I don't normally post blog posts, however, this post has merits for the purpose of figure 1 and figure 2. Figure 1 highlights the different omega 3:omega 6 of different fish and figure 2 highlights the different omega3;6 in wild versus farm raised fish.
Epigenetic and really nutrigenomics: 6 week study of 3 gram omega 3 intake induced methylation changes. Get that? Only 6 weeks of omega 3 intake induces a change in genetic expression.
Health fat intake associated with improved fertility in overweight and obese women undergoing IVF. Higher intake of polyunsaturated fats were associated with improved fertile rates: specifically omega 6 and Linoleum acid. Only a trend was seen with omega 3's.
The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
DHA deficiency further elevates TBI-induced production of SBDPs
less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
marine n-3 PUFAs have also been shown to alter the production of inflammatory proteins including chemokines, cytokines, growth factors and matrix proteases
Two transcription factors that are likely to play a role in inflammation are nuclear factor κ B (NFκB) and PPAR-γ
NFκB is the principal transcription factor involved in upregulation of inflammatory cytokine, adhesion molecule and cyclooxygenase-2 genes
PPAR-γ, is believed to act in an anti-inflammatory manner
PPAR-γ directly regulates inflammatory gene expression, it also interferes with the activation of NFκB creating an intriguing interaction between these two transcription factors
Both NFκB and PPAR-γ may be regulated by n-3 PUFAs.
great review of the anti-inflammatory effects of omega 3 DHA and EPA. EPA inhibits COX and 5-LOX and their downstream prostaglandin and leukotrienes. EPA/DHA inhibited endotoxin-stimulated IL-6, IL-8,TNF-alpha, and NFkappaB.
It is estimated that approximately 30% of children and adolescents in the United States and about 15–30% of those in Europe can be classified as overweight or obese
An increasing body of evidence now suggests that the nutritional environment encountered in utero and the early postnatal life may elicit permanent alterations in adipose tissue structure or function and, thereby, programme the individual’s propensity to later obesity
The composition of fatty acids in the Western diets has shifted toward an increasing dominance of n-6 relative to n-3 LCPUFAs over the past decades.9,10 This shift is also reflected in the fatty acid composition of breast milk
Evidence from animal studies suggests that the n-6 LCPUFA arachidonic acid promotes adipose tissue deposition, whereas the n-3 LCPUFAs eicosapentaenoic acid and docosahexaenoic acid seem to exert an opposite effect
Overall, no effect of supplementation was found on BMI in preschool (<5 years) and school-aged (6–12 years) children
increased adiposity, once established in childhood, tends to track into adulthood
Many studies have shown that even children <2 years with a high BMI are at increased risk of developing obesity later in life
The acquisition of fat cells early in life appears to be an irreversible process
Evidence from cell culture and animal studies suggests that early exposure to n-3 LCPUFAs has the potential to limit adipose tissue deposition mainly by attenuating the production of the arachidonic acid metabolite prostacyclin, which has been shown to enhance adipogenesis
In conclusion, there is currently no evidence to support that maternal n-3 LCPUFA supplementation during pregnancy and/or lactation exerts a favourable programming effect on adiposity status in childhood
our systematic review highlights that most of the trials reviewed were prone to methodological limitations
Literature review finds limited data (9 studies, only 6 RCTs) of omega-3 during pregnancy. No data was found that supported reduced obesity in children by mothers taking n-3 during pregnancy. No harm was found either. Data was sparse.
Take home: not enough data, no harm to pregnancy, children, thus if indications are present for mother, then recommend n-3. At this point not studies have pointed to reduced obesity in children.
Linoleic acid (LA), an essential n-6 polyunsaturated fatty acid (PUFA), was identified as an agent in dietary fat that is responsible for an up-regulation of tumor growth in vivo
A voluminous amount of information is also available in the literature linking increased fat consumption, particularly polyunsaturated fat, and stimulation of mammary tumorigenesis