The Impact Of Chronic Inflammation On Weight Loss – PROBLEM OF SYSTEMASIS, as indicated by higher circulating levels of mediators such as C-reactive protein, interleukin-6 and tumor necrosis factor-α, is a major risk factor for many chronic diseases. There is data showing that reducing energy intake and increasing physical activity may be effective therapies to reduce overall inflammation. Evidence is strong that circulating levels of inflammatory markers are elevated with general and abdominal obesity, possibly due to increased secretion of cytokines by adipose tissue in obese individuals. Additionally, low-energy weight loss reduces both circulating markers of inflammation and adipose-tissue cytokine production. Data from several large cohorts show an association between systemic inflammatory markers and physical activity or fitness status; Small intervention studies support that exercise training reduces inflammation. Weight loss combined with exercise may be more effective than weight loss alone in reducing inflammation. To date, data from randomized, controlled trials designed to confirm the effects of weight loss or exercise training, or both, on inflammation are limited. Future studies are needed to determine the amount of weight loss required for clinically meaningful weight loss; In addition, full control and studies are necessary to explain the effect of exercise training on chronic, systemic inflammation.
The biological complex of factors that create the body’s natural defenses against injury or infection is an important part of the immune system. Normally, this process is a critical response that results in a rapid, large increase in mediators released into the circulation.1
The Impact Of Chronic Inflammation On Weight Loss
2 In healthy, healthy, non-elderly individuals, for example, serum levels of C-reactive protein (CRP), which are usually less than 2 mg/L in men3 and less than 2.5 mg/L in women, 4 will can increase more than 1000 times in response to infection or injury.2
Chronic Inflammation: What It Is, Why It’s Bad, And How You Can Reduce It
Generally, CRP values of 10 mg/L or more are considered clinical signs of inflammation.7 However, recent evidence has shown that the persistence of signs of inflammation, even in the range of al Clinical practice is a risk factor for cardiovascular disease. both middle aged8
19 people. Recently, the American Centers for Disease Control and Prevention and the American Heart Association stated that people with CRP levels in the highest population (>3.0 mg/L) have a higher risk of heart disease and blood vessels that are twice as large as those of infected people. CRP levels are not less than 1.0 mg/L.20 In addition to CRP, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), along with other growth factor proteins, cytokines and cytokine- soluble receptors, are strongly associated with an increased risk for many diseases, including heart disease, 12
28 It is not yet known which of these factors may be the strongest predictor of inflammation, or whether the effects of these biomarkers are additive in predicting risk.
As illustrated in Figure 1, the characteristic features are associated with normal, low levels of inflammation (as measured by micro-organisms), and therefore with many diseases and associated with inflammatory states. Since risk estimates associated with increased inflammation appear linear (for example, the cut-off of CRP to evaluate cardiovascular diseases20 have low risk 3.0 mg /L), reactions that lead to a reduction in inflammation may have clinical benefits. Some effective drugs such as angiotensin-converting enzyme inhibitors and statins reduce inflammation, as shown by reductions in CRP levels in prospective clinical trials.29
Inflammation: Causes, Effects, Treatments
32 In addition, there is an impressive amount of data showing that weight loss and increased physical activity are just as effective as medication to reduce overall inflammation. The published literature on the effects of weight loss and exercise training on inflammatory markers is reviewed here.
Figure 1: Behavioral factors reported to be associated with chronic subclinical inflammation, and diseases and serious health conditions in which inflammation is a risk factor. ↓ = decrease; BMI = Body Mass Index.
Association between high adipose tissue (measured either indirectly by body mass index [BMI] or directly by assessment of body composition) and elevated CRP33 levels
50 and people suffering from metabolic syndrome, 49 diabetes48 and heart disease.52 In fact, obesity can account for a large part of the variation in CRP concentrations; in a population-based study involving healthy, middle-aged women, 35 for example, BMI explained 30% of the variance in CRP values. In a study33 of the Third National Health and Nutrition Examination Survey, the proportion of people with a CRP level above 10 mg/L (the traditional clinical level indicating infection) was 20% in obese women, but Only 4% of women are overweight. was within the normal range. Obese participants were more likely than normal-weight participants to have elevated CRP levels, by an odds ratio of 2.13 for men (95% confidence interval [CI] 1.56–2.91) and 6.21 for women (95% CI 4.94 -7.81). 33 Similarly, in a study involving 1929 middle-aged men and women, 49 15% of obese participants had a CRP level above 10 mg / L, compared to only 3% of overweight people.
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73 grow in obese people. Haptoglobin and serum amyloid protein A, both proteins involved in the acute response to inflammation, have also been shown to circulate in higher concentrations in obese individuals.74
76 The sample sizes in these studies were smaller and usually not population-based, but in these studies the data were consistent. In an interesting study63 involving identical twins with no difference in obesity (the average difference in body weight between twin pairs is 18 kg), levels of TNF-α and soluble TNF-αreceptor 2 (sTNFR2 ) were higher in obese than lean twins, suggesting that obesity more than other genes is a major determinant of these inflammatory markers.
Finally, there is some evidence from studies involving men and women that, in addition to total body fat, body (abdominal) fat may be an independent predictor of inflammatory markers.37
78 the amount of visceral fat was a better predictor of CRP levels than other measures of obesity, including total body fat. The location of body fat, independent of the total amount, is therefore an important factor that affects chronic inflammation.
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81 The source of these “adipokines” is probably not the adipocyte itself, but the infiltration of inflammatory cells (macrophages) into the adipose tissue. 82
83 In vivo release of IL-6 and TNF-soluble receptors from subcutaneous adipose tissue of the abdominal cavity has been shown to correlate with BMI and body-weight ratio. in the obese than in the obese.85
86 In one in-vitro study 87 the release of TNF-α from abdominal subcutaneous adipose tissue was 7.5 times higher than in tissue from obese (BMI 30- 40 kg/m
) subjects.87 Ouchi and associates81 reported not only that CRP is expressed in adipose tissue, but also that the levels of CRP and adiponectin mRNA are highly correlated. (Adiponectin is a protein that has anti-inflammatory properties.)
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Therefore, both in vivo and in vitro studies confirm that adipose tissue expression and cytokine release are increased in people with a higher adipose mass.
The hypothesis that an expanded adipose-tissue mass contributes to an elevated state of chronic inflammation is corroborated by data (summarized in Table 1) showing that weight loss reduces inflammation. Many inflammatory markers, including CRP, IL-6, IL-18, TNF-α and TNF-α receptors, are reduced after weight loss through short-term food restriction, 53.
64 The results of liposuction are contradictory: Although one such study99 that resulted in a weight loss of 3 kg found the levels of IL-6, IL-18, TNF-α and CRP to decrease after a 6-month period of stability, another96 who reduced body fat by 9.8 kg on average found IL-6, TNF-α and CRP concentrations to be unchanged 10-12 weeks after surgery. The effect of weight loss through liposuction to reduce inflammation therefore requires further research.
Most diet weight loss studies have shown the magnitude of the reduction in inflammatory markers to be inversely related to the amount of weight lost. For example, when CRP levels were reduced from 3.1 mg/L (standard deviation [SD] 0.7 mg/L) to 1.6 (SD 0.8) mg/L in postmenopausal women who followed a 14-month weight loss program, 42 and reductions associated with changes in body weight and body fat. Decreases in CRP, IL-6, IL-18 and TNF-α in a group of pre-existing women after a 10% weight loss were associated with changes in BMI but were more consistent with changes- changes in the ratio-hip ratio.43
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58 Those women were healthy, without diabetes or metabolic syndrome, and their mean reduction in CRP (from 3.4 [SD 0.7] to 1.9 [SD 0.2] mg/L) mimicked the reported in healthy women by Tchernof and coauthors.42 In others. study, weight loss reduced CRP levels (from 5.0 [SD 0.5] to 4.3 [SD 0.5] mg/L) in women with metabolic syndrome, 91 and IL-6 concentration (2.75 [SD 1.51] to 2.3 [SD 0.91] pg / mL) in women with insulin resistance.93
97 investigated the weight loss effects of diet on inflammation. Esposito and colleagues56 compared obese women who participated in a behavioral counseling program designed to achieve a 10% weight loss through monthly counseling on a low-calorie diet and increased physical activity with obese women in the control group who did not receive the diet.
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