Protect Against Damage Caused by Excess WeightPrint
By Robert Anderson
Obesity is a major threat to longevity and health.
In addition to physically burdening the body’s structure, fat cells accelerate disease risk and aging. They do this by churning out enormous amounts of inflammatory factors.1
Quercetin is a bioactive flavonoid found in onions, apples, and other botanical sources.
With more than 2 in 3 adults considered overweight or obese,2 these new results show that quercetin may represent a defense against the age-accelerating consequences of excess fat.
The Dangers of Excess Fat
Obesity imposes grave risks on our health, especially as we age.
It increases the wear and tear on all body systems and raises blood lipid levels.It also has ongoing effects that are less visible yet are more life-threatening.
When fat cells (adipocytes) and fat storage sites (adipose tissue) increase in size, an environment of insufficient oxygen supply (hypoxia) sets in, leading to cellular and biochemical changes.3
For example, hypoxia alters how fat cells express their genes, with the ultimate development of system-wide inflammation.4
Widespread inflammation is accompanied by metabolic disruptions. These include not only insulin resistance, type II diabetes, and fatty liver disease, but also atherosclerotic changes in blood vessels, heart disease, and stroke.5,6
Inflammatory changes in the brain and bone lead to neurodegenerative disorders and osteoporosis, respectively.7,8 At some point, DNA repair mechanisms and cell replication controls are lost, with a concomitant spike in cancer development.6,9
In short, fat tissue is perhaps the most powerful accelerator of aging.
Quercetin Prevents Obesity
The first step in protecting against obesity-related health dangers is to prevent diet-induced obesity in the first place.
Quercetin’s Multi-Targeted Effects
Two animal studies published in the past several years have demonstrated that supplementing with quercetin contributes to significant reductions in body weight—while also protecting against the dangerous impact of diet-induced accumulation of fat.12,13
Together, these studies offer a comprehensive picture of quercetin’s ability to attack obesity on multiple levels.
Here are the four primary ways quercetin accomplishes these feats.
Quercetin Reduces Fat-Generated Inflammation
First, quercetin precisely controls the genetic expression of pro-inflammatory signaling molecules (cytokines). In addition, this nutrient combination has been shown to produce significant reductions in the size of body-fat stores, to lower body weight, result in smaller fat- cell sizes, and reduce blood lipid levels.14
An even more striking finding is quercetin’s effect on the hypothalamus, the body’s central metabolic regulatory center.15
Obesity can activate the immune cells of the central nervous system, called microglia, producing destructive, localized inflammation, including in the hypothalamus. Inflammation in the hypothalamus has far-reaching consequences because of its intimate involvement in everything from core body temperature to basal metabolic rate to appetite and activity.
By activating microglia, obesity has been implicated in upsetting the ways the body manages its energy balance, as well as in metabolic complications like diabetes, and in neurodegenerative diseases.16-20
By reducing fat-generated inflammation, quercetin combats a potent age-accelerator.14,21
Quercetin Upregulates AMPK
AMPK is one of the body’s central metabolic regulatory signaling enzymes and is found in every living cell. It is considered one of the body’s most powerful anti-aging tools.
When activated, AMPK enhances rates of energy extraction by burning fat, and accelerating cleanup of toxic debris that accumulates inside aging cells (autophagy).
Quercetin has been shown to activate AMPK.13,14 Doing so promotes a more youthful cell type in terms of activity and vulnerability to stress of all kinds.22-24
Quercetin Promotes a Healthy Gut Microbiome
The gut microbiome is the community of millions of microorganisms that live in the intestinal tract. Obesity contributes to an imbalanced microbiome (called dysbiosis), a problem that is closely related to a wide range of human health issues, including diabetes and cardiovascular disease.25-27
Research suggests that obesity-related dysbiosis may produce “leaky gut,”29 a condition that allows bacterial toxins to enter the bloodstream, while promoting liver damage and excessive inflammation.
Supplementing with quercetin achieves specific gut-microbiome-related results by interacting with the many species that make up the gut microbiome. It stops the growth of bacteria that have pro-inflammatory and other harmful properties, while promoting the growth of bacteria known to protect the gut by producing mucous and anti-inflammatory compounds.21,32
In short, quercetin harnesses gut bacteria as allies in the fight against total-body impacts of obesity.
Quercetin Converts White Fat to Brown Fat
The bulk of fat tissue in adults is composed of white adipose tissue, or simply “white fat.”
This type of fat is what provides our energy supply between meals.34 Unfortunately, it is also the source of inflammation and other harmful metabolic changes associated with excessive fat stores.11,25
But infants (and many small mammals) have fat deposits that are made up of brown adipose tissue, or simply “brown fat.” Unlike the white variety, brown fat has the capability of converting energy stored as fat into heat.34,35
We’re now learning that it’s possible to boost brown-fat-cell content in human adults by triggering the cellular switch from white to brown.33-41 The result is the conversion of stored fat into fat that is burned for energy and readily shed from the body.
It’s a discovery that is revolutionizing our approach to obesity—and quercetin could play a major role.
Obesity is a major threat to human health and longevity.
Excessive amounts of certain types of fat tissue generate inflammation that accelerates the aging process and leads to numerous health issues.
Quercetin has been shown to help protect against obesity itself, as well as its age-accelerating consequences.
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- Available at: https://www.niddk.nih.gov/health-information/health-statistics/overweight-obesity. Accessed December 3, 2018.
- Pasarica M, Sereda OR, Redman LM, et al. Reduced adipose tissue oxygenation in human obesity: evidence for rarefaction, macrophage chemotaxis, and inflammation without an angiogenic response. 2009 Mar;58(3):718-25.
- Leiherer A, Stoemmer K, Muendlein A, et al. Quercetin Impacts Expression of Metabolism- and Obesity-Associated Genes in SGBS Adipocytes. Nutrients. 2016 May 12;8(5).
- Bonaccio M, Di Castelnuovo A, Pounis G, et al. A score of low-grade inflammation and risk of mortality: prospective findings from the Moli-sani study. Haemato2016 Nov;101(11):1434-41.
- Shimizu I, Yoshida Y, Suda M, et al. DNA damage response and metabolic disease. Cell Metab. 2014 Dec 2;20(6):967-77.
- Lacativa PG, Farias ML. Osteoporosis and inflammation. Arq Bras Endocrinol Metabol. 2010 Mar;54(2):123-32.
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- Kawanishi S, Ohnishi S, Ma N, et al. Crosstalk between DNA Damage and Inflammation in the Multiple Steps of Carcinogenesis. Int J Mol Sci. 2017 Aug 19;18(8):1808.
- Trayhurn P, Bing C, Wood IS. Adipose tissue and adipokines--energy regulation from the human perspective. J Nutr. 2006 Jul;136(7 Suppl):1935S-9S.
- Kuo FC, Huang YH, Lin FH, et al. Circulating Soluble IL-6 Receptor Concentration and Visceral Adipocyte Size Are Related to Insulin Resistance in Taiwanese Adults with Morbid Obesity. Metab Syndr Relat Disord. 2017 May;15(4):187-93.
- Jung CH, Cho I, Ahn J, et al. Quercetin reduces high-fat diet-induced fat accumulation in the liver by regulating lipid metabolism genes. Phytother Res. 2013 Jan;27(1):139-43.
- Dong J, Zhang X, Zhang L, et al. Quercetin reduces obesity-associated ATM infiltration and inflammation in mice: a mechanism including AMPKalpha1/SIRT1. J Lipid Res. 2014 Mar;55(3):363-74.
- Zhao L, Cen F, Tian F, et al. Combination treatment with quercetin and resveratrol attenuates high fat diet-induced obesity and associated inflammation in rats via the AMPKalpha1/SIRT1 signaling pathway. Exp Ther Med. 2017 Dec;14(6):5942-8.
- Yang J, Kim CS, Tu TH, et al. Quercetin Protects Obesity-Induced Hypothalamic Inflammation by Reducing Microglia-Mediated Inflammatory Responses via HO-1 Induction. 2017 Jun 23;9(7).
- de Kloet AD, Pioquinto DJ, Nguyen D, et al. Obesity induces neuroinflammation mediated by altered expression of the renin-angiotensin system in mouse forebrain nuclei. Physiol Behav. 2014 Sep;136:31-8.
- Politis M, Pavese N, Tai YF, et al. Microglial activation in regions related to cognitive function predicts disease onset in Huntington’s disease: a multimodal imaging study. Hum Brain Mapp. 2011 Feb;32(2):258-70.
- Rana I, Badoer E, Alahmadi E, et al. Microglia are selectively activated in endocrine and cardiovascular control centres in streptozotocin-induced diabetic rats. J Neuroendocrinol. 2014 Jul;26(7):413-25.
- Sugama S. Stress-induced microglial activation may facilitate the progression of neurodegenerative disorders. Med Hypotheses. 2009 Dec;73(6):1031-4.
- Valdearcos M, Douglass JD, Robblee MM, et al. Microglial Inflammatory Signaling Orchestrates the Hypothalamic Immune Response to Dietary Excess and Mediates Obesity Susceptibility. Cell Metab. 2017 Jul 5;26(1):185-97 e3.
- Valdearcos M, Robblee MM, Benjamin DI, et al. Microglia dictate the impact of saturated fat consumption on hypothalamic inflammation and neuronal function. Cell Rep. 2014 Dec 24;9(6):2124-38.
- Zhao L, Zhang Q, Ma W, et al. A combination of quercetin and resveratrol reduces obesity in high-fat diet-fed rats by modulation of gut microbiota. Food Funct. 2017 Dec 13;8(12):4644-56.
- Angin Y, Beauloye C, Horman S, et al. Regulation of Carbohydrate Metabolism, Lipid Metabolism, and Protein Metabolism by AMPK. 2016;107:23-43.
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- Li C, Yu L, Xue H, et al. Nuclear AMPK regulated CARM1 stabilization impacts autophagy in aged heart. Biochem Biophys Res Commun. 2017 Apr 29;486(2):398-405.
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- Porras D, Nistal E, Martinez-Florez S, et al. Protective effect of quercetin on high-fat diet-induced non-alcoholic fatty liver disease in mice is mediated by modulating intestinal microbiota imbalance and related gut-liver axis activation. Free Radic Biol Med. 2017 Jan;102:188-202.
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