Lauric acid promotes neuronal maturation mediated by astrocytes in primary cortical cultures

This sounds useful, enhances the presynaptic maturation. But two problems with this;

1.  It is in cell cultures so human testing will never occur under current stroke leadership

2.  You'll have to get by the fact that lauric acid is a main component of coconut oil and these are the roadblocks;

   The Hype About Coconut Oil Benefit Is False

   A Harvard professor just busted the myth that coconut oil is good for you, calling it 'pure poison'

    

    Lauric acid promotes neuronal maturation mediated by astrocytes in primary cortical cultures

Author links open overlay panelShingoNakajima^aHiroshiKunugi^ab

https://doi.org/10.1016/j.heliyon.2020.e03892Get rights and content

Under a Creative Commons license

open access

Abstract

Previous studies have suggested the potential efficacy of middle chain fatty acids (MCFAs) in the treatment of mood disorders and cognitive dysfunction. MCFAs are metabolized to ketone bodies in astrocytes; however, their effects on neuronal development including neurotrophic factor level are not well-understood. In the present study, we examined the effect of MCFAs on the mRNA expression of growth factors and cytokines in primary cultures of cortical astrocytes. The effect of MCFAs on neuron-astrocyte interaction in neuronal maturation was also determined using co-culture and astrocyte-conditioned medium. Lauric acid (LA) typically increased the mRNA expression of glial-derived neurotrophic factor (Gdnf), interleukin-6 (Il6), and C–C motif chemokine 2 (Ccl2) in astrocytes. LA-induced phosphorylation of extracellular signal-regulated kinase contributed to these changes. In primary cultures of cortical neurons containing astrocytes, LA enhanced the presynaptic protein levels. Astrocyte-conditioned medium after LA treatment also enhanced the presynaptic protein levels in the cortical neuron cultures. These results suggest that LA increase the mRNA expression of GDNF and cytokines in astrocytes, and thereby, enhances the presynaptic maturation.

Lauric Acid Alleviates Neuroinflammatory Responses by Activated Microglia: Involvement of the GPR40-Dependent Pathway

Your doctor needs to follow this closely to setup protocols to prevent your likely descent into dementia. Her responsibility, don't let her weasel her way out of it. I use coconut oil to fry my breakfast eggs and bake salmon in it. I use coconut milk as coffee creamer and the liquid for my oatmeal. Don't follow me, I'm not medically trained.

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?

   May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research.   July 2013.

Lauric Acid Alleviates Neuroinflammatory Responses by Activated Microglia: Involvement of the GPR40-Dependent Pathway 

• Authors
• Authors and affiliations

• Yasunori Nishimura
• Mitsuaki MoriyamaEmail author
• Kenji Kawabe
• Hideyo Satoh
• Katsura Takano
• Yasu-Taka Azuma
• Yoichi Nakamura

• Yasunori Nishimura
  • 1
• Mitsuaki Moriyama
  • 1
  Email authorView author's OrcID profile
• Kenji Kawabe
  • 1
  • 2
• Hideyo Satoh
  • 1
• Katsura Takano
  • 1
• Yasu-Taka Azuma
  • 3
• Yoichi Nakamura
  • 1

1. 1.Laboratory of Integrative Physiology in Veterinary SciencesOsaka Prefecture UniversityIzumisanoJapan
2. 2.Department of Regenerative ScienceOkayama University Graduate School of Medicine, Dentistry and Pharmaceutical SciencesOkayamaJapan
3. 3.Laboratory of Veterinary PharmacologyOsaka Prefecture UniversityIzumisanoJapan

Original Paper

First Online: 26 June 2018

• 25 Downloads

Abstract

In several neurodegenerative diseases such as Alzheimer’s disease (AD), microglia are hyperactivated and release nitric oxide (NO) and proinflammatory cytokines, resulting its neuropathology. Mounting evidence indicates that dietary supplementation with coconut oil (CNO) reduces the cognitive deficits associated with AD; however, the precise mechanism(s) underlying the beneficial effect of CNO are unknown. In the present study, we examined the effects of lauric acid (LA), a major constituent of CNO, on microglia activated experimentally by lipopolysaccharide (LPS), using primary cultured rat microglia and the mouse microglial cell line, BV-2. LA attenuated LPS-stimulated NO production and the expression of inducible NO synthase protein without affecting cell viability. In addition, LA suppressed LPS-induced reactive oxygen species and proinflammatory cytokine production, as well as phosphorylation of p38-mitogen activated protein kinase and c-Jun N-terminal kinase. LA-induced suppression of NO production was partially but significantly reversed in the presence of GW1100, an antagonist of G protein-coupled receptor (GPR) 40, which is an LA receptor on the plasma membrane. LA also decreased LPS-induced phagocytosis, which was completely reversed by co-treatment with GW1100. Moreover, LA alleviated amyloid-β-induced enhancement of phagocytosis. These results suggest that attenuation of microglial activation by LA may occur via the GPR40-dependent pathway. Such effects of LA may reduce glial activation and the subsequent neuronal damage in AD patients who consume CNO.

 

Effects of coconut oil on lipid accumulation in 3T3-L1 cells

Would this result in less deposits of arterial plaque? We'll never know. Don't do this on your own.
https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0036-1596845
J Rabalert¹, N Munkong¹, W Parklak¹, A Wongnopavich², P Hansakul³, N Lerdvuthisopon³

• ¹Graduate Studies, Faculty of Medicine, Thammasat University, Pathumthani 12120, Thailand
• ²Department of Biochemistry, Faculty of Medicine, Chiangmai University, Chiangmai 50100, Thailand
• ³Institue of Preclinical Science, Faculty of medicine, Thammasat University, Pathumthani 12120, Thailand

Further Information

• Congress Abstract
• Full Text

 

Consumption of medium-chain triglyceride as coconut (Cocos nucifera L., Arecaceae) oil was shown to reduce fat deposition both in human and animals [1, 2]. Since coconut oil (CO) consisted of 47% lauric acid (decanoate, LaA), mechanism of CO in comparison to LaA on fat deposition was verified in 3T3-L1 cells. Cell viability was assessed by tetrazolium/formazan assay. Density of Oil Red O stained material (OROSM) was observed. Both assays were expressed as % of control (1% ethanol and 1% dimethyl sulfoxide instead of CO and LaA, respectively). Relative gene expression of adipogenic nuclear factors, peroxisome proliferator activated receptor gamma (PPARγ) and CCAAT-enhancer-binding protein alpha (C/EBPα) were assessed by real-time quantitative PCR. The results showed that % cell viability was significantly (p < 0.05) lower than control when cells were treated with the highest dose of LaA (100 µg/mL) for 8 days indicating the potential toxicity. Both CO and LaA were significantly reduced mean ± SEM of the % OROSM density at day 8 (67.17 ± 4.40, 69.27 ± 3.89 and 74.66 ± 5.02 when cells were treated with 670, 1340 and 2012 µg CO/mL, respectively; 59.37 ± 3.22 and 65.96 ± 6.27 when cells were treated with 20 and 40 µg LaA/mL, respectively). Relative gene expressions were significantly reduced by both CO and LaA at day 8 (PPARγ: 0.54 ± 0.02 and 0.62 ± 0.02; C/EBPα: 0.37 ± 0.04 and 0.49 ± 0.09 when cells were treated with 670 and 1340 µg CO/mL or PPARγ: 0.38 ± 0.03 and 0.55 ± 0.03; C/EBPα: 0.49 ± 0.01 and 0.37 ± 0.03 when cells were treated with 20 and 40 µg LaA/mL, respectively). In conclusion, the medium-chain fatty acid both in CO and as LaA were able to reduce fat accumulation in adipocyte during its differentiation. It is worth, then, to study its effect on the ectopic fat deposition as well.
Acknowledgements: Two institutes were acknowledged for their funding: Research Unit, Faculty of Medicine, Thammasat University; Higher Education research Promotion and National Research Project of Thailand.
Keywords: Lauric acid, OROSM, PPARγ, C/EBPα.
References:
[1] Assunção ML, Ferreira HS, dos Santos AF. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids 2009; 44: 593 – 601
[2] Portillo MP, Serra F, Simon E, del Barrio AS, Palou A. Energy restriction with high-fat diet enriched with coconut oil gives higher UCP1 and lower white fat in rats. Int J Obesity 1998; 22: 974 – 979

Acute Treatment with Lauric Acid Reduces Blood Pressure and Oxidative Stress in Spontaneously Hypertensive Rats

Not to be done on your own until research has created protocols in at least 50 years, because we have NO stroke leaders or strategy.
http://onlinelibrary.wiley.com/doi/10.1111/bcpt.12700/full

• Accepted manuscript online: 7 November 2016Full publication history
• DOI: 10.1111/bcpt.12700View/save citation
• Cited by: 0 articles

• 
  

• This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/bcpt.12700
  

Abstract

The effects of acute administration of lauric acid (LA), the most abundant medium chain fatty acid of coconut oil, on blood pressure, heart rate and oxidative stress were investigated in spontaneously hypertensive rats (SHR). Intravenous doses of LA reduced blood pressure in a dose-dependent fashion (1, 3, 4, 8 and 10 mg/kg) in both SHR and Wistar Kyoto rats. LA (10^-8 to 3 x 10^-3 M) induced vasorelaxation in isolated superior mesenteric artery rings of SHR in the presence (n = 7) or absence (n = 8) of functional endothelium [maximum effect (ME) = 104 ± 3 versus 103 ± 4 %]. After exposure to KCl (60 mM), LA also induced concentration-dependent vasorelaxation (n = 7) compared to that under Phe-induced contraction (ME = 113.5 + 5.1 versus 104.5 + 4.0 %). Furthermore, LA induced vasorelaxation in vessels contracted with S(−)-BayK8644 (200 nM), a L-type Ca²⁺ channel agonist (ME = 91.4 + 4.3 versus 104.5 + 4.0 %, n = 7). Lastly, LA (10^-3 M) reduced NADPH-dependent superoxide accumulation in the heart (18 ± 1 versus 25 ± 1 MLU/min/μg protein, n = 4, P < 0.05) and kidney (82 ± 3 versus 99 ± 4 MLU/min/μg protein, n = 4, P < 0.05). Our data show that LA reduces blood pressure in normotensive and hypertensive rats. In SHR, this effect might involve Ca⁺² channels in the resistance vessels and by its capability of reducing oxidative stress in heart and kidneys.

Insects are a sustainable source of omega-3

Here's a solution to the fish burps of Omega-3 capsules.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=159889&CultureCode=en

Insect oil is a possible new source of the healthy omega-3 fatty acid. Insects make fatty acids by nature and can live on organic waste. Wageningen University examines which insects can best be used for oil and what their optimal diet should be.
Insects are already used as a source of protein for man and beast. In the protein extraction process also oil is extracted. This insect oil is currently thrown away. That is a shame, proves researcher Daylan Tzompa Sosa of Wageningen University.
Fatty acids
In her PhD-research, Tzompa Sosa looks at milkfats. Out of curiosity, she once did similar fat analysis with oil that was left over after protein extraction of insects by a lab colleague. “The oil appeared to contain a lot of fatty acids, both saturated and unsaturated.” In addition, Tzompa Sosa demonstrated that the oil can be extracted in an environmentally friendly way, giving also the highest return and the best quality oil compared to other processes. Tzompa Sosa extracted oil from for instance meal worms, beetle larvae, crickets, cockroaches, grasshoppers and soldier flies. “All the oils smell differently, some nicer than others”, the Wageningen scientist says.
Fish
The industry is interested in sustainable fatty acids like omega-3 and lauric acid. The main source for omega-3 is currently fish. It is added to the feed of cats and farm raised salmon, to foodstuffs and put in capsules. “Cats die when they get a full vegetable diet without these additives. That is why they normally eat meat. Farm raised salmons get wild caught fish or fishmeal instead.” Also humans need to take in a certain amount of fatty acids. Lauric acid (also to be found in coconut oil for example) is supposed to have bactericidal and virus obliterate qualities. Furthermore, the use of insect oil in for example cosmetics is obvious.
Properties
To research breeding, diet and processing of insects for oil, the Wageningen fat researchers are working together with entomologists and bio based experts of Wageningen UR. One of these researches concerns an analysis of the different fractions in oil and their properties, because these fractions have different liquid and solid phase. Also a risk analysis of use of the oil for man and beast will be done.
http://www.wageningenur.nl/en/newsarticle/Insects-are-a-sustainable-source-of-omega3.htm

The Properties of Lauric Acid and Their Significance in Coconut Oil

I'm sure your doctor is not subscribing to Journal of the American Oil Chemists' Society
http://link.springer.com/article/10.1007/s11746-014-2562-7

• Fabian M. Dayrit

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Get Access

Abstract

The primary fatty acid of coconut oil is lauric acid, which is present at approximately 45–53 %. The metabolic and physiological properties of lauric acid account for many of the properties of coconut oil. Coconut oil is rapidly metabolized because it is easily absorbed and lauric acid is easily transported. Detailed studies have shown that the majority of ingested lauric acid is transported directly to the liver where it is directly converted to energy and other metabolites rather than being stored as fat. Such metabolites include ketone bodies, which can be used by extrahepatic tissues, such as the brain and heart, as an immediate form of energy. Studies on the effect of lauric acid on serum cholesterol are contradictory. Among saturated fatty acids, lauric acid has been shown to contribute the least to fat accumulation. Lauric acid and monolaurin have demonstrably significant antimicrobial activity against gram positive bacteria and a number of fungi and viruses. Today there are many commercial products that use lauric acid and monolaurin as antimicrobial agents. Because of the significant differences in the properties of lauric acid relative to longer chain fatty acids, they are typically differentiated as medium-chain fatty acids covering C6–C12, and long-chain fatty acids covering C14 and longer.

Replacement of saturated fat with polyunsaturated fat may reduce CHD risk

Rather incomplete analysis, What about good saturated fat? For example, lauric acid found in coconut oil?
Replacement of saturated fat with polyunsaturated fat may reduce CHD risk

Higher intake of dietary linoleic acid is associated with lower risk for CHD in a dose-response manner, according to results of a systematic review and meta-analysis of prospective cohort studies.

“These data provide support for current recommendations to replace saturated fat with polyunsaturated fat for primary prevention of CHD,” Maryam S. Farvid, PhD, from the department of nutrition, Harvard School of Public Health, and colleagues wrote in Circulation.
The systematic review and meta-analysis focused on 13 prospective cohort studies that assessed the link between dietary intake of linoleic acid, the main polyunsaturated fat found in vegetable oil, nuts and seeds, and the incidence of CHD. Three trials did not report total CHD events, and four provided separate data for men and women, resulting in 14 estimates for total CHD. Two trials did not include data on CHD-related mortality and one reported separate data according to sex, resulting in 12 estimates for CHD mortality. Follow-up ranged from 5.3 years to 30 years across the studies.
Overall, the study population included 310,602 participants and 12,479 total CHD events (5,882 CHD deaths).
Dietary intake of linoleic acid ranged from 1.5% to 6.4% of energy.
Across 10 studies with evaluable data on total CHD events, participants with the highest intake of dietary linoleic acid had a reduced risk for CHD events (pooled RR=0.85; 95% CI, 0.78-0.92 vs. lowest reported intake) in a fixed-effects model. A random-effects model yielded similar results (RR=0.86; 95% CI, 0.76-0.97).
Across the 11 trials that provided evaluable data on CHD mortality, participants with the highest intake of linoleic acid were at reduced risk (pooled RR=0.79; 95% CI, 0.71-0.89 vs. lowest reported intake).
In a dose-response analysis, the researchers observed linear associations between dietary linoleic acid consumption and total CHD events (P=.91 for nonlinearity) and CHD-related mortality (P=.72). Each 5% increment of energy intake from linoleic acid was associated with reduced risk for CHD (RR=0.9; 95% CI, 0.85-0.94) and CHD mortality (RR=0.87; 95% CI, 0.81-0.93).
Analysis of data from eight trials that assessed the substitution of 5% of caloric intake from saturated fats with linoleic acid indicated a 9% reduction in risk in a fixed-effects model (RR=0.91; 95% CI, 0.87-0.96) and a 10% reduction in a random-effects model (OR=0.9; 95% CI; 0.8-1.01). Substitution of 5% of caloric intake from carbohydrates for linoleic acid yielded similar results for total CHD (RR=0.9; 95% CI, 0.85-0.94) and CHD-related mortality (RR=0.87; 95% CI, 0.81-0.94).
According to the researchers, these results provide “robust evidence” of a dose-response relationship between increased linoleic acid intake and reduced CHD risk.
“Randomized clinical trials have shown that replacing saturated fat with polyunsaturated fat reduces total and HDL cholesterol,” Frank B. Hu, MD, PhD, professor of nutrition and epidemiology at Harvard School of Public Health, said in a press release. “Our comprehensive meta-analysis provides clear evidence to support the benefits of consuming polyunsaturated fat as a replacement for saturated fat.”

Lauric Acid as Potential Natural Product in the Treatment of Cardiovascular Disease: A Review

Lauric acid constitutes about half of the fatty acid content in coconut oil, laurel oil, and palm kernel oil.  I'm sure your doctor will never recommend this because they learned that all fat is bad.  I however look to the research. I have written 11 posts on coconut oil which is why I take this, but never listen to me since I have no medical designation behind my name.

11 posts on coconut oil

http://omicsonline.org/open-access/lauric-acid-as-potential-natural-product-in-the-treatment-of-cardiovascular-disease-a-review-1948-593X.1000107.pdf

It is only 3 pages long, but here is the conclusion;

Conclusions

Cardiovascular diseases are one of the leading cause for deaths

throughout the world. It is observed from various studies that saturated

and trans fatty acids have increased the cardiovascular risk. The risk of

heart diseases are tobacco consumption, smoking, physical inactivity

and unhealthy eating habits leading to obesity and Cardiovascular

diseases. Lauric acid is describing as ‘good’ cholesterol’ and a major

component in coconut oil. Consumption of coconut oil (Lauric acid,

a component) enhances in High-Density Lipoprotein (HDL) and

decreases the total/HDL cholesterol ratio which results in a decrease in

risk of cardiovascular diseases (atherosclerosis).