Food and Mood Flashcards
What is depression?
not 1 full definition but….
Depression is a low mood that lasts for a long time, and affects your everyday life.” (MIND, 2019)
“Depression is a mood disorder characterised by hopelessness, sadness and misery” (Thomas, 2002).
“Depression is a broad and heterogeneous diagnosis. Central to it is depressed mood and/or loss of pleasure in most activities” (NICE, 2009)
Depression Statistics (WHO, 2021)
Estimated 3.8% of the global population affected, including 5.0% among adults and 5.7% among adults older than 60 years
Approximately 280 million people in the world have depression
Over 700 000 people die due to suicide every year. Suicide is the fourth leading cause of death in 15-29-year-olds
What are the symptoms of depression?
Unable to cope
Feeling down, upset or tearful
Finding little pleasure in life
Suicidal thoughts
Feeling isolated
Low self-confidence or self-esteem
Numbness
Lethargy and tiredness
Loss of interest in activities
Restless, agitated or irritable
Sadness or feeling unhappy
Sleeping problems
Loss of appetite
Formal Diagnosis of depressive disorders?
ICD-10
classification system requires at least four out of ten criteria listed in the manual
DSM-V
system requires at least five out of nine criteria to be met for a diagnosis of major depressive disorder (depression).
Risk factors for depression
stress from work/school
relationship problems
family history
money problems
loss of social support
loss of parent before the age of 10
Contributors to onset of depression (Volker & Ng, 2006; Lopresti et al., 2013)
Psychological, Genetic, Social/environmental
Psychological Factors:
A persons style of thought and the way in which they interpret and react to life experiences may either protect or predispose them to mood disorders.
Make negative statements about themselves and their abilities
Personality traits
Distorted views of reality
Unrealistic goals
Genetic Factors:
Familial aggregation: Depressive disorders more common in the relatives of depressed subjects than in the population at large
Concordance rateofmajor depressive disorderfor MZtwinswas 46% and for non-identical (DZ)twinswas 20% (McGuffin et al., 1996).
This shows that there isa heritability factor formajor depression
Social/environmental Factors:
Clinical depression is usually preceded by a greater frequency of demanding life events
Acute adverse changes in environmental and social circumstances appear to have an effect on the onset, maintenance and relapse of depression.
Biological factors: dysregulated pathways in depression (Lopresti et al., 2013).
An increased size and activity of the pituitary and adrenal glands are found in major depression (Nemeroff et al., 1992).
- Decreased antioxidant status and elevated oxidative and nitrosative stress are found in patients with major depression (Maes et al., 2011).
Elevated levels of C-reactive protein (CRP), interleukin-1 (IL-1), and interleukin-6 (IL-6) are reported in depression (Howren et al., 2009)
- BDNF levels are low in people with major depression (Duman, 2009; Lee and Kim, 2010)
Depression is also associated with an increased availability of monoamine oxidase, an enzyme that metabolises serotonin in the brain (Meyer et al., 2006)
Protein and mood
tryptophan -> 5-HTP -> Serotonin
Serotonin (5-hydroxytryptamine; 5-HT) is synthesized from tryptophan.
Supplementation with this amino acid, or its metabolite, 5-HTP, is hypothesized to normalise serotonin synthesis and its function as an antidepressant within the brain (Parker & Brotchie, 2011).
Tryptophan – Research Evidence?
Both trials showed superiority of supplementation to placebo in alleviating depression, although side effects reported by some subjects.
Van Praag et al., (1972) tested 5-HTP in 10 severely depressed patients. The intervention involved 3 weeks of 5-HTP given as 200mg capsules at a dosage increasing to 3000mg daily and to a total of 50g for 3 weeks, followed by 2 weeks of placebo. Control group were given a placebo for duration of 5 week trial.
Thompson et al., (1982) tested tryptophan and involved 28 patients with mild depression and 26 controls. The patients with depression were given the placebo for 1 week followed by 12 weeks of tryptophan (3g/d), with 26 controls given placebo for 13 weeks.
Tryptophan supplementation: Systematic review (Kikuchi et al., 2020)
Systematic review that includes 11 RCTs that examined the effects of TRP intake on positive and negative mood in healthy adult populations:
Concluded that taking 0.14–3 g of TRP per day in addition to usual dietary intake can be expected to improve the mood of healthy individuals.
Carbohydrate and mood
facilitates the amino acid tryptophan into the brain to be converted into seritonin
Source of seretonin
banana
walnuts
Carbohydrate and mood – Research evidence?
Fernstrom (1981) showed that ingestion of a single carbohydrate-rich meal by rats raised brain tryptophan and 5-HT.
One week on a high fat/low-carb diet decreased serotonin release in the hypothalamus (Banas et al., 2009).
Various authors (Teff et al., 1989; Spring et al., 1987; Rogers, 1995; Soh & Walter, 2011) suggest that it is very difficult to alter blood tryptophan levels through dietary methods alone outside of a laboratory research setting.
Glycemic index/glycemic load and mood: Meta-analysis (Solari-Moghaddam et al., 2019)
This meta-analysis showed no significant association between either dietary GI or GL and odds of depression in cross-sectional studies.
They did find a significant positive association between dietary GI and risk of depression in cohort studies
They also found a significant change in depression score after consumption of a high-GL diet in clinical trials
Introduction to fatty acids - Structure
- A chain of carbon atoms with the required number of hydrogen atoms attached (Hydrocarbon chains)
- A carboxylic acid residue at one end of the chain
- A methyl group at the other end of the chain.
Can se saturated or unsaturated with hydrogen
Human desaturases
Human desaturase enzymes can only operate on the bonds between the first 9 carbons starting after the carboxyl group.
Food is the only supply of fatty acids with one or more double bonds in the out of range part of the molecule.
Therefore, fatty acids with one or more double bonds in the out of range part of the molecule are termed Essential Fatty Acids (EFAs).
Essential Fatty Acids
Linoleic acid – omega-6
Alpha linoleic acid - omega-3
Metabolism allows biosynthesis of other fatty acids
Factors influencing the efficiency of conversion of EFAs to LC-PUFAs
Conversion of LA to AA is typically very efficient
Conversion of ALA to EPA and DHA is much less efficient
For this reason omega-3 LC-PUFAs are sometimes referred to as ‘conditionally essential’
Dietary factors:
Competition for enzymes involved in fatty acid elongation and desaturation between n-3 and n-6 fatty acids.
Synthesis of longer chain n-3 fatty acids from LA within the body is competitively slowed by n-6 analogues.
High dietary intake of n-6 PUFAs can reduce n-3 fatty acid conversion by as much as 40%
Effect of type of fatty acid tail on membrane fluidity:
Incorporation of omega-3 fatty acids into neuronal cell membranes required in order for proper functioning of the membranes and ultimately neuronal functioning.
Suggested that Omega 3 has more anti-inflammitory effects compared to O6 (more fluid)
Omega-3 fatty acids: Observational evidence
Epidemiological data suggests lower prevalence of mood disorders with higher fish consumption (kamphuis et al., 2006; Appleton et al., 2007).
Some research suggests an association between low omega-3 status and depressive symptoms (Edwards et al., 1998; Mcnamara et al., 2007; Astorg et al., 2008; Feart et al., 2008; Lin & Su, 2010).
Omega-3 fatty acids - Intervention studies (Lin and Su, 2007)
Lin and Su (2007) analysed studies by different EPA dosages and suggested that doses >4000mg/d had significantly greater antidepressant effects than placebo.
> 2000mg/d had no effect.
Therefore, we may only see an effect in studies that have given larger doses and at doses way higher than is achievable through dietary means alone.
Limitations of this research on Omega 3 fatty acid?
Problems with this research to date:
These trials tended to be small (n=20-77)
Short duration
Use differing doses of omega-3 fatty acids - What is the optimum dose? Are they using enough to have an effect?
Different ratios of EPA/DHA – what ratio should we use?
Heterogeneous populations under study – makes it very difficult to compare findings
Different severity of depression
Different age categories
Etc…
And the does of omega-3 LCPUFA (up to 9.6g/d) associated with the largest effects in adults is very much higher than could be realistically achieved through diet alone.
Different measures/assessments of mood and depression used
Very difficult to measure/quantify
Potential mechanism of action?
Folate (B9) is a water soluble B vitamin:
Dihydrofolate – natural form
Leafy green vegetables, broccoli, asparagus, peas, legumes, chickpeas, brown rice, fortified breakfast cereals, etc..
Folic acid (synthetic form)
Neither of these forms is biologically active and must be converted to L-methylfolate
L-methylfolate and synthesis of neurotransmitters
folate
dihydrofolate
tetrahydrofolate
5,10 methylene THF
L-methylfolate
L-methylfolate = modulates transmitter to modulate the production of BH4
BH4 activates synthesis of translaters to make =
dopamine -> norepinephrine
serotonin
