeine - 1 of 2 people are slow metabolizers

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many studies have shown that slow metabolizers have increased risk of different diseases with higher caffeine intake

name examples of increased risks slow metabolizers of caffeine have

* case-control observational study found that: - coffee may **increase myocardial infraction risk** in slow metabolizers
* another study found same thing but only when caffeine intake was 200+ mg/day
* study found **risk of hypertension was higher** with higher caffeine intake in slow metabolizers
* study looking at **athlete performance** found that fast metabolizers had positive effect after caffeine, slow metabolizers had negative impact (longer cycling time)
* confidence because AC genotype had no change
* study found that there was **increased kidney dysfunction** only when large amount of caffeine consumed; no effect in fast metabolizers
* higher risk of **impaired fasting glucose** in slow metabolizers after increased coffee consumption (3 times higher risk)

if genetics could be acting as a confounder in big population studies, why isn’t genotyping done every time

* costly
* not always feasible in big studies
* innocence is bliss - people do not always want to know

What is the Health Canada recommendation of caffeine consumption?

can you tell if you’re a fast or slow metabolizer of caffeine from how you feel after drinking coffee?

NO! jittery vs no effect isn’t related to how fast you metabolize caffeine

what is the link between adenosine receptor genetics and response to caffeine?

DBPC trial found that people with the CC genotype of the gene ADORA2A gene displayed significantly higher anxiety than other genotypes

what are some pathophysiological changes obesity causes?

* changes to cardiac structure and function
* physical enlargement of various tissues and organs because because of increased body mass
* causes higher prevalence of sleep apnea as enlarged soft tissue block airway during sleep
* chronic inflammatory state because adipose tissue has endocrine functions so it produces adipokines which are pro-inflammatory
* obesity = excess adiposity

name the common health risks associated with obesity (7)

* hypertension
* dyslipidemias (high LDL, low HDL)
* metabolic syndrome
* coronary artery disease
* heart failure
* atrial fibrillation
* T2D

define metabolically healthy obesity (MHO)

individuals who have a high BMI, but no other evidence of poor health, cardiovascular risk factors

from the POV the MHO is it’s own disease, what does this suggest about obesity?

obesity is a **risk factor** of chronic disease instead of **being** a chronic disease

When it comes to MHO, what did early evidence suggest, and what does newer evidence suggest?

early evidence: MHO had similar CVD morbidity and mortality to non-obese, metabolically healthy individuals

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newer evidence: any level of obesity increases the risk of heart failure, any other cardiometabolic diseases

what factors affect dietary intake?

* genetics
* attitudes/perceptions towards food
* income
* education/work
* geography
* psychology
* medical conditions
* sleep
* ETC

what factors affect weight? is it just calories and exercise?

* individuality - different people respond differently to the same nutritional intake
* **genetics**; study showed people which specific gene had higher fat mass loss after low, or moderate-to-high protein diet
* sleep
* smoking
* stress
* history of weight-cycling (people who have cycled have higher body setpoint than those who maintain 1 weight)
* ethnicity
* medications (anti-anxiety, anti-depression increase weight)

do people who lose weight eventually regain it back often?

yes… at least 80% of people regain it all based on studies; loss maintenance was usually oinly 3 kg less which isn’t that clinically relevant

______________ is likely more harmful to health than sustaining an elevated BMI

weight cycling

according to multiple studies, what disease’s risk was significantly increased through weight cycling

endometrial cancer risk (increase 1.23-2.33 times)

in terms of adipose cells, elevated body weight is associated with:

* adipose hypertrophy
* more fat stored within adipocytes
* increase in number and size of fat cells

T/F: lifestyle intervention can reduce the number and size of fat cell

FALSE: you can only reduce size of fat cells not the number

a large weight loss leads to a metabolic rate that is _____________ compared to someone who is their size

much lower

what is the impact of people who have been through weight loss having a lower resting metabolic rate, and what makes it non-sustainable

low metabolic rate = low calorie (50 kcal) to maintain which is not realistic for a human

give two examples of the body/biological factors ‘fighting’ sustained weight loss

* low metabolic rate = very low calories to maintain, not sustainable
* neural responsivity: decrease in leptin (satiety hormone) and increase in ghrelin (hunger hormone); people always feel more hungry

why is weight loss relevant in the context of FFN?

* many nutraceutical products are marketed as weight loss aids
* not many long-term studies on weight loss products exist, long-term sustained weight loss product doesn’t exist

What are the FFN products marketed for weight loss that were covered in class?

* Herbal Magic
* Green Coffee Bean

Weight loss nutraceutical case study 1: what is the Health Canada claim vs Herbal Magic’s claim?

Health Canada: provides support for healthy glucose metabolism. Helps the body to metabolize carbs, fats and proteins. A factor in maintenance of good health

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Herbal Magic: supports healthy carbohydrate metalobism and lean muscle mass. Regulates blood sugar and insulin levels **resulting in reduced appetite and sugar cravings**

Weight loss nutraceutical case study 1: what are the issues with the research Herbal Magic uses to make claims on thier ‘Chromagic’ product?

* study: chromium improves HbA1c in diabetics BUT only if subject had very poorly controlled diabetes; dose in chromium in study and product are 6x different
* study: chromium improves body composition BUT there was a high drop out rate, and there was no control of diet and exercise (could change body composition); in follow up, huge variability surrounding weight loss

Weight loss nutraceutical case study 1: summarize the issue with the Chromagic product (3)

* some data provides use of chromium to enhance glucose management in patients with very poorly controlled diabetes, NOT in healthy individuals
* limited good quality data exists examining chromium and weight loss/body composition
* Chromagic is very unlikely to do what their claim says (reduce appetite and weight loss)

Weight loss nutraceutical case study 1: for the Essience product, what is the main difference between the Health Canada and Herbal Magic claim?

Health Canada = maintain weight/metabolism

Herbal Magic = improve metabolism

Weight loss nutraceutical case study 1: how do still people still lose weight with the Essience product?

they have a whole health plan with reducing calories, portion control, diet, food diary, pedometers

what are the main summary points of Weight loss nutraceutical case study 1: for the Essience product

* these supplements are unlikely to cause any clinically meaningful weight loss
* studies they use are not relevant to humans, the general pop, not specific to weight loss, not well designed

from Case study 2 in weight loss, how is green coffee extract supposed to work?

* CGA level in green coffee beans are the highest (they decrease with roasting)
* in experimental animals, CGA shows: reduced formation of triglycerides in liver, reduced weight gain in high-fat fed mice
* in V EARLY human studies. CGA may faciliate absorption of glucose from distal instead of proximal portion of the gut

Weight loss nutraceutical case study 2: green coffee beans; explains the study Dr. Oz cites on this product

* study done by Vinson et al.
* RDBPC, crossover (3 different treatments, combos of treatments used) study
* small sample size (16 adults)
* 3 treatments:
* placebo
* low dose CGA
* high dose (HD) CGA
* short term study: supplement taken for 6 weeks, then 2 weeks washout period, then repeat until everyone had taken all 3 treatments
* results: starting weights were not the same, couldn’t compare weight loss; HD CGA did not have highest weight loss as expected
* looking at overall weight loss, it is 17 lbs like Dr Oz claims, BUT looking at individual weight loss in individual groups, only \~2 kg
* overall study had a lot of methodological concerns

Weight loss nutraceutical case study 2: what does the meta analysis on green coffee extra show?

favours GCE, so it does help with weight loss, but not 17 kg like Dr. Oz was claiming

statistical signifiance _____________ clinical relevance

DOES NOT MEAN

Weight loss nutraceutical case study 2: if we wanted to assess the safety and efficacy of GCE properly, what needs to be done?

more rigorous trials that have a longer duration

what are the 3 types of fatty acids; give 2-3 examples of each

1. saturated (SFA): butyric acid, palmitic acid
2. monounsaturated (MUFA): oleic acid (cis), elaidic acid (trans)
3. polyunsaturated (PUFA): cis-9, 12-linoleic acid, cis-9, trans-11-CLA, arachidonic acid

PUFA and LC-PUFA include omega ___ and _. give example of both

* omega 3
* alpha-linolenic acid (ALA)
* eicosapentoanoic acid (EPA)
* docosahexaenoic acid (DHA)
* omega 6
* linoleic acid (LA)
* arachidonic acid (AA)

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define essential fatty acid, and give 2 example of PUFA/LC-PUFA

a type of nutrient that is required for normal physiological function but cannot be synthesized by the body in sufficient amounts, so must be obtained by the diet

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LA and ALA and essential PUFAs; we lack the enzymes to insert double bonds to make these acids, they are produced in plants

what studies in history showed importance of fat in diet?

1. 1929, George and Mildred Barr fed rats fat-free diets, they had stunted growth, lost fur, inflamed & scaly tails
2. in 1963, infants fed diets differing in fat content, lowest fat = poor growth, thickened dry skin

after fatty acids are consumed, what are the series of steps for LC-PUFA synthesis?

desaturates (inserting double bond in certain position)

elongases (elongating chain by 2 carbons)

T/F: there is limited conversion of ALA to EPA and DHA. Why?

TRUE: ALA tends to get oxidated before it can get elongated

What are the main things LC-PUFAs do in the body (health wise) (3)

1. constitute cell membranes phospholipids - influence physiochemical properties of membrane
2. act as signalling molecules - interact with other components; act as ligands of transcription factors, influencing gene expression
3. are precursors of bioactive lipid mediators; eg eicosanoids; important role in inflammation

describe the study on Omega-3 FA and triglycerides (cardiovascular health)

* subjects with moderatae hypertriglyceridiemia were supplemented with 0.85 and 3.4 g/day of EPA and DHA
* EPA and DHA went up in blood in dose-dependent way
* triglycerides lowered by 27% (no other markers)

what is the omega 3 index?

EPA + DHA in RBC