Some people gain weight from chronic inflammation, while others lose weight. The kind of inflammation you’re experiencing will determine if you gain or lose weight. This post will go into what types of inflammation cause weight gain.
What’s interesting is that people who are affected by environmental toxins are more likely to gain weight, and markers that are associated with weight gain are elevated.
TGF-beta causes weight gain.
TGF-beta is correlated with obesity in rodents and humans (R).
Smad3 (which is activated by TGF) acts as a repressor of PGC-1a expression.
Complement 3 (C3) generates C3a. C3a converts to ASP or acylation-stimulating-protein (R).
C3a and the complement immune system is often elevated in mold illness.
- SelfDecode has SNPs for C3a.
SOCS3 causes weight gain.
SOCS3 is often elevated in mold illness.
There is growing evidence that MMPs play an important role in causing obesity.
An MMP-2 gene was associated with percentage of body fat in childhood obesity in New Zealand (R).
In one study, obese children and adolescents had higher MMP-8 [R].
VEGF causes weight gain.
Vascular endothelial growth factor (VEGF) is abundantly secreted from fat cells and plays a key role in the process of fat tissue formation through increasing angiogenesis.
A positive correlation between the concentrations of circulating VEGF levels and BMI was demonstrated in healthy male subjects under highly controlled conditions [R].
Angiogenesis has been associated with fat tissue (visceral and subcutaneous) in severe human obesity [R].
Mice treated with an angiogenesis inhibitor had smaller fat cells [R].
Different angiogenesis inhibitors have been shown to significantly decrease body and fat tissue weights [R].
VEGF-B specifically controlled the uptake of fatty acids [R].
- SelfDecode has SNPs for VEGF-A and VEGF-B.
TLR4 causes weight gain.
Substantial evidence exists supporting the important role of Toll Like Receptors (TLRs) in the cause of obesity.
Chronic low-grade inflammation found (in endoxinemia) has been demonstrated to be due to activation of TLR-4 by LPS (lipopolysaccharide).
Mice, lacking TLR-4, have been found to be resistant to diet-induced obesity and insulin resistance [R].
TLR-4-deficient mice were protected against obesity-induced by diets high in saturated fat.
Prostaglandins promote weight gain.
Prostaglandins (PGs) play a role in inflammatory processes.
PGE2 enhanced fat accumulation in the liver and caused fatty liver [R].
Nf-kB seems to cause weight gain.
The fancy term is “endoplasmic reticulum stress”, which basically means we’re overloading our cells with calories, without the ability of the mitochondria to utilize it.
Most studies use fat to do this, but any macronutrient can theoretically do this (R).
NF-κB activity was higher in animals fed a high fat diet. Increased stomach fat was associated with higher Nf-kB in these tissues (R).
MyD88 causes weight gain in some circumstances.
When scientists inactivated part of the intestinal immune system in mice (a protein called MyD88), they were much more resistant to diabetes and obesity (diabesity) (R).
This MyD88 protein also causes gut permeability (R).
PAI-1 causes obesity.
PAI-1 results in the overgrowth of tissue (fibrosis) (R).
TGF-beta increases PAI-1, which is reversed by curcumin (R).
- Buy Curcumin (IHERB).
Glutamate causes weight gain.
Glutamate is an excitatory neurotransmitter and it stimulates appetite (R).
People with chronic inflammation will have higher glutamate in various brain regions.
NADPH causes weight gain.
Nicotinamide adenine dinucleotide phosphate (NADPH).
13) Nitric Oxide Synthase (NOS)
NOS causes weight gain.
Nitric oxide synthase (NOS) is an enzyme that is involved in the synthesis of nitric oxide (NO). It’s increased in inflammatory states.
Platelet NO production has been significantly correlated with BMI, waist circumference, and triglyceride concentrations, thus suggesting an association between increased platelet NO production, obesity, and high triglycerides, independent of the degree of insulin-resistance [R].
Chronic NOS blockade in mice ameliorated diet-induced weight gain and glucose intolerance, accompanied by reduced fat tissue inflammation and improved insulin sensitivity in muscle, suggesting that NO plays a role in the development of obesity-related insulin resistance [R].
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