Atherosclerosis, Glucorticoids & The Fried Lard Diet

[OhNoYo]

Do these studies isolate SFA as the ONLY variable that is causing the problem? In other words, what is the dietary context in which these studies were done where they see inflammation?

Two of the articles are reviews, so they will cite many different types of research studies. Have you not read any of the articles, or can you not understand them?

If you can't open them, then you need to down Adobe Acrobat Reader.

Adobe - Adobe Reader download - All versions

 

[zkt]

Houston we have a problem
FUCK
We need to investigate this further especially as to the SFA chain lenght and the resultant response.

ScienceDirect - Journal of Allergy and Clinical Immunology : A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma

Asthma and lower airway disease
A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma


Lisa G. Wood PhDa, , , Manohar L. Garg PhDb and Peter G. Gibson MBBSa, c

a Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia

b Nutraceuticals Research Group, School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia

c Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, Australia

Received 3 September 2010; revised 13 January 2011; accepted 17 January 2011. Available online 5 March 2011.

Background
Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.

Objective
To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma.

Methods
Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-?, high-sensitivity C-reactive protein, and IL-6 concentrations.

Results
In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV1/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV1, % FVC, and FEV1/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal.

Conclusion
A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma.

 

[CubbieBlue]

Houston we have a problem
FUCK
We need to investigate this further especially as to the SFA chain lenght and the resultant response.

ScienceDirect - Journal of Allergy and Clinical Immunology : A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma

Asthma and lower airway disease
A high-fat challenge increases airway inflammation and impairs bronchodilator recovery in asthma


Lisa G. Wood PhDa, , , Manohar L. Garg PhDb and Peter G. Gibson MBBSa, c

a Centre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, Australia

b Nutraceuticals Research Group, School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia

c Department of Respiratory and Sleep Medicine, John Hunter Hospital, Newcastle, Australia

Received 3 September 2010; revised 13 January 2011; accepted 17 January 2011. Available online 5 March 2011.

Background
Dietary fat activates systemic innate immune responses, but the effect on airway responses is unknown.

Objective
To examine effects of a high-fat versus low-fat meal on systemic and airway inflammation in asthma.

Methods
Nonobese subjects with asthma were randomized to consume a high-fat (n = 19; 48% [49 g] fat) or low-fat (n = 18; 15% [3 g] fat) meal. Fourteen obese patients with asthma and 21 healthy controls also consumed a high-fat meal. Another group of patients with asthma consumed a high-trans (n = 5; 5.2 g trans fat) or nontrans (n = 5, <0.3 g trans fat) fatty acid meal. Lung function was measured at baseline (prebronchodilator) and 2, 3, and 4 hours after bronchodilator. Airway inflammation was assessed by using induced sputum cell counts and Toll-like receptor 4 mRNA expression by real-time PCR. Systemic inflammation was measured by ELISA quantification of plasma TNF-?, high-sensitivity C-reactive protein, and IL-6 concentrations.

Results
In patients with asthma, at 4 hours postmeal, increases in sputum % neutrophils and Toll-like receptor 4 mRNA expression were higher and increases in FEV1/forced vital capacity (FVC) were lower in the high-fat versus low-fat groups. Changes in plasma fatty acids correlated with changes in sputum % neutrophils and were negatively associated with changes in % FEV1, % FVC, and FEV1/FVC. After the high-trans fatty acid meal, sputum % neutrophils were significantly higher than after the nontrans meal.

Conclusion
A high-fat meal augments neutrophilic airway inflammation, with the effect dependent on the type of fat consumed. A high-fat meal also suppresses bronchodilator recovery in asthma. Modifying dietary fat intake may be useful in asthma.

What else was in the diet? I bet it wasn't devoid of carbs, grains, and any of the other shit you are (probably) avoiding. How has your asthma been since changing diets?

 

[zkt]

What else was in the diet? I bet it wasn't devoid of carbs, grains, and any of the other shit you are (probably) avoiding. How has your asthma been since changing diets?

One would have to assume that the researchers had the common sense to keep the diet the same except for the experimentqal variables.
Hard to say the heat and humidity has a big effect.
This is a real bitch. There is a lot of evidence connecting SFA to TLR4 and systemic inflammation. The only saving grace is that it appears maybe to also be associated with adipose tissue. Taubes`c CRP was within range and he aint fat at all.
Just when ya think ya have a handle on it they snatch it away.
But this is the part that I have wanted to investigate since the get-go.

 

[LW64]

One would have to assume that the researchers had the common sense to keep the diet the same except for the experimentqal variables.

I would not assume that.

Dietary context is everything. Each study has to be looked at carefully for the macronutrient content - if it's there at all. There's something of a 'default' bias built in to many, many studies that carbs are healthy and fats are evil, so they feed subjects lots of fat along with lots of carbs (100 gm/day carbs is NOT a 'low-carb' diet!) and then blame the fat for the (no surprise!) negative outcome.

I dont doubt there are deleterious effects to eating SFA when it's in the context of a high carb intake.Restricting carbs changes everything and if there's a paper somewhere showing inflammation increasing with SFA intake while carbs are also restricted, that's the one I'd like to look at.

 

[zkt]

I would not assume that.

Dietary context is everything. Each study has to be looked at carefully for the macronutrient content - if it's there at all. There's something of a 'default' bias built in to many, many studies that carbs are healthy and fats are evil, so they feed subjects lots of fat along with lots of carbs (100 gm/day carbs is NOT a 'low-carb' diet!) and then blame the fat for the (no surprise!) negative outcome.

I dont doubt there are deleterious effects to eating SFA when it's in the context of a high carb intake.Restricting carbs changes everything and if there's a paper somewhere showing inflammation increasing with SFA intake while carbs are also restricted, that's the one I'd like to look at.

Yes this is true. I`ve noticed that the effect of serum glucose is mentioned in some studies, and goes along with and increases the inflammatory effect. I doubt that the effect of SFA in a low carb diet has been studied. The inflammatory effect of SFA qppears to not be dependant upon dietary carbs tho but amplified by them.
So the question in my mind is how much of an effect do SFAs have on inflammation and does the chain lenght mattter.?
Wouldnt mind understanding the mechanism of action a little better too.

 

[OhNoYo]

I would not assume that.

Dietary context is everything. Each study has to be looked at carefully for the macronutrient content - if it's there at all. There's something of a 'default' bias built in to many, many studies that carbs are healthy and fats are evil, so they feed subjects lots of fat along with lots of carbs (100 gm/day carbs is NOT a 'low-carb' diet!) and then blame the fat for the (no surprise!) negative outcome.

I dont doubt there are deleterious effects to eating SFA when it's in the context of a high carb intake.Restricting carbs changes everything and if there's a paper somewhere showing inflammation increasing with SFA intake while carbs are also restricted, that's the one I'd like to look at.

SFA activate TLR's independent of CHO intake.

 

[LW64]

Yes this is true. I`ve noticed that the effect of serum glucose is mentioned in some studies, and goes along with and increases the inflammatory effect. I doubt that the effect of SFA in a low carb diet has been studied.

http://www.nmsociety.org/App_Themes/Images/AboutFat/Comparison%20of%20Low%20Fat%20and%20Low%20Carbohydrate%20Diets.pdf

"...reducing carbohydrate led to considerably greater reductions in a number of proinflammatory cytokines, chemokines, and adhesion molecules. These data implicate dietary carbohydrate rather than dietary fat as a more significant nutritional factor contributing to inflammatory processes; although increased fat in the presence of high carbohydrate may be
particularly deleterious."

The inflammatory effect of SFA qppears to not be dependant upon dietary carbs tho but amplified by them.
So the question in my mind is how much of an effect do SFAs have on inflammation and does the chain lenght mattter.?
Wouldnt mind understanding the mechanism of action a little better too.

Chain length is one part of it but insulin level, oxidation and glycation are in there as variables too. It's complicated.

 

[zkt]

SFA activate TLR's independent of CHO intake.

http://www.nmsociety.org/App_Themes/Images/AboutFat/Comparison%20of%20Low%20Fat%20and%20Low%20Carbohydrate%20Diets.pdf

"...reducing carbohydrate led to considerably greater reductions in a number of proinflammatory cytokines, chemokines, and adhesion molecules. These data implicate dietary carbohydrate rather than dietary fat as a more significant nutritional factor contributing to inflammatory processes; although increased fat in the presence of high carbohydrate may be
particularly deleterious."



Chain length is one part of it but insulin level, oxidation and glycation are in there as variables too. It's complicated.

Its way complicated.

File this under anechdoal evidence if you like:
I have a number of (auto) imflammatory conditions:
1. asthma
2. PVD
3. contact dermatitus to several substances, wool is one.

Over the course of the past month or so several problems have developed which could have multiple causes.
The first was a burning sensation in my left leg when I turned my back a certain way- sciatica- inflammation of the nerve roos. But I have been crawling and rapelling around the roof . Could have strained my back.
Developed a case of pusticular psoriasis. Used to get it as a kid. Probable too much sun exposure brought it on.
Left knee is swollen and painful to the extent that circulation in impaired in the left foot- left is colder as compared to right foot. But working on the roof caused more stress on the left knee that the right.
CB asked about the breathing. Definitely worse but could be the heat and humidity.

Just to complicate things further I have been titrating exogenous GCs down for the past 9 months. Had to back up several times already. Currently at HC 10mg/d and have been problem free until I started this roof project.

I`m am upping the HC to 10mg/3xd for a few days.
All this could be coincidental- or not.
What really bothers me is WTF might be going on inside my arteries. I`ve considered GC therapy for a while now.

 

[LW64]

Did you get around to having blood work done? Maybe follow-up sooner rather than later to see what - if anything - has changed.

 

[zkt]

Did you get around to having blood work done? Maybe follow-up sooner rather than later to see what - if anything - has changed.

Hell no. But what would it show? . What would you test? CRP maybe something...

 

[CubbieBlue]

Its way complicated.

File this under anechdoal evidence if you like:
I have a number of (auto) imflammatory conditions:
1. asthma
2. PVD
3. contact dermatitus to several substances, wool is one.

Over the course of the past month or so several problems have developed which could have multiple causes.
The first was a burning sensation in my left leg when I turned my back a certain way- sciatica- inflammation of the nerve roos. But I have been crawling and rapelling around the roof . Could have strained my back.
Developed a case of pusticular psoriasis. Used to get it as a kid. Probable too much sun exposure brought it on.
Left knee is swollen and painful to the extent that circulation in impaired in the left foot- left is colder as compared to right foot. But working on the roof caused more stress on the left knee that the right.
CB asked about the breathing. Definitely worse but could be the heat and humidity.

Just to complicate things further I have been titrating exogenous GCs down for the past 9 months. Had to back up several times already. Currently at HC 10mg/d and have been problem free until I started this roof project.

I`m am upping the HC to 10mg/3xd for a few days.
All this could be coincidental- or not.
What really bothers me is WTF might be going on inside my arteries. I`ve considered GC therapy for a while now.

Sounds to me like you need to get off the freakin' roof.

I will let you guys know how this sort of diet effects my (maybe inflammatory) condition. NSAIDs seem to stop the pain, so there must be some sort of inflammatory component.

 

[zkt]

Sounds to me like you need to get off the freakin' roof.

I will let you guys know how this sort of diet effects my (maybe inflammatory) condition. NSAIDs seem to stop the pain, so there must be some sort of inflammatory component.

Yea, thats an idea. But I dont quit. I might lose interest and wander off sometimes ....
I`m on T for the long run. Why not GC?
I think you are right in that GH is a BIG part of trauma recovery. I have clearly exceeded my limits but I`m in way too deep to quit.
Why not GH too?
And I thought that exceeding the vodka 3oz/d was my biggest problem insofaras inflammation goes now. LOL

 

[LW64]

Hell no. But what would it show? . What would you test? CRP maybe something...

That would be a start; at least you can compare it to where you were before.

 

[zkt]

That would be a start; at least you can compare it to where you were before.

All I have as far as history is standard lipids, the ocassional CRP and glucose, chem14, and CBC. Inflammatory markers arent routinely checked. There is nothing to compare. Even if I had a Hx of LDL particle size, I really dont think it would be relevant. Now we are into the mechanism that causes LDL to become athrogenic and inactivates the protective action of HDL. I posted a lecture: HDL When Good Cholesterol goes Bad. Thats where I am at. A lot of research and/or go with the GC therapy.
You know that the inflammation aspect has concerned me from the very beginning. Time to figure it out.
BTW, I posted some stuff re renal function and the DA1 receptor and AT1 and AT2 receptors in the MHF yesterday. It relates to prami and chronic renal insufficiency.
This just fuckin pisses me off. I`m about one step away from getting a prescription tablet and writing labs.

 

[CubbieBlue]

Yea, thats an idea. But I dont quit. I might lose interest and wander off sometimes ....
I`m on T for the long run. Why not GC?
I think you are right in that GH is a BIG part of trauma recovery. I have clearly exceeded my limits but I`m in way too deep to quit.
Why not GH too?
And I thought that exceeding the vodka 3oz/d was my biggest problem insofaras inflammation goes now. LOL

Because if you miss a T shot or two you won't drop dead if you get in a serious accident (like you could if you are relying on exogenous HC). Also, your bodies endogenous GC output is very variable. It waxes and wanes depending on what you are doing. You can't begin to control that to the extent that your body can naturally. I just think it is one system you are better off leaving alone.

 

[zkt]

Because if you miss a T shot or two you won't drop dead if you get in a serious accident (like you could if you are relying on exogenous HC). Also, your bodies endogenous GC output is very variable. It waxes and wanes depending on what you are doing. You can't begin to control that to the extent that your body can naturally. I just think it is one system you are better off leaving alone.

Good points and well taken. Thanks.

 

[zkt]

Another one.
But how significant is all this?

Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3

summary, the intake of a modest amount of glucose or cream results in a significant induction of SOCS3 mRNA and protein in parallel with the induction of an inflammatory response characterized by an increase in NF-?B binding in MNCs and the induction of two of the cytokines, TNF-? and IL-1?, which are known to induce SOCS3 in experimental animals. In addition, the intake of cream but not of glucose also induces an increase in the expression of TLR-4 mRNA and protein while also inducing an increase in plasma LPS concentrations. Both SOCS3 and TLR-4 are putative mediators of insulin resistance. In contrast, orange juice intake does not induce oxidative stress, inflammation, SOCS3, TLR-4, or an increase in plasma LPS concentrations.

BUT LOOK WHO FUNDED THE STUDY
The study was supported in part by a grant from the State of Florida, Department of Citrus.

 

[zkt]

Excellent overview of the inflammatory processes and factors effecting it.

http://www.agehealthy.org/pdf/chap6_0926.pdf

Lipopolysaccharide (LPS), associated with the cell wall of common bacteria, is the best recognized stimulant of TLR activation.q 99
The activation of TLR4, the most studied of the Toll-like receptors, causes inflammation and a variety of downstream consequences. These consequences include the disruption of insulin signaling and its associated problems—hyperglycemia, elevated triglycerides/VLDL, reduced nitric oxide production, and increased risks for cardiovascular disease and Alzheimer’s disease.
Recent evidence demonstrates that nonmicrobial substancesr
can also activate TLRs or may heighten the TLR response to a pathogen.100 101 In particular, a substantial body of evidence (summarized by Lee and Hwang 2006)102 indicates that TLR4 activation is also triggered or exacerbated by saturated fat. In addition, omega-3 fatty acids have been shown to reduce TLR4 stimulation by saturated fat and LPS.103-106 Other poly- and monounsaturated fats also inhibit TLR activation, though they are far less effective than omega-3
fatty acids.107
Thus, the modulation of TLR4 by fatty acids provides a
mechanism that may explain some of the emerging links between dietary fatty acids—notably saturated fats and omega-3s—and chronic inflammatory disease, including cardiovascular disease, hyperlipidemia, and possibly diabetes.108-111 The interaction of fatty acids, LPS, TLR, and insulin cell signaling provides a sub-cellular framework that may explain, at least in part, the observed Western chronic disease cluster and its relation to the Western dietary pattern.
Limited data (neurobiological and nutritional epidemiology) suggest that TLR4 activation may play a role in Alzheimer’s disease as well. Little evidence is available at this time to clarify whether TLR4 activation, with or without saturated fat or LPS exposure, may play a role in Parkinson’s disease. However, LPS has been shown to cause dopaminergic degeneration in vitro and in vivo, suggesting the possibility of a TLR4 mechanism in Parkinson’s disease that merits further investigation. (See chapter 8.)
A summary of some of the key studies linking TLR4 and/
or its ligands (triggers) with chronic disease is provided in the
diagram below.112-132

 

[CubbieBlue]

Excellent overview of the inflammatory processes and factors effecting it.

http://www.agehealthy.org/pdf/chap6_0926.pdf

Lipopolysaccharide (LPS), associated with the cell wall of common bacteria, is the best recognized stimulant of TLR activation.q 99
The activation of TLR4, the most studied of the Toll-like receptors, causes inflammation and a variety of downstream consequences. These consequences include the disruption of insulin signaling and its associated problems—hyperglycemia, elevated triglycerides/VLDL, reduced nitric oxide production, and increased risks for cardiovascular disease and Alzheimer’s disease.
Recent evidence demonstrates that nonmicrobial substancesr
can also activate TLRs or may heighten the TLR response to a pathogen.100 101 In particular, a substantial body of evidence (summarized by Lee and Hwang 2006)102 indicates that TLR4 activation is also triggered or exacerbated by saturated fat. In addition, omega-3 fatty acids have been shown to reduce TLR4 stimulation by saturated fat and LPS.103-106 Other poly- and monounsaturated fats also inhibit TLR activation, though they are far less effective than omega-3
fatty acids.107
Thus, the modulation of TLR4 by fatty acids provides a
mechanism that may explain some of the emerging links between dietary fatty acids—notably saturated fats and omega-3s—and chronic inflammatory disease, including cardiovascular disease, hyperlipidemia, and possibly diabetes.108-111 The interaction of fatty acids, LPS, TLR, and insulin cell signaling provides a sub-cellular framework that may explain, at least in part, the observed Western chronic disease cluster and its relation to the Western dietary pattern.
Limited data (neurobiological and nutritional epidemiology) suggest that TLR4 activation may play a role in Alzheimer’s disease as well. Little evidence is available at this time to clarify whether TLR4 activation, with or without saturated fat or LPS exposure, may play a role in Parkinson’s disease. However, LPS has been shown to cause dopaminergic degeneration in vitro and in vivo, suggesting the possibility of a TLR4 mechanism in Parkinson’s disease that merits further investigation. (See chapter 8.)
A summary of some of the key studies linking TLR4 and/
or its ligands (triggers) with chronic disease is provided in the
diagram below.112-132

JUST what I was looking for. Thank you kindly sir.

BTW, LW, gots some heavy cream in my coffee as we speak. Makes the swill my office serves a hell of a lot better, that's for sure.