Jump to content

Does inflammation peak after meals?


Recommended Posts



Yes, inflammation does peak after meals, and it appears to be more a function of the meal's fat content than its influence on blood glucose, although glucose levels may play a factor in triggering inflammation as well [1]. Endotoxins, particularly in animal products, are another cause of postprandial inflammation, as discussed in this Nutritionfacts.org video. Below is a picture from this review [2] of the factors that most affect postprandial lipemia (fat in the blood) resulting in inflammation, ranging from most beneficial at the top to most detrimental at the bottom:




Note - these authors say:


Since humans are postprandial most of the day, the continuous 
generation of [lipoproteins] remnants after each meal may be one
of the triggers for the development of atherosclerosis.
This might help you get motivated to cut back from three meals per day, as you asked about on this other thread!


[1] Adv Exp Med Biol. 2014;824:161-70. doi: 10.1007/978-3-319-07320-0_12.

Postprandial inflammation: targeting glucose and lipids.
de Vries MA(1), Klop B, Janssen HW, Njo TL, Westerman EM, Castro Cabezas M.
Author information: 
(1)Department of Internal Medicine, Center for Diabetes and Vascular Medicine,
Sint Franciscus Gasthuis, 10900, Rotterdam, 3004 BA, The Netherlands,
Many risk factors have been identified as being responsible for the process of
atherogenesis. Several of these risk factors are related to inflammation, which
is an obligatory feature of the atherosclerotic plaque. Increasing evidence
suggests that postprandial lipoproteins and glucose may be involved in the
inflammatory process preceding the development of atherosclerosis. During the
postprandial situation, remnants of chylomicrons and very low-density
lipoproteins bind to circulating leukocytes and endothelial cells, leading to a
state of acute activation with the expression of integrins on different cells,
the generation of oxidative stress, production of cytokines and complement
activation. Elevated plasma glucose levels may also induce leukocyte activation
in humans. In addition, advanced glycation end products, formed during
hyperglycemia, cause inflammation and endothelial damage. This chain of events
results in a situation of acute inflammation causing endothelial dysfunction,
which may be one of the earliest defects in atherogenesis. Interestingly, while
this may occur several times each day after each meal, there is only limited
information on the contribution of different nutrients on the postprandial
inflammatory processes. In this review, we will focus on the available evidence
and we will discuss the role of lifestyle and pharmaceutical interventions in
modulating postprandial inflammation.
PMID: 25038999

[2] Int J Vasc Med. 2012;2012:947417. doi: 10.1155/2012/947417. Epub 2011 Sep 25.

Understanding postprandial inflammation and its relationship to lifestyle
behaviour and metabolic diseases.
Klop B(1), Proctor SD, Mamo JC, Botham KM, Castro Cabezas M.
Author information: 
(1)Department of Internal Medicine, Center for Diabetes and Vascular Medicine,
Sint Franciscus Gasthuis, 3004 BA Rotterdam, The Netherlands.
Postprandial hyperlipidemia with accumulation of remnant lipoproteins is a common
metabolic disturbance associated with atherosclerosis and vascular dysfunction,
particularly during chronic disease states such as obesity, the metabolic
syndrome and, diabetes. Remnant lipoproteins become attached to the vascular
wall, where they can penetrate intact endothelium causing foam cell formation.
Postprandial remnant lipoproteins can activate circulating leukocytes, upregulate
the expression of endothelial adhesion molecules, facilitate adhesion and
migration of inflammatory cells into the subendothelial space, and activate the
complement system. Since humans are postprandial most of the day, the continuous 
generation of remnants after each meal may be one of the triggers for the
development of atherosclerosis. Modulation of postprandial lipemia by lifestyle
changes and pharmacological interventions could result in a further decrease of
cardiovascular mortality and morbidity. This paper will provide an update on
current concepts concerning the relationship between postprandial lipemia,
inflammation, vascular function, and therapeutic options.
PMCID: PMC3179890
PMID: 21961070
Link to comment
Share on other sites

Wouldn't MUFAs decrease inflammation after meals? Or is there a certain limit after which MUFAs would start increasing it again?


You would think MUFA would decrease (or at least not increase) post-meal inflammation. Michael may correct me if I'm wrong, but I'm not sure this is the case however.


Study [1] suggests little difference between MUFA and SFA on post-meal lipid metabolism - e.g. ApoB was similarly elevated by the two type of fats. In study [2], carbohydrates were better than MUFA for post meal inflammation markers like ApoB, at least in Type 1 diabetics:


Our data suggest that in patients with type 1
diabetes, a CHO diet might be preferable to a Mono diet, since adherence to the
former results in a lower number of circulating postprandial lipoprotein
particles that are potentially atherogenic.





[1] Br J Nutr. 1998 May;79(5):419-24.

The effect of test meal monounsaturated fatty acid: saturated fatty acid ratio on
postprandial lipid metabolism.
Roche HM(1), Zampelas A, Jackson KG, Williams CM, Gibney MJ.
Author information: 
(1)Unit of Nutrition, Trinity Centre for Health Sciences, St James's Hospital,
Dublin, Ireland. hmroche@tcd.ie
Epidemiological evidence shows that a diet high in monounsaturated fatty acids
(MUFA) but low in saturated fatty acids (SFA) is associated with reduced risk of 
CHD. The hypocholesterolaemic effect of MUFA is known but there has been little
research on the effect of test meal MUFA and SFA composition on postprandial
lipid metabolism. The present study investigated the effect of meals containing
different proportions of MUFA and SFA on postprandial triacylglycerol and
non-esterified fatty acid (NEFA) metabolism. Thirty healthy male volunteers
consumed three meals containing equal amounts of fat (40 g), but different
proportions of MUFA (12, 17 and 24% energy) in random order. Postprandial plasma 
triacylglycerol, apolipoprotein B-48, cholesterol, HDL-cholesterol, glucose and
insulin concentrations and lipoprotein lipase (EC activity were not
significantly different following the three meals which varied in their levels of
SFA and MUFA. There was a significant difference in the postprandial NEFA
response between meals. The incremental area under the curve of postprandial
plasma NEFA concentrations was significantly (P = 0.03) lower following the
high-MUFA meal. Regression analysis showed that the non-significant difference in
fasting NEFA concentrations was the most important factor determining difference 
between meals, and that the test meal MUFA content had only a minor effect. In
conclusion, varying the levels of MUFA and SFA in test meals has little or no
effect on postprandial lipid metabolism.
PMID: 9682660
[2] Arterioscler Thromb Vasc Biol. 1998 May;18(5):773-82.
Differences in the metabolism of postprandial lipoproteins after a
high-monounsaturated-fat versus a high-carbohydrate diet in patients with type 1 
diabetes mellitus.
Georgopoulos A(1), Bantle JP, Noutsou M, Swaim WR, Parker SJ.
Author information: 
(1)Minneapolis Veterans Affairs Medical Center, MN 55417, USA.
There is little information comparing the effects of a high-monounsaturated
(Mono)-fat versus a high-carbohydrate (CHO) diet in patients with type 1 diabetes
mellitus. In the present study, the effects of these diets on a number of
metabolic parameters were compared. Seventeen normolipidemic, nonobese patients
with type 1 diabetes were provided with the diets for 4 weeks each in a
randomized, crossover design. The percentages of Mono fat of the two diets were
25 Mono versus 9 CHO, with a corresponding total fat content of 40% versus 24%
and a total CHO content of 45% versus 61%. At the end of each dietary period,
parameters of glycemic control, coagulation factors, and fasting and postprandial
lipoproteins were assessed. There were no differences in weight, glycemia,
insulin dose, fasting lipid profile, or coagulation factors between the two
diets. However, the metabolism of postprandial lipoproteins after a fat load
differed; viz, after the Mono diet compared with the CHO diet, mean plasma
triglyceride levels over 10 hours were higher (P=.0025, by repeated-measures
ANOVA). The levels of triglyceride (P=.0045) and retinyl esters (P=.0046) in
chylomicrons (Sf>400) and chylomicron remnants (Sf 100 to 400) (P=.0047 and
P=.043, respectively), and the total particle number (apolipoprotein B levels) in
chylomicron remnants (P=.001) and small, very low density lipoprotein (Sf 20 to
100, P=.016) were also higher. Our data suggest that in patients with type 1
diabetes, a CHO diet might be preferable to a Mono diet, since adherence to the
former results in a lower number of circulating postprandial lipoprotein
particles that are potentially atherogenic.
PMID: 9598837
Link to comment
Share on other sites

Qualifier - to avoid Michael jumping down my throat.  :)xyz


MUFA, including low phenolic olive oil, appears to increase postprandial inflammation as mentioned above, but high phenolic content, extra virgin olive oil appears not to, or at least not as much, according to [1].





[1] Food Chem. 2014 Nov 1;162:161-71. doi: 10.1016/j.foodchem.2014.04.047. Epub 2014 

Apr 24.
Olive oil phenolic compounds decrease the postprandial inflammatory response by
reducing postprandial plasma lipopolysaccharide levels.
Camargo A(1), Rangel-Zuñiga OA(2), Haro C(2), Meza-Miranda ER(2), Peña-Orihuela
P(2), Meneses ME(2), Marin C(2), Yubero-Serrano EM(2), Perez-Martinez P(2),
Delgado-Lista J(2), Fernandez-Real JM(3), Luque de Castro MD(4), Tinahones FJ(5),
Lopez-Miranda J(2), Perez-Jimenez F(2).
We investigated the molecular mechanisms by which phenolic compounds (phenols) in
virgin olive oil reduce the postprandial inflammatory response with the aim of
identifying the transcription factor involved and the downstream effects. Olive
oil-based breakfasts prepared with virgin olive oil (VOO) with high (398 ppm),
intermediate (149 ppm) and low (70 ppm) phenol content were administered to 49
metabolic syndrome patients following a randomized crossover design. The
consumption of a high-phenol VOO-based breakfast limited the increase of
lipopolysaccharide plasma levels, TLR4, and SOCS3 proteins (p<0.001, p=0.041 and 
p=0.008, respectively), the activation of NF-κB (p=0.016) and the IL6 (p=0.007
and p=0.048, low and intermediate oil, respectively), IL1B (p=0.002, intermediate
oil), and CXCL1 (p=0.001) postprandial gene expression, in peripheral blood
mononuclear cells, as compared with the consumption of a breakfast prepared with 
the same oil but with low or intermediate phenol content. Virgin olive oil
phenolic compounds reduce the postprandial inflammatory response in association
with postprandial plasma lipopolysaccharide levels.
Copyright © 2014 Elsevier Ltd. All rights reserved.
PMID: 24874372
Link to comment
Share on other sites


This topic is now archived and is closed to further replies.

  • Create New...