Chemical changes triggered by the Metabolic Syndrome can cause degradation of cartilage, which normally protects the joints, and therefore results in joint destruction.

Losing belly fat and lowering the overall body mass BMI helps arthritic joint pain and slows down the process of joint degeneration. Increased BMI, on the other hand, has been shown to be associated with increased incidence of knee replacement surgery, and with worse outcomes after surgery.

One of the chemical agents released by visceral fat is called Leptin. High levels of Leptin, as seen with increased BMI, are associated with osteoarthritis. Tests of the synovial fluid of osteoarthritic joints usually reveal high concentrations of Leptin.

Therefore, Leptin is believed to play an important role in the pathogenesis of osteoarthritis. Another important inflammatory marker in osteoarthritis is Interleukin-6 Il-6 , a protein, or cytokine, that is elevated in states of chronic inflammation.

This cytokine, which is elevated in obese people, has also been implicated in the etiology of cardiovascular disease and some forms of cancer. Increased levels of Leptin, IL-6, and other inflammatory markers are important factors in the development of joint arthritis and poor outcome after joint surgeries.

So, to improve the health of your joints and to prevent early osteoarthritis, lose your belly fat: exercise regularly; avoid inflammatory foods like refined carbohydrates, trans-fats, or processed foods; eat more vegetables and fruits.

Nutritional supplementation, especially in obese patients, may play a significant role in the modulation of osteoarthritis, and in alleviating chronic muscle, joint, and bone aches.

Vitamin D supplementation, for example, has been shown to result in a significant drop of Il-6 levels. The lesson to be learned here is that body fat can damage your joints, not only because of the increased mechanical stress, but also due to chemical reactions triggered by fat tissue.

Joint pain can be reduced by losing your body fat. Baseline DXA scans were used to measure total body fat and visceral and subcutaneous fat in the torso.

The association of fat depot size with structural outcomes incident radiographic OA and cartilage loss and synovitis on MRI and with pain outcomes worsening knee pain, number of painful joints, and widespread pain was assessed.

Regression analyses were adjusted for age, sex, race, education level, smoking status, physical activity, body mass index BMI , and depressive symptoms.

Results: Of the 2, participants at baseline, The mean age was After adjustment for covariates, no fat measures were associated with any structural outcomes.

Get the latest news and tips about living with Gout in the Living Your Yes! How Fat Affects Gout Excess weight increases your risk of gout and health problems that go along with it. Quick Links Managing Pain Treatment Nutrition Exercise Emotional Well-being Daily Living.

Gout Related Articles Find More Gout Articles. Gout Gout Gout is an inflammatory type of arthritis that can come and go. Gout A New View on Gout Flares and Treatments New research is revealing further insights into the causes of gout and gout flares as well as the best gout treatments.

Gout What Role Does Diet Play in Gout Management? Learn what role diet plays in gout management and other steps that need to be taken to help stop gout attacks. Connect with Others Local support groups bring together people with arthritis to exchange tips, share concerns and encourage each other.

Diagnosed With Gout? I Want to Donate. After adjustment for covariates, no fat measures were associated with any structural outcomes.

Conclusion: Our findings indicate that visceral fat is associated with an increased risk of musculoskeletal and widespread pain. Abstract Objective: Osteoarthritis OA and pain are both made more severe by low-grade inflammation.

Publication types Observational Study Research Support, N. What is certain is that being overweight or obese plays a role in PsA. Systemic lupus erythematosus is a chronic, inflammatory autoimmune disease that primarily affects women of color. Several studies have found that the rates of obesity are higher in people with lupus than in the general population.

Obesity in patients with lupus is associated with high levels of disability and possibly cognitive impairment. As in OA and RA, the cytokines that fat releases create inflammation in different parts of the body. For example, people with lupus have a higher risk of heart disease.

Learn more about the association between lupus and fat. In the U. Additionally, being overweight raises the risk of developing fibromyalgia, especially among those who are not active, according to a large Norwegian study. Both fibromyalgia and obesity are characterized by the malfunctioning of the HPA axis — communication system between glands that helps regulate the immune system, digestion, mood, hormones and other functions.

Understanding the HPA axis issue could lead to better treatments for both conditions, says Akiko Okifuji, PhD, a psychologist at the Pain Research and Management Center and professor at the University of Utah in Salt Lake City. Read more about how fat affects fibromyalgia. Get involved with the arthritis community.

How Fat Can Worsen Arthritis Excess fat increases not only pressure on joints but also inflammation. Why Obesity Matters The inflammatory chemicals from fat are culprits in RA. FAT AND GOUT Gout is a form of inflammatory arthritis that occurs when an excess of uric acid in the body leads to the formation of uric acid crystals in the joints, triggering painful attacks, most commonly in the big toe.

Why Obesity Matters According to studies, obesity is a risk factor for psoriasis and is associated with more severe disease. Why Obesity Matters Several studies have found that the rates of obesity are higher in people with lupus than in the general population.

For continuous variables, independent t -test or Mann—Whitney U test was performed for parametric and non-parametric data respectively. R-squared was calculated as a goodness-of-fit for each regression model. Pearson correlation coefficients were employed to depict covariance of body composition variables in the context of physical activity, disease activity, function and metabolic dysfunction.

At recruitment, median PsD disease duration was The two groups did differ in their ages median age 52 [IQR 18] vs. However, MDA scores were counterbalanced by entheseal, VAS and HAQ scores which were modest, thereby enhancing the aggregate effect of overall PsD activity.

PsD-derived data are summarised in Table 2. All group-specific outcomes including metabolic and body composition variables are shown in Supplementary Table 1.

BODPOD®-derived body composition measures in patients with PsD according to disease activity are summarised in Table 3 and illustrated in Fig. Overall, whole-body mass by ADP was BODPOD®-derived body composition and MRI segmentation in patients with PsD according to sex and disease activity.

Similar to the BODPOD®-derived data, MRI identified a 5. Furthermore, MRI segmentation revealed that the PsD group had a 5. Figure 2 depicts overlay of fat segmentation using FatSegNet PsD vs. A 3D fat imaging. B Axial fat segmentation in a year-old male patient compared to that of an age-, sex- and BMI-matched control visceral fat depicted in green.

C Coronal fat segmentation in a year-old male patient compared to that of an age-, sex- and BMI-matched control visceral fat depicted in green. Based on data derived from ADP, participants with active PsD had an 8. Between the subgroups of PsD including PsO and PA , both disease activity levels and ADP-derived measures of body composition were equivalent Table 4.

None of the other ADP-derived body composition measures independently associated with PsD disease activity. Older participants had greater whole-body VAT: unstandardised ꞵ Correlations between body composition and physical activity, quality of life and metabolic indices are shown in Supplementary Table 2.

As shown, body mass, total body fat, whole-body volume and whole-body VAT correlated with higher fasting serum triglyceride levels and cholesterol:HDL ratio.

The premise of this pilot study was to understand in more depth body composition in psoriatic disease, particularly its phenotypic and metabolic associations. Several aspects of body composition, specifically, the amount and distribution of body fat and lean mass, are now understood to be independent health predictors in adults and may form an important part of the ongoing clinical assessment of patients with psoriatic disease.

As expected, patients represented the whole spectrum of psoriatic disease; those with chronic plaque psoriasis and concomitant psoriatic arthritis being by far the largest group. In our cohort, women revealed overall lower body mass and volumes yet higher body fat when compared to men, whereas men revealed comparatively higher visceral fat; such characteristic sex differences in body composition have been well established [ 29 , 30 ].

Sex dimorphism in the heritability suggests that female fat distribution may be more genetically affected than males, and biological pathways are differentially involved in the determination of body fat distribution [ 31 ].

The molecular mechanism for this sex dimorphism may also be beyond the modulation of sex hormones [ 32 ]. Regarding the psoriatic group, they demonstrated adverse body composition profiles across the board, including higher body mass, whole-body volume, subcutaneous and visceral fat.

This relationship could not be explained by lifestyle factors such as physical activity levels, diet or smoking; ironically, patients with PsD were seen to be maintaining as much vigorous exercise as their healthy counterparts.

More patients in the PsA subgroup had active disease, as measured by MDA, and demonstrated higher visceral fat, although this effect was not revealed in the purely cutaneous PsO patients, exemplifying the fact that there are often more diverse contributory factors and nuances to disease activity in a PsA population.

If we consider the observed dysmetabolism is a consequence of inflammation, it is however, not clear if the underlying psoriasis itself or the visceral adipose tissue is the key player.

Moreover, the association between psoriatic disease activity and MRI-derived visceral fat distribution was noted to be starker in men than women. Epidemiological studies have tended to focus on weight or BMI to define obesity rather than altered body composition.

Interestingly, there is conflicting data on the association between psoriasis severity, such as PASI, and body composition parameters, indicating that a causal link is by no means definitive. Previous studies have alluded to a dose—response relationship between psoriasis severity and metabolic syndrome [ 33 ], supported by translational studies showing T-helper cell cytokine upregulation in the blood and skin of psoriasis patients, leading to effects on lipid metabolism and insulin resistance [ 34 ].

Quantification and accurate localisation of various adipose tissue depots is of high research interest in chronic disease particularly those of an inflammatory nature. The last decade has seen an impetus in the development and validation of new modalities for the assessment of body composition.

Whole-body fat quantities derived from a continuously moving table Dixon sequence MRI have shown high reproducibility of results ratifying its potential for future research studies [ 37 ].

Moreover, the accuracy of this method and the high reproducibility of results indicate its potential for clinical applications. FatSegNet is a novel, fully automated deep learning pipeline that utilises a competitive dense fully convolutional network CDFNet architecture to localise VAT and SAT on abdominal Dixon MR images.

It can accurately segment visceral and subcutaneous adipose tissue inside a consistent anatomically defined abdominal region and has been shown to outperform manual rating of VAT 0. In accordance with previous studies on small datasets [ 38 , 39 ], our data showed a sex- and age-specific difference of VAT accumulation, wherein men and older patients were more likely to have higher VAT compared to women and younger patients.

This method of fat segmentation is efficient, well-tolerated and reliable [ 26 ]. Furthermore, FatSegNet has been shown to go one better than other architectures employed in body composition mapping and, in our case, proved to be far more informative than the technique of air displacement plethysmography for demonstrating important phenotypic and metabolic differences between psoriatic patients and controls.

Some studies have employed manual techniques for the assessment of visceral fat in chronic disease, such as the visceral adiposity index VAI , a gender-specific empirical mathematical model based on simple anthropometric BMI and waist circumference and functional parameters TG and HDL and indicative of fat distribution and function [ 40 ].

Studies of spondyloarthritis, RA and psoriasis have reported a reduced efficacy, drug survival and adherence to tumour necrosis factor inhibitors TNFis in obese patients [ 41 , 42 , 43 , 44 , 45 , 46 ].

There are also data linking the human TNF receptor fusion protein, Etanercept, with weight gain [ 47 ]. In PsD, the impact of obesity on TNFis remains unclear since available studies are small, present diverging results and lack long-term follow-up data.

IL, one of the key proinflammatory cytokines in psoriasis, mechanistically links inflammation with insulin resistance and adipocyte dysfunction [ 50 ].

ILA-producing cells are thought to be pathogenic in driving inflammation in obesity and progression of obesity-related inflammatory diseases, suggesting that causality between psoriasis and adipogenesis is likely to be bidirectional [ 51 ].

A recent prospective, open-label study Immune Metabolic Associations in Psoriatic Arthritis evaluated the effect of the phosphodiesterase-4 PDE4 inhibitor apremilast on body weight and composition and observed weight loss, principally abdominal subcutaneous fat, and improvement in psoriatic disease activity independent of weight change [ 52 ].

These findings were paralleled by the results of the VIP-A trial, a single-arm, open-label, interventional, non-randomised clinical trial, in which CT imaging and laboratory outcomes were measured in patients taking apremilast. Patients showed reductions in visceral and subcutaneous fat as well as beneficial effects on cardiometabolic biomarkers [ 53 ].

Considering this, we postulate that further individualised treatment strategies based on multimodal insight into adverse metabolic profiles and biomarkers, such as high visceral fat, may improve outcomes and overall care of psoriatic patients.

An automated model of fat segmentation—being less expensive and time-consuming than manual segmentation—could facilitate future research of similar patients using large population-based cohorts.

To our knowledge, this is the first time that a deep learning application for MRI-derived body composition, especially that of VAT and its metabolic significance, has been studied in psoriatic disease and compared to matched controls. We have reported on a novel, automated method for image acquisition and validated its functionality in a clinical cohort with chronic inflammatory disease.

We are aware that this is a pilot study and as such will likely need to be repeated on a wider scale. The cross-sectional nature of the study confers challenges with determining causal relationships. The relatively small sample size of patients and controls and diverse age range will also have hampered the data analysis and ability to draw certain conclusions.

We believe that further research in this field will enhance the validity of our results whilst keeping a realistic view of the expected numbers of patients that can be recruited to a similar study.

This study shows that visceral adipose [a more metabolically active depot] can provide additional value to current measures of obesity such as BMI and waist-to-hip ratio and contribute to the unfavourable metabolic dysfunction seen in psoriatic disease. Our data support the concept that defined body composition changes are independent of the customary metabolic syndrome and that disease activity, not just occurrence of psoriasis, is unequivocally more than skin-deep and seems to correlate with underlying visceral fat.

These indices may serve as useful biomarkers of an adverse inflammatory state seen in psoriatic disease. A deep learning algorithm employing automated MRI-determined fat segmentation shows good association with disease activity and metabolic dysfunction, findings that cannot be simulated by anthropometric assessment or air displacement plethysmography.

MR imaging and automated fat analysis could serve as a prototype for the valuable assessment of the metabolic and body composition effects of targeted therapies in complex inflammatory disease.

It is possible that such novel systems will eventually supplement less sophisticated bedside measurements and influence key aspects of risk assessment, prognostication and management in patients with psoriatic disease.

Further prospective studies are needed to confirm these preliminary results. The data underlying this article will be shared on reasonable request to the corresponding author.

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Ann Rheum Dis. di Minno MN, Peluso R, Iervolino S, Lupoli R, Russolillo A, Scarpa R, et al. This syndrome causes changes in the chemical environment of the joints. Chemical changes triggered by the Metabolic Syndrome can cause degradation of cartilage, which normally protects the joints, and therefore results in joint destruction.

Losing belly fat and lowering the overall body mass BMI helps arthritic joint pain and slows down the process of joint degeneration. Increased BMI, on the other hand, has been shown to be associated with increased incidence of knee replacement surgery, and with worse outcomes after surgery.

One of the chemical agents released by visceral fat is called Leptin. High levels of Leptin, as seen with increased BMI, are associated with osteoarthritis. Tests of the synovial fluid of osteoarthritic joints usually reveal high concentrations of Leptin.

Therefore, Leptin is believed to play an important role in the pathogenesis of osteoarthritis. Another important inflammatory marker in osteoarthritis is Interleukin-6 Il-6 , a protein, or cytokine, that is elevated in states of chronic inflammation.

This cytokine, which is elevated in obese people, has also been implicated in the etiology of cardiovascular disease and some forms of cancer. Increased levels of Leptin, IL-6, and other inflammatory markers are important factors in the development of joint arthritis and poor outcome after joint surgeries.

So, to improve the health of your joints and to prevent early osteoarthritis, lose your belly fat: exercise regularly; avoid inflammatory foods like refined carbohydrates, trans-fats, or processed foods; eat more vegetables and fruits.

Nutritional supplementation, especially in obese patients, may play a significant role in the modulation of osteoarthritis, and in alleviating chronic muscle, joint, and bone aches.

Vitamin D supplementation, for example, has been shown to result in a significant drop of Il-6 levels. The lesson to be learned here is that body fat can damage your joints, not only because of the increased mechanical stress, but also due to chemical reactions triggered by fat tissue.