![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 72 to 96 of 98. Go back in thread:
Posted by Phillipa on December 27, 2012, at 23:49:02
In reply to Re: Bifidobacteria reduce depression, posted by larryhoover on December 27, 2012, at 23:15:56
Lar years ago I was on the original Atkins diet of all protein & fat with only carb source a small amount of salad basically greens. I have a 4 hour glucose tolerance test during this time and came out diabetic. When the doc found out the diet I was on. I was told to go home and eat high carbs for two weeks repeat the test which I did and was completly normal. And was told I had low blood sugar. And to eat protein every 4 hours which did til lost Taste & smell so now it dark chocolate. Taste buds sweet, sour, bitter, spicy. Texture is important to me. Any ideas after 4 specialists who said no way how to restore smell & taste? Supposedly some virus destroyed the neurons in nose. It's a loss like no other. thanks, P
Posted by rca on December 28, 2012, at 8:55:02
In reply to Re: Bifidobacteria reduce depression, posted by Trotter on December 27, 2012, at 21:15:58
I think it is safe to assume that a meal high in saturated fat causes inflammation; that is a well-established fact accepted for at least 15 years. But the prevailing thought had been that saturated fat causes our gut lining to become leaky and allow our own bacteria (endotoxins) to slip into our blood stream and cause the inflammation. Then came the study cited below (Erridge, 201). We now know that the high load of bacteria in animal products contain endotoxins (even in dead bacteria so doesnt matter if cook at high temperatures or expose to highly acidic environments like the stomach). And animal fat may play a profound role in the pathogenesis of this after-meal inflammation by increasing the absorption of the endotoxins, since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the blood stream (Deopurkar et al., 2010, below).
So what can you do? Whole food plant based diet.
Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23.
Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, Viswanathan P, Chaudhuri A, Dandona P. 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. Diabetes Care. 2010 May; 33(5):991-7.
Posted by rca on December 28, 2012, at 9:14:39
In reply to Re: High fat diet -) inflammation -) depression » rca, posted by larryhoover on December 27, 2012, at 15:19:59
On obesity: Of course one can be thin or overweight on a preponderance of protein, fat, or carbohydrates in our diet, depending upon the quantities involved (disregarding other effects than weight gain/ loss, like morbidity and mortality). Whole food plant based diet contains a lot of water and fiber so the tendency is to eat fewer calories to reach satiety.
But there may be more involved than that. Since this thread features gut flora, consider this: Our good gut bacteria, while technically unable to digest fiber, can break it down to an extent to make a compound called propionate which is absorbed into our blood stream. What does propionate do? Well, it inhibits cholesterol synthesis and it has a hypophagic effect meaning it helps us eat less. Apparently it does this by slowing down the rate at which our food empties from our stomachs thereby making us feel fuller, longer. Propionate may be able to regulate food intake or the generation of new fat cells, resulting in an overall anti-obesity effect.
Arora T, Sharma R, Frost G. Propionate. Anti-obesity and satiety enhancing factor? Appetite. 2011 Apr;56(2):511-5.
Posted by rca on December 28, 2012, at 9:39:28
In reply to Re: High fat diet -) inflammation -) depression » rca, posted by larryhoover on December 27, 2012, at 15:19:59
A plant-based diet high in fiber may lower bad cholesterol; only in individuals with a type of familial hypercholesterolemia will diet be unable to lower levels into the safe range. For example see the review from the editor and chief of the Journal of American Cardiology below (Roberts, 2010). The literature supporting cholesterol lowering through plant based diet is just too vast to summaries but see for example Ferdowsian, 2009 below.
The new USDA Dietary Guidelines (heavily influenced by meat and dairy industries) even recommend a more plant-based diet to lower cholesterol intake.
Roberts WC. It's the cholesterol, stupid! Am J Cardiol. 2010 Nov 1;106(9):1364-6.
Ferdowsian HR, Barnard ND. Effects of plant-based diets on plasma lipids. Am J Cardiol. 2009 Oct 1;104(7):947-56
US Department of Agriculture. 2011. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010.
Posted by rca on December 28, 2012, at 9:47:39
In reply to High fat diet -) inflammation -) depression, posted by Trotter on December 19, 2012, at 23:44:21
This very large study was published this week on the association of inflammation and psychological stress: http://archpsyc.jamanetwork.com/article.aspx?articleid=1485898
Posted by larryhoover on December 28, 2012, at 10:44:25
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 28, 2012, at 8:55:02
> I think it is safe to assume that a meal high in saturated fat causes inflammation; that is a well-established fact accepted for at least 15 years.
In mice, yes. In humans, it's a different story. And, in humans, it also depends on how sick their metabolism already is, and what other nutrients are co-ingested.
For example, this study comparing challenge tests of bolus ingestion of fats of differing composition.
http://www.ncbi.nlm.nih.gov/pubmed/21736782
"In addition, ALA and EPA were shown to elicit different effects on the release and mRNA expression levels of inflammatory markers in PBMC cultured ex vivo, with EPA having the most prominent pro-inflammatory potential."The so-called pro-inflammatory PUFA arichadonic acid wasn't pro-inflammatory, but the anti-inflammatory eicosapentaenoic acid was? Hmmmm. In this case PUFAs were inflammatory, but not saturated fat.
Here's a full-text article discussing various fatty acid challenges in people with differing metabolic health. The responses are quite variable across the groups.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402390/Now, as to your references, let's see what they really say.
> Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23.
"The ingestion of fatty meals is associated with a transient, low-grade systemic inflammatory response in human subjects, involving the activation of circulating monocytes and the secretion of pro-inflammatory cytokines."
Note, they do not implicate saturated fats. Moreover, they do not discuss the fact that this is only seen in people simultaneously exposed to both carbs and fat.
The actual study performed was in vitro, which means that the cells were not in a normal matrix, with the normal complex of homeostatic influences. And, having done in vitro work myself, I can assure you that the nutrient broth used is high-carb. Can you say confound?
> Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, Viswanathan P, Chaudhuri A, Dandona P. 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. Diabetes Care. 2010 May; 33(5):991-7.
Full-text here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858203/
Interesting opening remark: "We have recently shown that a high-fat high-carbohydrate (HFHC) meal induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation."
High-fat HIGH-CARB combination. There it is, plain as day.
From the full-text article's conclusion section: "It would thus appear that the oxidative stress and inflammation-inducing actions of the HFHC meal are due to the combination of saturated fat and the carbohydrate (glucose) at least."
In that conclusion, they are referring to an earlier study they did comparing high-fat high-carb meal to a fruit and fiber meal. They presented no evidence to implicate the saturated fat, however. It's funny how these assumptions persist, without evidence.
This article is quite interesting in one sense, as the only difference in inflammatory response between glucose and cream was with respect to lipopolysaccharides. Glucose itself was extremely inflammatory, and more rapidly than was the cream. I'm going to take a closer look at lipopolysaccharides.
I'll close with a nice summary piece.
http://www.ncbi.nlm.nih.gov/pubmed/19082851
Lipids. 2009 Apr;44(4):297-309. doi: 10.1007/s11745-008-3274-2. Epub 2008 Dec 12.Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet.
Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD.
SourceDepartment of Kinesiology, University of Connecticut, 2095 Hillside Road, Storrs, CT 06269-1110, USA. jeff.volek@uconn.edu
AbstractWe recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (-47%), the Apo B/Apo A-1 ratio (-16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.
Lar
Posted by Trotter on December 28, 2012, at 13:40:31
In reply to Re: High fat diet -) inflammation -) depression » Trotter, posted by rca on December 28, 2012, at 9:47:39
> This very large study was published this week on the association of inflammation and psychological stress: http://archpsyc.jamanetwork.com/article.aspx?articleid=1485898
Yes, it is my understanding that chronic low grade inflammation, such as caused by endotoxemia, causes depression.
Posted by Trotter on December 28, 2012, at 13:50:52
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 28, 2012, at 8:55:02
> I think it is safe to assume that a meal high in saturated fat causes inflammation; that is a well-established fact accepted for at least 15 years. But the prevailing thought had been that saturated fat causes our gut lining to become leaky and allow our own bacteria (endotoxins) to slip into our blood stream and cause the inflammation. Then came the study cited below (Erridge, 201). We now know that the high load of bacteria in animal products contain endotoxins (even in dead bacteria so doesnt matter if cook at high temperatures or expose to highly acidic environments like the stomach). And animal fat may play a profound role in the pathogenesis of this after-meal inflammation by increasing the absorption of the endotoxins, since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the blood stream (Deopurkar et al., 2010, below).
>
> So what can you do? Whole food plant based diet.
>
> Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23.
>
> Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, Mohanty P, Viswanathan P, Chaudhuri A, Dandona P. 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. Diabetes Care. 2010 May; 33(5):991-7.
>
>You seem to assume that this laboratory study proves that endotoxemia is caused by endotoxins in protein or refined foods and not from the lumen via a permeable intestine. I agree it establishes that such foods contain some endotoxin, but that is all.
The bowel has massive amounts of endotoxin. I think the amount of endotoxin in the bowel regardless of whether one is on a plant or protein orientated diet dwarfs any endotoxin ingested in food. I still firmly believe a high fat diet causes endotoxemia due to increased intestinal permeability. I think this has been pretty well established in rodent studies which looked at high fat diets, not high protein diets.
Posted by Trotter on December 28, 2012, at 13:59:26
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 28, 2012, at 8:55:02
>since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the blood stream (Deopurkar et al., 2010, below).
>Can you please provide evidence to support your statement that the translocation of endotoxin is facilitated by a "saturated fat transport system"? It is my current understanding that a high fat diet increases endotoxemia by affecting the bowel bacterial composition, specifically by reducing bifidobacteria. I think it is the bifidobacteria which help maintain intestinal integrity.
Posted by SLS on December 28, 2012, at 14:26:54
In reply to Re: High fat diet -) inflammation -) depression, posted by Trotter on December 28, 2012, at 13:40:31
> > This very large study was published this week on the association of inflammation and psychological stress: http://archpsyc.jamanetwork.com/article.aspx?articleid=1485898
>
> Yes, it is my understanding that chronic low grade inflammation, such as caused by endotoxemia, causes depression.Am I failing to find indications of causation or directionality in this study?
I don't understand why whenever depression is associated with a biological finding, there is an immediate conclusion drawn that the observed biological phenomenon must be the cause of that depression. I sometimes think that authors like to see their names in lights.
- Scott
Posted by Trotter on December 28, 2012, at 15:47:59
In reply to Re: High fat diet -) inflammation -) depression » Trotter, posted by SLS on December 28, 2012, at 14:26:54
> > > This very large study was published this week on the association of inflammation and psychological stress: http://archpsyc.jamanetwork.com/article.aspx?articleid=1485898
> >
> > Yes, it is my understanding that chronic low grade inflammation, such as caused by endotoxemia, causes depression.
>
> Am I failing to find indications of causation or directionality in this study?
>
> I don't understand why whenever depression is associated with a biological finding, there is an immediate conclusion drawn that the observed biological phenomenon must be the cause of that depression. I sometimes think that authors like to see their names in lights.
>
>
> - ScottYes, they did not prove cause and effect in this particular study, only that a link exists. However there is a lot of cause and effect evidence to show that inflammation causes depression. I have presented some of that evidence to you already.
You seem to be married to your belief that inflammation is caued by depression and not the other way round.
Posted by SLS on December 28, 2012, at 18:28:02
In reply to Re: High fat diet -) inflammation -) depression, posted by Trotter on December 28, 2012, at 15:47:59
> > > > This very large study was published this week on the association of inflammation and psychological stress: http://archpsyc.jamanetwork.com/article.aspx?articleid=1485898
> > > Yes, it is my understanding that chronic low grade inflammation, such as caused by endotoxemia, causes depression.
> > Am I failing to find indications of causation or directionality in this study?
> >
> > I don't understand why whenever depression is associated with a biological finding, there is an immediate conclusion drawn that the observed biological phenomenon must be the cause of that depression. I sometimes think that authors like to see their names in lights.
> Yes, they did not prove cause and effect in this particular study, only that a link exists.Yeah, well...
> However there is a lot of cause and effect evidence to show that inflammation causes depression.
Instead of throwing a URL at me, perhaps you can summarize this evidence as you understand it? I still have a difficult time reading stuff.
> I have presented some of that evidence to you already.
Maybe I'll go back and take a look. My problem is that I have not seen a convincing demonstration that inflammation causes Major Depressive Disorder (MDD), only an associative link for which directionality is ambiguous. How do we know when the true onset of the MDD disorder begins? There might be a convergence in time of separate processes. Inflammation might be a prosyndromal consequence of the onset of disease, so it would show up before the depressive symptoms would.
Can immune activation and inflammatory processes cause someone feel depressed? Perhaps. After all, interferon certainly does. However, no one has produced evidence that interferon causes MDD. Like I said, I think it possible that once induced, MDD and the inflammatory reaction to that pathology converge and "feed on each other", producing a positive feedback loop. Inflammation by itself might not be the inducer.
I don't know. I just haven't seen what I would call proof that inflammation leads to Axis I disorders. If you really want to see something interesting, perform a Medline search on schizophrenia and inflammation and tell me what you come up with.
> You seem to be married to your belief that inflammation is caued by depression and not the other way round.
I am married to my feeble intellect and relative ignorance.
No big deal. The idea isn't to prove whether I am right or wrong. It is simply to challenge an idea that might influence people to seek ineffective treatments if that idea is wrong.
I have no idea what you suffer from. I look forward to you confirming for yourself that your illness is indeed MDD, and how your current belief system helps you to make treatment decisions.
- Scott
Posted by SLS on December 28, 2012, at 20:42:04
In reply to Re: High fat diet -) inflammation -) depression, posted by Trotter on December 28, 2012, at 15:47:59
> Instead of throwing a URL at me, perhaps you can summarize this evidence as you understand it? I still have a difficult time reading stuff.
I apologize. That is asking a bit much of you, and you have probably explained things in a previous post. I'll just keep reading.
- Scott
Posted by rca on December 29, 2012, at 9:29:19
In reply to Re: Bifidobacteria reduce depression » rca, posted by larryhoover on December 28, 2012, at 10:44:25
Thanks for your thoughtful reply - haven't "digested" it all but can respond to one comment here.
>High-fat HIGH-CARB combination. There it is, plain as day.
The study (quote below) involved comparison of a high fat high carb (HFHC) group compared to an American Heart Association recommended food group (AHA). But you know what they were actually eating? The HFHC groups ate egg muffin and sausage muffin sandwiches and two hash browns, which contain 88 g carbohydrates, 51 g fat [33% saturated] and 34 g protein [carbohydrates 41%, protein 17%, and fat 42%]; the second group ate oatmeal, milk, orange juice, raisins, peanut butter, and English muffin (carbohydrates 58%, protein 15%, and fat 27%). I think their choice of these two groups were unfortunate and their labeling misleading.
The HFHC group ate a typical SAD diet of animal products and simple carbohydrates; the second group still included some animal product and was predominately a high carbohydrate meal, but had a significant amount of complex carbohydrates too.
Their data indicated a pronounced inflammation after the HFHC (SAD) diet compared to the AHA diet (even with the milk , juice, and English muffin Id prefer comparing to a whole plant based diet something like whole rolled oats, blueberries, crushed flax seeds in soy milk).
The entire article is available on-line here: http://www.ncbi.nlm.nih.gov/pubmed?term=Diabetes%20Care.%202009%20Dec%3B%2032(12)%3A2281-7.
Heres the interesting part. Please examine the two figures (each with three figures on them), showing the inflammatory marker rise (figure 1) and the endotoxin rise (Figure 2). Notice anything strange? In all cases these parameters rise in just ONE HOUR after the meal certainly not time enough to reach the leaky gut colon where all the bacteria are. I see no explanation other than there are endotoxins in the animal products that are being absorbed in the small intestine.
Yep. Look at (Erridge, 2011) below. For the first time ever, they aimed to determine whether common foodstuffs may contain appreciable quantities of endotoxin. Forty extracts were therefore prepared from twenty-seven foodstuffs common to the Western diet, and the capacity of each to induce the secretion of inflammatory signals from human white blood cells was measured. They found whopping doses of endotoxin equivalents in pork, poultry, dairy.
Conclusion is that animal products may cause inflammation because of their endotoxins.
Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, Dandona P. Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance. Diabetes Care. 2009 Dec; 32(12):2281-7.Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23. http://www.ncbi.nlm.nih.gov/pubmed/20849668
Posted by rca on December 29, 2012, at 11:25:12
In reply to Re: Bifidobacteria reduce depression, posted by Trotter on December 28, 2012, at 13:59:26
> >since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the blood stream (Deopurkar et al., 2010, below).
> >
>
> Can you please provide evidence to support your statement that the translocation of endotoxin is facilitated by a "saturated fat transport system"? It is my current understanding that a high fat diet increases endotoxemia by affecting the bowel bacterial composition, specifically by reducing bifidobacteria. I think it is the bifidobacteria which help maintain intestinal integrity.Yes. Animal fat may play a profound role in the pathogenesis of after-meal inflammation by increasing the absorption of the endotoxins, since endotoxin has a strong affinity for the saturated fat transport system (chylomicrons lipoproteins that transport dietary long chain saturated fatty acids through the gut wall and into the blood stream). So animal fat may play a role in boosting endotoxin absorption, but the primary reason all those studies show increased inflammation from animal foods, but not from unfermented plant foods, may be the load of dead bacteria, which release endotoxins that are absorbed into our system leading to the endotoxemic inflammation we see after meat, egg, and dairy consumption.
The transport system is nicely explained here: http://www.google.com/url?sa=t&rct=j&q=&esrc=s&frm=1&source=web&cd=1&ved=0CDQQFjAA&url=http%3A%2F%2Fwww.jlr.org%2Fcontent%2Fearly%2F2008%2F10%2F28%2Fjlr.E800018-JLR200.full.pdf&ei=oSTfUISRLufg2wXLjIHoBQ&usg=AFQjCNEiN37xnCExm09raRc1iapzMaLxZQ&sig2=qh8SmOEKpm3S84kDmqMW_A
Posted by SLS on December 29, 2012, at 12:18:42
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 29, 2012, at 11:25:12
Fascinating stuff. I feel so wonderfully dumb.
- Scott
> > >since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the blood stream (Deopurkar et al., 2010, below).
> > >
> >
> > Can you please provide evidence to support your statement that the translocation of endotoxin is facilitated by a "saturated fat transport system"? It is my current understanding that a high fat diet increases endotoxemia by affecting the bowel bacterial composition, specifically by reducing bifidobacteria. I think it is the bifidobacteria which help maintain intestinal integrity.
>
> Yes. Animal fat may play a profound role in the pathogenesis of after-meal inflammation by increasing the absorption of the endotoxins, since endotoxin has a strong affinity for the saturated fat transport system (chylomicrons lipoproteins that transport dietary long chain saturated fatty acids through the gut wall and into the blood stream). So animal fat may play a role in boosting endotoxin absorption, but the primary reason all those studies show increased inflammation from animal foods, but not from unfermented plant foods, may be the load of dead bacteria, which release endotoxins that are absorbed into our system leading to the endotoxemic inflammation we see after meat, egg, and dairy consumption.
>
> The transport system is nicely explained here: http://www.google.com/url?sa=t&rct=j&q=&esrc=s&frm=1&source=web&cd=1&ved=0CDQQFjAA&url=http%3A%2F%2Fwww.jlr.org%2Fcontent%2Fearly%2F2008%2F10%2F28%2Fjlr.E800018-JLR200.full.pdf&ei=oSTfUISRLufg2wXLjIHoBQ&usg=AFQjCNEiN37xnCExm09raRc1iapzMaLxZQ&sig2=qh8SmOEKpm3S84kDmqMW_A
>
> http://www.ncbi.nlm.nih.gov/pubmed/22210577
>
Posted by Trotter on December 29, 2012, at 14:40:16
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 29, 2012, at 11:25:12
> > >since endotoxin has a strong affinity for the saturated fat transport system through the gut wall and into the blood stream (Deopurkar et al., 2010, below).
> > >
> >
> > Can you please provide evidence to support your statement that the translocation of endotoxin is facilitated by a "saturated fat transport system"? It is my current understanding that a high fat diet increases endotoxemia by affecting the bowel bacterial composition, specifically by reducing bifidobacteria. I think it is the bifidobacteria which help maintain intestinal integrity.
>
> Yes. Animal fat may play a profound role in the pathogenesis of after-meal inflammation by increasing the absorption of the endotoxins, since endotoxin has a strong affinity for the saturated fat transport system (chylomicrons lipoproteins that transport dietary long chain saturated fatty acids through the gut wall and into the blood stream). So animal fat may play a role in boosting endotoxin absorption, but the primary reason all those studies show increased inflammation from animal foods, but not from unfermented plant foods, may be the load of dead bacteria, which release endotoxins that are absorbed into our system leading to the endotoxemic inflammation we see after meat, egg, and dairy consumption.
>
> The transport system is nicely explained here: http://www.google.com/url?sa=t&rct=j&q=&esrc=s&frm=1&source=web&cd=1&ved=0CDQQFjAA&url=http%3A%2F%2Fwww.jlr.org%2Fcontent%2Fearly%2F2008%2F10%2F28%2Fjlr.E800018-JLR200.full.pdf&ei=oSTfUISRLufg2wXLjIHoBQ&usg=AFQjCNEiN37xnCExm09raRc1iapzMaLxZQ&sig2=qh8SmOEKpm3S84kDmqMW_A
>
> http://www.ncbi.nlm.nih.gov/pubmed/22210577
>Very interesting. As you indicated, this is pretty compelling evidence that a high fat meal results in facilitated 'transportation' of endotoxins from the bowel into the bloodstream, causing inflammation.
Have you read the research showing that increasing bifidobacterial levels reverse endotoxemia caused by high fat diet? This has been shown in two separate studies. I wonder how this fits in with the above?
Posted by Trotter on December 29, 2012, at 14:50:06
In reply to Re: Bifidobacteria reduce depression » larryhoover, posted by rca on December 29, 2012, at 9:29:19
You are a smart guy rca but I think your argument is slightly flawed. Yes, you have shown that animal protein does contain endotoxins. However you have not shown, not is it possible to show, that it is the endotoxins in the animal protein that causes endotoxemia. Given the massive amounts of endotoxins in the bowel, it seems logical to me that 99.9% of endotoxemia is not caused by the ingested endotoxins you refer to. Further, increased 'transportation' of endotoxins across the bowel wall caused by a high fat meal occurs regardless of the fat source, animal or vegetable.
> Thanks for your thoughtful reply - haven't "digested" it all but can respond to one comment here.
>
> >High-fat HIGH-CARB combination. There it is, plain as day.
>
> The study (quote below) involved comparison of a high fat high carb (HFHC) group compared to an American Heart Association recommended food group (AHA). But you know what they were actually eating? The HFHC groups ate egg muffin and sausage muffin sandwiches and two hash browns, which contain 88 g carbohydrates, 51 g fat [33% saturated] and 34 g protein [carbohydrates 41%, protein 17%, and fat 42%]; the second group ate oatmeal, milk, orange juice, raisins, peanut butter, and English muffin (carbohydrates 58%, protein 15%, and fat 27%). I think their choice of these two groups were unfortunate and their labeling misleading.
>
> The HFHC group ate a typical SAD diet of animal products and simple carbohydrates; the second group still included some animal product and was predominately a high carbohydrate meal, but had a significant amount of complex carbohydrates too.
>
> Their data indicated a pronounced inflammation after the HFHC (SAD) diet compared to the AHA diet (even with the milk , juice, and English muffin Id prefer comparing to a whole plant based diet something like whole rolled oats, blueberries, crushed flax seeds in soy milk).
>
> The entire article is available on-line here: http://www.ncbi.nlm.nih.gov/pubmed?term=Diabetes%20Care.%202009%20Dec%3B%2032(12)%3A2281-7.
>
> Heres the interesting part. Please examine the two figures (each with three figures on them), showing the inflammatory marker rise (figure 1) and the endotoxin rise (Figure 2). Notice anything strange? In all cases these parameters rise in just ONE HOUR after the meal certainly not time enough to reach the leaky gut colon where all the bacteria are. I see no explanation other than there are endotoxins in the animal products that are being absorbed in the small intestine.
>
> Yep. Look at (Erridge, 2011) below. For the first time ever, they aimed to determine whether common foodstuffs may contain appreciable quantities of endotoxin. Forty extracts were therefore prepared from twenty-seven foodstuffs common to the Western diet, and the capacity of each to induce the secretion of inflammatory signals from human white blood cells was measured. They found whopping doses of endotoxin equivalents in pork, poultry, dairy.
>
> Conclusion is that animal products may cause inflammation because of their endotoxins.
>
>
> Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, Dandona P. Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance. Diabetes Care. 2009 Dec; 32(12):2281-7.
>
> Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23. http://www.ncbi.nlm.nih.gov/pubmed/20849668
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Posted by rca on December 30, 2012, at 11:11:29
In reply to Re: Bifidobacteria reduce depression » rca, posted by Trotter on December 29, 2012, at 14:50:06
Thanks for the kind word and I agree that one would initially logically think that the endotoxins would emerge from the resident flora in the large bowel except for at least two reasons. The first is the cited Ghanim et al. study that shows emergence of the endotoxins in the bloodstream within one hour and peaking at 2 -3 hours (bolus hasnt reached colon) and the second is what kind of a crummy body design would have our natural bacterial flora attaching us. I think the key is understanding that while its been quite handy to be an omnivore as people migrated to all regions of the globe, the key to healthy nutrition is whole plant based diet. No endotoxins, negligible saturated fat (compared to animal products).
So while the question of the mechanism of endotoxin emergence may be in question, the solution appears to be dietary changes we can acquire and recommend to our patients.
> You are a smart guy rca but I think your argument is slightly flawed. Yes, you have shown that animal protein does contain endotoxins. However you have not shown, not is it possible to show, that it is the endotoxins in the animal protein that causes endotoxemia. Given the massive amounts of endotoxins in the bowel, it seems logical to me that 99.9% of endotoxemia is not caused by the ingested endotoxins you refer to. Further, increased 'transportation' of endotoxins across the bowel wall caused by a high fat meal occurs regardless of the fat source, animal or vegetable.
>
>
>
>
> > Thanks for your thoughtful reply - haven't "digested" it all but can respond to one comment here.
> >
> > >High-fat HIGH-CARB combination. There it is, plain as day.
> >
> > The study (quote below) involved comparison of a high fat high carb (HFHC) group compared to an American Heart Association recommended food group (AHA). But you know what they were actually eating? The HFHC groups ate egg muffin and sausage muffin sandwiches and two hash browns, which contain 88 g carbohydrates, 51 g fat [33% saturated] and 34 g protein [carbohydrates 41%, protein 17%, and fat 42%]; the second group ate oatmeal, milk, orange juice, raisins, peanut butter, and English muffin (carbohydrates 58%, protein 15%, and fat 27%). I think their choice of these two groups were unfortunate and their labeling misleading.
> >
> > The HFHC group ate a typical SAD diet of animal products and simple carbohydrates; the second group still included some animal product and was predominately a high carbohydrate meal, but had a significant amount of complex carbohydrates too.
> >
> > Their data indicated a pronounced inflammation after the HFHC (SAD) diet compared to the AHA diet (even with the milk , juice, and English muffin Id prefer comparing to a whole plant based diet something like whole rolled oats, blueberries, crushed flax seeds in soy milk).
> >
> > The entire article is available on-line here: http://www.ncbi.nlm.nih.gov/pubmed?term=Diabetes%20Care.%202009%20Dec%3B%2032(12)%3A2281-7.
> >
> > Heres the interesting part. Please examine the two figures (each with three figures on them), showing the inflammatory marker rise (figure 1) and the endotoxin rise (Figure 2). Notice anything strange? In all cases these parameters rise in just ONE HOUR after the meal certainly not time enough to reach the leaky gut colon where all the bacteria are. I see no explanation other than there are endotoxins in the animal products that are being absorbed in the small intestine.
> >
> > Yep. Look at (Erridge, 2011) below. For the first time ever, they aimed to determine whether common foodstuffs may contain appreciable quantities of endotoxin. Forty extracts were therefore prepared from twenty-seven foodstuffs common to the Western diet, and the capacity of each to induce the secretion of inflammatory signals from human white blood cells was measured. They found whopping doses of endotoxin equivalents in pork, poultry, dairy.
> >
> > Conclusion is that animal products may cause inflammation because of their endotoxins.
> >
> >
> > Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, Dandona P. Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance. Diabetes Care. 2009 Dec; 32(12):2281-7.
> >
> > Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23. http://www.ncbi.nlm.nih.gov/pubmed/20849668
> >
> >
> >
> >
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Posted by Trotter on December 30, 2012, at 16:19:21
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 30, 2012, at 11:11:29
Can't argue with your logic with regards the timing of endotoxins in blood plasma following a meal. It does suggest that some endotoxins are coming from the food itself.
Not sure I agree with your second point though, regarding "our natural bacterial flora attacking us." Technically, the contents of the lumen are not part of our bodies. Our intestinal wall is designed to keep most of the intestinal contents out of our bodies. Further, one study in mice showed that commensal bacteria in our bowel do not cause endotoxemia, only invasive (bad) bacteria. Friendly bacteria such as lactobacilli and bifidobacteria do not attack the body, while some strains (not all) of E. coli (and other gram negative bacteria) are responsible for endotoxemia.
While I agree you have presented a good case that food endotoxins can cause endotoxemia, it has also been shown through antibodies to certain gram negative intestinal bacteria that bowel bacteria certainly cause endotoxemia too.
Regarding plant vs animal fat, it is my understanding that they both increase endotoxemia. While a plant based diet low in fat would reduce endotoxemia, I'm not convinced a plant diet with similar fat level to an animal based diet would have significantly lower plasma endotxins. You might be right, I'm just not convinced.
I guess in the back of my mind also is the logic behind the paleo diet. We are designed to eat meat.
> Thanks for the kind word and I agree that one would initially logically think that the endotoxins would emerge from the resident flora in the large bowel except for at least two reasons. The first is the cited Ghanim et al. study that shows emergence of the endotoxins in the bloodstream within one hour and peaking at 2 -3 hours (bolus hasnt reached colon) and the second is what kind of a crummy body design would have our natural bacterial flora attaching us. I think the key is understanding that while its been quite handy to be an omnivore as people migrated to all regions of the globe, the key to healthy nutrition is whole plant based diet. No endotoxins, negligible saturated fat (compared to animal products).
>
> So while the question of the mechanism of endotoxin emergence may be in question, the solution appears to be dietary changes we can acquire and recommend to our patients.
>
> > You are a smart guy rca but I think your argument is slightly flawed. Yes, you have shown that animal protein does contain endotoxins. However you have not shown, not is it possible to show, that it is the endotoxins in the animal protein that causes endotoxemia. Given the massive amounts of endotoxins in the bowel, it seems logical to me that 99.9% of endotoxemia is not caused by the ingested endotoxins you refer to. Further, increased 'transportation' of endotoxins across the bowel wall caused by a high fat meal occurs regardless of the fat source, animal or vegetable.
> >
> >
> >
> >
> > > Thanks for your thoughtful reply - haven't "digested" it all but can respond to one comment here.
> > >
> > > >High-fat HIGH-CARB combination. There it is, plain as day.
> > >
> > > The study (quote below) involved comparison of a high fat high carb (HFHC) group compared to an American Heart Association recommended food group (AHA). But you know what they were actually eating? The HFHC groups ate egg muffin and sausage muffin sandwiches and two hash browns, which contain 88 g carbohydrates, 51 g fat [33% saturated] and 34 g protein [carbohydrates 41%, protein 17%, and fat 42%]; the second group ate oatmeal, milk, orange juice, raisins, peanut butter, and English muffin (carbohydrates 58%, protein 15%, and fat 27%). I think their choice of these two groups were unfortunate and their labeling misleading.
> > >
> > > The HFHC group ate a typical SAD diet of animal products and simple carbohydrates; the second group still included some animal product and was predominately a high carbohydrate meal, but had a significant amount of complex carbohydrates too.
> > >
> > > Their data indicated a pronounced inflammation after the HFHC (SAD) diet compared to the AHA diet (even with the milk , juice, and English muffin Id prefer comparing to a whole plant based diet something like whole rolled oats, blueberries, crushed flax seeds in soy milk).
> > >
> > > The entire article is available on-line here: http://www.ncbi.nlm.nih.gov/pubmed?term=Diabetes%20Care.%202009%20Dec%3B%2032(12)%3A2281-7.
> > >
> > > Heres the interesting part. Please examine the two figures (each with three figures on them), showing the inflammatory marker rise (figure 1) and the endotoxin rise (Figure 2). Notice anything strange? In all cases these parameters rise in just ONE HOUR after the meal certainly not time enough to reach the leaky gut colon where all the bacteria are. I see no explanation other than there are endotoxins in the animal products that are being absorbed in the small intestine.
> > >
> > > Yep. Look at (Erridge, 2011) below. For the first time ever, they aimed to determine whether common foodstuffs may contain appreciable quantities of endotoxin. Forty extracts were therefore prepared from twenty-seven foodstuffs common to the Western diet, and the capacity of each to induce the secretion of inflammatory signals from human white blood cells was measured. They found whopping doses of endotoxin equivalents in pork, poultry, dairy.
> > >
> > > Conclusion is that animal products may cause inflammation because of their endotoxins.
> > >
> > >
> > > Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, Dandona P. Increase in plasma endotoxin concentrations and the expression of Toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal: implications for insulin resistance. Diabetes Care. 2009 Dec; 32(12):2281-7.
> > >
> > > Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011 Jan; 105(1):15-23. http://www.ncbi.nlm.nih.gov/pubmed/20849668
> > >
> > >
> > >
> > >
> > >
> >
> >
>
>
Posted by Trotter on December 30, 2012, at 23:27:27
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 30, 2012, at 11:11:29
I've spent a bit of time analysing the two studies you referenced. It has challenged my understanding of endotoxemia. Here are some of my observations.
It seems likely the endotoxemia measured in the Ghanim study was due to LPS translocation within the small bowel.
The researchers believe the LPS came primarily from the food due to the relatively small numbers of resident bacteria in the small bowel. I'm still not 100% convinced of this, but I concede it is likely.
There was around 3x increase in plasma endotoxins after the HFHC meal, compared to the AHA meal. I think this is likely explained by three factors. Firsly, the HFHC meal had a higher fat content. Secondly, orange juice (in the AHA meal) has been shown to reduce translocation of LPS. Thirdly, the higher fibre in the AHA meal may have absorbed some of the fat.
According to the reseachers, both meals had similar LPS in spite of the fact one was vegetarian and the other meat/egg based.
In the Erridge study, the main foodstuffs linked to possible increased endotoxemia were ice cream, chocolate, turkey and pork. I agree that all these foodstuffs come from milk or meat, however other meats like beef, lamb and chicken had negligible LPS. So, yes, plant foods may have low LPS, but most animal foods were low as well.
This has been an eye opener for me. Thank you for the references.
I'm not sure how this research ties in with the high fat diet rodent studies. In these two studies (linked below) a high fat diet caused endotoxemia. However in both the endotoxemia was completely avoided by increasing bifidobacteria. In the first via feeding a prebiotic, and the second by directly feeding probiotic bifidobacteria. In the OFS fed mice, presumably the increase in bifidobacteria occured primarily in the large bowel. Bifidobacteria are anaerobic so very few exist in the small bowel. This suggests the bifidobacteria reduced translocation of LPS in the large bowel. This suggest to me two different models of endoxemia. One that occurs in the hours following a high fat meal (in the small bowel), and another that occurs in the large bowel.
http://www.ncbi.nlm.nih.gov/pubmed/17823788
http://www.ncbi.nlm.nih.gov/pubmed/21685239I find it all rather confusing. I tend to think the small bowel endotoxemia may involve ingested LPS, whereas I think the large bowel endotoxemia involves resident bacteria. Which is more important? I suspect the latter. I base this on the fact that increasing bifidobacteria was able to reverse high fat induced endotoxemia.
Here are a few other studies I found interesting regarding bifidobacteria, intestinal permeability and endotoxemia.
http://www.medbc.com/annals/review/vol_10/num_1/text/vol10n1p45.htm
http://www.ncbi.nlm.nih.gov/pubmed/16773690
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702831/
Posted by SLS on December 31, 2012, at 7:16:26
In reply to Re: Bifidobacteria reduce depression, posted by Trotter on December 30, 2012, at 23:27:27
Are there differences in the composition of the endotoxins coming from the upper GI versus the colon? Is there any way to track some sort of endotoxin molecular signature?
Also, have you guys come to any conclusion as to which process allows endotoxins to exit the bowel - transport or translocation?
Do all endotoxins produce exactly the same immune reaction, or are there differences in the types and ratios of interleukins, cytokines, and interferons?
Thanks.
- Scott
Posted by Trotter on December 31, 2012, at 13:23:18
In reply to Re: Bifidobacteria reduce depression, posted by SLS on December 31, 2012, at 7:16:26
> Are there differences in the composition of the endotoxins coming from the upper GI versus the colon?
At a guess I would say there are different, since it seems the endotoxins from the upper GI are from food, and from the colon from resident bacteria. However I have no actual evidence to back this up.
Is there any way to track some sort of endotoxin molecular signature?
Yes. I remember reading somewhere that they tracked an ingested endotoxin into the blood plasma. From memory it was radioactive, but not sure. Further, they can measure antibodies to specific bacterial LPS.
>
> Also, have you guys come to any conclusion as to which process allows endotoxins to exit the bowel - transport or translocation?I think it is always translocation. Fat seems to facilitate translocation of LPS. This has been referred to as 'transportation', as the LPS is carried by the fat, but it still involves translocation across the intestine wall.
>
> Do all endotoxins produce exactly the same immune reaction, or are there differences in the types and ratios of interleukins, cytokines, and interferons?I'm not sure, but I have not come across any differences, so my guess is that it's pretty much the same.
>
> Thanks.
>
>
> - Scott
Posted by Trotter on December 31, 2012, at 19:41:12
In reply to Re: Bifidobacteria reduce depression » SLS, posted by Trotter on December 31, 2012, at 13:23:18
In this study of people with MDD there was a very strong link between antibodies for LPS bacteria and depression. No cause and effect was proven, but the obvious suggestion is that endotoxemia causes systemic inflammation, which causes depression.
Posted by SLS on January 3, 2013, at 7:52:38
In reply to High fat diet -) inflammation -) depression, posted by Trotter on December 19, 2012, at 23:44:21
Here's an interesting short article:
- Scott
"The Impact of Obesity on Brain and Behavior
December 21, 2012 · Posted in Risk Factors · CommentOverweight Santa Claus
In an abstract presented at the 5th Biennial Conference of the International Society for Bipolar Disorders, K. Sim and colleagues discussed the impact of increased body mass index on the integrity of white matter in the brain during a first episode of mania. The researchers found significant abnormalities in white matter integrity in the temporal pole and occipital brain regions in overweight and obese patients compared to patients of normal weight. These data highlight the need to clarify the neural mechanisms that link obesity and poorer functional outcomes in bipolar disorder.
Other investigators have reported that bipolar patients with obesity have a less robust response to naturalistic treatment compared to those of normal weight. At least one study suggested that patients with overweight and obesity experience more cognitive difficulties.
Editors Note: The pathophysiological mechanisms involved in the relationship between weight and brain function are not yet clear, although one possibility is that in obese patients, some fat cells in the abdominal area become too big to survive and are scavenged by other cytokine-producing cells. These inflammatory cytokines are then able to cross the blood-brain barrier, enter the brain, and affect neuronal functioning. Whether a mechanism like this is at play in relation to these particular findings remains for further investigation.
Nonetheless, these data suggest the importance of good diet, exercise, and other means of maintaining a good body weight in order to attempt to avoid some of the adverse associations of obesity with deficits in cognition, white matter integrity, and treatment outcome."
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