Adiponectin is a fat regulator, and if we do not have enough of it circulating in our systems, it could cause our body to accumulate more fat than necessary. Studies have demonstrated that visceral fat and adiponectin were independently associated with the clustering of metabolic risk factors such as high cholesterol, higher triglycerides and lower LDL low-density lipoprotein and HDL high-density lipoprotein.

Yet another effect of accumulated and increased visceral fat seems to be on cognition. One study demonstrated how visceral fat is harmful to the brain because it allows the inflammatory cytokine interleukin-1 beta to heavily infiltrate the brain The interleukin-1 beta cytokine is produced by visceral fat, which then travels through the bloodstream, passes through the blood—brain barrier and enters the brain, where it causes the microglia to become dysfunctional and hampers cognition.

Microglia are the immune cells in the brain which regulate neuronal function indirectly by clearing dead cells and extracellular debris, and directly by releasing signalling molecules that support or suppress neuroplasticity.

Inflammation is our immune response to a threat, injury or infection. During the process of inflammation, inflammatory cells and cytokines are released. Acute or temporary inflammation occurs when there is a sudden body change, or damage or injury to our system.

For example, if we cut ourselves, if we have an infection or if we work out. Chronic inflammation, on the other hand, is when the body continues to send out inflammatory cells and there is a continuous inflammatory response.

Major sources of inflammation also include environmental stressors, environmental toxins as well as psychological stress. Shifts in the inflammatory response from short- to long-lived can cause a breakdown of immune tolerance, which leads to oxidative stress and damage to tissues and cells.

It has been seen that chronic inflammation also contributes to the pathophysiology of a number of metabolic diseases. Systemic chronic inflammation can lead to a number of conditions such as metabolic syndrome a triad of hypertension, hyperglycemia and dyslipidemia , cancer, diabetes, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders.

It is established that the levels of cortisol in the blood increase with age. This is mainly considered to be on account of the HPA axis getting activated by many non-specific stressors.

Over time, the phenomenon of anti-inflammaging, mainly exerted by cortisol, gives rise to a tangible decrease in immunological functions. The coexistence of anti-inflammaging alongside the increased levels of proinflammatory cytokines of inflammaging ultimately negatively impact metabolism, bone density, strength, exercise tolerance, the vascular system, cognitive function as well as mood.

Inflammation plays a critical role in the development of insulin resistance. There are various established mechanisms that play a part in this process. When we eat highly processed, high-sugar foods, it can trigger inflammation and the release of proinflammatory compounds.

High-sugar foods cause a spike in insulin and, over time, these types of diets could also lead to insulin resistance. Dietary fat might play a role in the production of inflammatory molecules by way of modifying the intestinal microbiota, which might result in an inappropriate immune reaction, through processes like leaky gut, and can also lead to autoimmune conditions like rheumatoid arthritis, lupus, psoriasis, etc.

Seemingly, the interaction between immune cells and metabolic cells has a major role to play in the disturbance of metabolic homeostasis. High levels of dietary saturated fatty acids or of their metabolites can be detected by immune sensors, leading to the synthesis of inflammatory cytokines in different metabolic tissues.

Intestinal microbiota, which produce different inflammatory molecules, can also be modified by dietary fat, which can lead to an inappropriate immune reaction. The inflammatory cytokines, saturated fatty acids and lipopolysaccharides activate a network of signalling pathways that impinges on insulin signalling, leading to alterations in metabolic cell functions.

There is evidence to show that physical exercise and activity has an anti-inflammatory effect, where exercise-induced cytokines may impact cardiometabolic diseases. Interleukin IL -1β is involved in pancreatic β-cell damage, whereas TNF-α is a key molecule in peripheral insulin resistance.

A marked increase in IL-6 and IL is provoked by exercise and exerts direct anti-inflammatory effects by an inhibition of TNF-α and by stimulating IL-1ra, thereby limiting IL-1β signalling. Or, it can be systemic and travel via the blood, injuring your heart and brain.

Our rising obesity rate means the problem is getting worse. In Ohio, for instance, the adult obesity rate is currently The report also says Ohio has the 19th-highest adult obesity rate in the nation.

If you want to know how you rate, many doctors now use waist circumference as a way to measure obesity. You can determine this easily, Dr. Buchinsky says, by using a measuring tape. Another tool is to take your waist-to-height ratio and divide by two.

For example, if you're 5 feet, 10 inches — or 70 inches — tall, divide 70 in half. Your swelling belly doesn't have to stop you from living the life you want, however. If you want to improve your health, Dr. Buchinsky offers these tips:. Use meals as medicine.

The biggest culprits are foods that Dr. Those foods, coupled with sugar, cause an outpouring of insulin into the pancreas, which sets inflammation in motion.

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Preliminary data suggested that fat embolism could explain the importance of visceral obesity as a critical determinant of coronavirus disease COVID Human adipocytes hMADS infected with SARS-CoV-2 were also studied.

Consistently, human adipocytes were successfully infected by SARS-CoV-2 in vitro and displayed lower cell viability. Being VAT inflammation associated with lipids spill-over from dead adipocytes, we studied lipids distribution by ORO. Importantly, transition aspects between embolic fat and hyaline membranes were also observed.

Franziska Hornung, Luise Schulz, … Stefanie Deinhardt-Emmer. Gemma Bogard, Johanna Barthelemy, … Isabelle Wolowczuk.

Yuki Goto, Yuiko Nagamine, … Takeo Fujiwara. Since December , the severe acute respiratory syndrome coronavirus 2 SARS-CoV-2 , responsible for the development of coronavirus disease COVID , has spread globally, resulting in a worldwide health crisis that caused over five million deaths [ 1 ].

Published data support interstitial fibrosis with alveolar hyaline membrane HM formation as the main underlying histopathologic event responsible for pneumonia and acute respiratory syndrome distress [ 5 , 6 ]. The reasons for HM bilateral expression, histogenesis, and sudden clinical appearance during COVID early stages are not completely understood [ 7 ].

Obesity and impaired metabolic health are in fact strongly associated with COVID unfavorable prognosis and pose also young patients at higher risks [ 10 , 11 ].

Significantly, visceral obesity increases the risk of COVIDrelated complications, independently of age, gender, body mass index [ 12 ], total and subcutaneous adipose tissue areas [ 13 , 14 , 15 , 16 ].

Visceral obesity is, in fact, strongly associated with chronic low-grade inflammation, blood hypercoagulability, impaired metabolic health, and higher risk of cardiovascular events, all risk factors for COVID severity [ 8 , 11 , 16 , 17 , 18 ]. Visceral adipose tissue VAT excessive expansion is paralleled by adipocytes hypertrophy, death, and lipids spill-over, phenomena resulting in macrophages infiltration, crown-like structures CLS development and inflammation, in turn contributing to the obesity-related complications [ 19 , 20 , — 21 ].

The elevated adipocytes ACE2 expression in obesity [ 22 ], receptor exploited by SARS-CoV-2 for cell entry, has been often speculated as a possible pathophysiological mechanism responsible for obesity-related COVID severity [ 8 , 23 , 24 ].

However, although obesity has been strongly associated with COVID severity, original articles comprehensively analyzing adipose tissue samples belonging to subjects with COVID and providing direct evidence of SARS-CoV-2 infection are lacking [ 16 ]. In our preliminary study, we described the presence of embolic fat in the lung of patients with obesity died from COVID and we hypothesized that such histopathologic hallmark could be due to adipocytes stress induced by SARS-CoV-2 infection [ 23 ].

We observed novel SARS-CoVrelated histopathological features, i. Autoptic VAT, lung and liver samples belonging to 49 subjects were collected and screened to be included in the study.

Forty-two subjects were considered suitable for the study i. Subject characteristics, including gender, age, BMI, comorbidities, and cause of death, are reported in Supplementary Tables 1 and 2. SARS-CoV-2 infection was assessed by RT-qPCR performed on nasal pharyngeal or pharyngeal swab samples.

Study population mean age was However, although there were no between-group differences in BMI and VAT adipocytes size Fig. Other inflammatory cells were represented mainly by lymphocytes, but their number was negligible in all investigated cases.

E Transmission electron microscopy TEM : normal adipocyte adjacent to a stressed adipocyte showing dilated endoplasmic reticulum arrows. G TEM : free lipid droplets of variable size were frequently found in COVID subjects asterisks. H Enlargement of the squared area in G showing lipid droplets inside endothelial cells arrows.

J TEM: a capillary filled with embolic fat near a stressed adipocyte. K LM: mesenteric fat sample showing lipid-rich embolic material in a vein squared area, enlarged in inset.

Perilipin 1 PLIN1 immunohistochemistry is a reliable method for identifying and quantifying dead adipocytes [ 19 , 25 ]. However, in the present study, all samples display PLIN1 negative adipocytes, probably due to the autoptic nature of the specimens.

We thus performed a morphologic and ultrastructural study to assess VAT adipocyte stress and death. In line with the observed widespread death, cell remnants were evident in closed proximity of dying adipocytes, while free lipid droplets were often found in fat interstitial spaces Fig.

Notably, large lipid vacuoles were frequently observed: 1 inside endothelial cells belonging to capillaries adjacent to free lipid droplets Fig. We then aimed at assessing whether the observed VAT alterations were associated with SARS-CoV-2 presence in the tissue or if they were a consequence of the systemic inflammation.

Although SARS-CoV-2 ability to infect human adipose tissue has been frequently speculated [ 8 , 13 , 18 , 23 ], direct evidence of such phenomenon are scarce in the literature [ 16 , 28 , 29 ]. While SARS-CoV-2 genomic RNA, nucleocapsid and spike proteins were not detectable in VAT samples of patients affected by COVID, virus-like structures with morphology and size resembling those present in SARS-CoVinfected VeroE6 cells Fig.

Furthermore, the presence of ribosome-like clusters described in virus-infected cells [ 30 ] was evident in visceral adipocytes of individuals with COVID, although rarely, Fig. Next, to provide direct evidence of SARS-CoV-2 ability to infect human adipocytes, leading to cell stress and death, we infected differentiated human multipotent adipocytes hMADS Fig.

Consistently, SARS-CoV-2 genomic RNA was also detected in the hMADS adipocytes pellet after h of infection Fig. Importantly, the infected hMADS adipocytes displayed lower cell viability Fig.

We hence performed a time-course analysis of hMADS expression of putative SARS-CoV-2 receptors Fig. ACE2 receptor was expressed at very low levels in both differentiated and undifferentiated hMADS, even though we used specifically designed primers holding a On the other side, the BASIGIN receptor was preferentially detected in differentiated hMADS which displayed an increased expression after 14 days.

Concerning proteases expression, while differentiated hMADS expressed the protease FURIN , the undifferentiated ones preferentially expressed DPPIV. The expression of CATHEPSIN L did not differs between the two conditions, while we did not detect TMPRSS2 in both differentiated and undifferentiated hMADS data not shown.

A Transmission electron microscopy TEM : VeroE6 infected cell showing several virions into the rough endoplasmic reticulum RER , some indicated by arrows. Inset: enlargement of squared area. D Enlargement of squared area in C shows a ribosome-like cluster and a virion-like structure into the dilated RER arrow.

E TEM: SARS-CoVinfected VeroE6 cells showing a ribosome-like cluster squared area , enlarged in the inset. F Kinetic of SARS-CoV-2 infection in undifferentiated and differentiated hMADS.

G SARS-CoV-2 quantification in supernatant and cell pellets of hMADS infected cells. I Hoechst nuclear staining showing pyknotic nuclei arrows. Expression of putative SARS-CoV-2 receptors L or proteases M assessed by RT-qPCR and normalized for the expression of 36B4 mRNA.

Expressions were measured in cells that received red bars or did not receive blue bars the differentiation cocktail for the indicated number of days.

Given our previous observation [ 23 ] and the widespread lipid droplets presence in the capillary lumen of VAT and in some mesenteric adipose depots, we studied lipid distribution in lung samples employing Oil Red O staining ORO, i.

Lipids were evidenced within lungs alveolar septa, interstitial spaces, endothelial cells, vessel lumen, and in alveolar and interstitial macrophages Fig. E LM: resin embedded, toluidine-blue stained tissue.

Large free lipid droplets yellow are evident in the capillaries lumen in alveolar septa arrows. F Transmission electron microscopy TEM : showing lipid droplet LD into an alveolar septum mixed with erythrocytes. G TEM: alveolar macrophage M in a COVID subject. Note: diffuse dilated rough endoplasmic reticulum RER denoting cellular stress arrows H TEM: enlargement of the squared area in G showing two virions at stages 1—2 and 5 of the reproductive cycle into the dilated RER similar to what observed in I TEM: 1 to 5 stages of the reproductive cycle of SARS-CoV-2 virions in VeroE6 infected cells.

Reference in the main text. Consistently, all subjects with type 2 diabetes had fat embolism. Of note, electron microscopy observations revealed several structures with size and morphology compatible with those of SARS-CoV-2 viruses [ 6 ] in pneumocytes, endothelial cells and macrophages, the last of which displayed disseminated, dilated endoplasmic reticulum denoting cellular stress [ 26 , 32 ] and signs of virus presence only in subjects with COVID Fig.

Several Weibel-Palade bodies, signs of activated coagulative phenomena [ 31 ], were also observed in most of the capillary endothelial cells of subjects with COVID data not shown.

Unexpectedly, the used lipid-specific histochemistry technique evidenced that all alveolar structures reminiscent of HM were ORO-positive Fig. Interestingly, this last subject displayed a fainted HM positivity for ORO staining, suggesting a lower lipidic presence.

This finding is consistent with other reports describing HM in the lungs of patients with non-COVIDrelated pneumonia [ 7 ]. Several aspects suggesting a direct role of embolic fat in HM formation were observed. Specifically, free lipid droplets occupying the alveolar space and lining and spreading on the alveolar surface were observed Fig.

A Light microscopy LM : hyaline membranes lining alveolar surfaces arrows at low magnification. Lipid-rich macrophages free in the alveolar space red arrows and inside hyaline membranes red arrow. D LM: enlargement of the squared area in C.

Arrows indicate lipid vacuoles. F TEM: free lipid droplets lining the alveolar surface composed by pneumocytes type II PT2 with classic surfactant granules arrow. Lastly, since the embolic material from abdominal visceral tissues should necessarily pass through the liver parenchyma to reach the lung, we exploited the ORO staining technique to study liver samples belonging to 9 individuals with COVID and 8 control subjects.

Liver autoptic samples showed focal, macrovesicular steatosis with lipid droplets of very variable size Supplementary Fig. In particular, signs consistent with fat embolism, i. This is the first study investigating the ultrastructural features of VAT among individuals with COVID and assessing lipid distribution in lungs and liver samples by histomorphology.

Our data support the presence of higher local VAT inflammation and higher prevalence of fat embolism and lipidic HM formations in the lungs of subjects dead due to COVID compared to control individuals dead for different reasons. In addition, our data support SARS-CoV-2 ability to infect human adipocytes in vitro.

Considering the strong association between COVIDrelated complications and obesity, especially with visceral adipose content excess [ 10 , 11 , 13 , 14 , 15 , 16 ], the comprehension of the biological phenomenon at the basis of such association holds critical clinical implications in the era of the COVID pandemic.

Our study provides the first evidence of higher local VAT inflammation among subjects with COVID, independently of obesity status and support an exacerbation of obesity-related inflammation by SARS-CoV-2 infection, a novel finding consistent with studies reporting higher systemic inflammation among infected patients [ 18 ].

Adipocyte inflammation is associated with cell stress, death, and lipid release in the extracellular space [ 19 , 20 , 25 , 26 ]. We hence studied adipocyte features by TEM and revealed the presence of the typical signs of cellular stress, together with prominent features of lipids spill-over from suffering adipocytes.

Of note, these data are supported by a recent work showing an increased number of autoimmune antibodies against the malondialdehyde and the adipocyte-derived protein antigen markers of lipid peroxidation and adipocytes death, respectively [ 35 ] among subjects with COVID and obesity as compared to individuals suffering from each condition independently [ 36 ].

In addition, hyperglycemia among subjects with COVID was demonstrated to be strongly associated with insulin resistance and low plasma adiponectin levels [ 29 ]. The authors from the same study also demonstrated that SARS-CoV-2 could infect hamster adipose tissue, leading to reduced adiponectin production and speculated that SARS-CoV-2 infection might result in adipocyte dysfunction driving insulin resistance.

Importantly, we detected lipids in the extracellular space, inside endothelial cells, inside the capillary lumen, and extruding from endothelial cells into the capillary lumen, all features indicative of fat embolism.

Although virus-like structures were evidenced by TEM in the same VAT depots, the lack of SARS-CoV-2 detection by qPCR did not allow us to conclude that such inflammation, cellular stress, and death were all related to the presence of the virus.

It is, in fact, possible that the described VAT features were secondary to the systemic inflammation induced by COVID or due to the presence of different viruses within the depot.

On the other side, we demonstrated that SARS-CoV-2 could infect human adipocytes even though neither adipocytes nor adipocyte progenitors gathered all of the known molecular requirements for the virus entry e.

This set of data is in part consistent with other findings and suggests that additional, not yet characterized, receptors and proteases may be exploited for this purpose [ 16 , 37 ]. Puray-Chavez et al. in fact indicated that human H lung adenocarcinoma cells are permissive to SARS-CoV-2 infection despite complete ACE2 absence and that virus entry is dependent on heparan sulfate in this cell line [ 37 ].

Importantly, despite being the first SARS-CoV-2 targets, olfactory and respiratory epithelial cells express low ACE2 protein levels [ 38 ]. For these reasons, additional co-factors facilitating the virus-host cell interaction e. In our study, BASIGIN receptor and FURIN protease were highly expressed in differentiated hMADS and could be exploited for SARS-CoV-2 infection.

However, it should be noted that, although FURIN critical role in mediating SARS-CoV-2 infection is widely accepted and seem to be of relevance in patients with type 2 diabetes where the protease is highly expressed [ 41 ], the role of BASIGIN has been recently questioned [ 42 ].

Given the widespread presence of lipid droplets in the capillary lumen of VAT and our preliminary data [ 23 ], we studied lipid distribution in lung and liver samples and confirmed the presence of fat embolism.

Fat embolism in the lungs was not exclusive to, but more prevalent among subjects with COVID; it was in fact also detected among subjects with obesity independently of SARS-CoV-2 infection.

These data are not surprising given that adipocyte death and release of lipids are both phenomena occurring in obesity [ 19 , 25 , 26 ]. This finding provides the first evidence pointing out fat embolism as a complication of obesity and obesity plus type 2 diabetes , determined by adipocyte death and possibly exacerbated by the COVIDinduced inflammatory status.

HM were present in all patients with COVID and in only one control who died for pneumonia, a finding consistent with other reports describing HM presence in this latter disease [ 7 ].

Our histomorphologic assessment revealed several aspects indicative of a direct role of embolic fat in HM formation. Consistently, the presence of lung HM of lipidic nature in the lungs was associated with VAT inflammation. Our findings on intestinal and liver fat embolism strongly support the embolic nature of lipid droplets in the lungs.

As the portal system drains venous blood from most abdominal fat depots to the liver, the embolic fat originated in the VAT necessarily pass through the liver to reach other organs. The unequivocal presence of lipid droplets into sinusoids and liver veins supports the fat embolic production by abdominal fat.

In summary, in our case series, although fat embolism may be present in obesity and type 2 diabetes independently of COVID, the embolic lipidic material could contribute to the formation of HM only in the case of COVIDrelated pneumonia.

This novel finding holds critical clinical implications and deserves further investigation. Furthermore, these data provide insights into HM nature, as their formation process has not been characterized yet [ 44 ].

Additional studies investigating the HM nature of non-COVIDrelated pneumonia are required to detail such histopathological features. Collectively our data reveal higher local VAT inflammation in subjects with COVID and SARS-CoV-2 ability to infect human adipocytes.

In addition, we provide the first evidence that supports the fat embolism as a complication of obesity, likely determined by adipocyte death and exacerbated by the COVIDinduced inflammatory status.

Consistently, fat embolism displays similar signs and symptoms as observed in COVID, in line with a recently published case report [ 45 ].

When fat embolism and COVID are suspected, differential diagnosis is critical for proper patient care. Based on our findings, the assessment of fat embolism symptoms is mandatory in the context of the COVID pandemic, especially among patients with pulmonary symptoms, obesity, and high waist circumference, last two of which are recognized as signs of high visceral adipose accumulation.

Such complex clinical status should be therefore adequately assessed and properly addressed. Our data hold critical clinical implications in the context of obesity and COVID pandemics and need to be confirmed by additional studies with larger sample size.

Our study did not entail any physical risk for the subjects. In Italy, the evaluation of non-pharmacological observational studies is not governed by the same normative references provided for the evaluation of clinical trials and observational studies concerning drugs.

Furthermore, as reported in the above report [ 46 ] in the section dedicated to our type of study in conditions of pandemic and therefore of high risk for the communities, some administrative steps may be abolished.

Therefore, our Institutional Review Board does not require ethical approval for studies conducted on autoptic specimens and not collecting personal or sensitive data.

Autoptic lung, liver, and VAT samples of 49 subjects were collected at the Department of Legal Medicine of the Ospedali Riuniti of Ancona between March and May Twenty-four subjects were affected by COVID, while the remaining 25 were not and died for different reasons.

SARS-CoV-2 infection was assessed in all subjects by RT-PCR tests on a nasopharyngeal swab. Among the studied subjects, 15 had documented respiratory conditions, i. VAT was sampled from the omentum and mesentery region. Lungs were extensively sampled across central and peripheral regions of each lobe bilaterally.

A median of seven tissue blocks range five to nine were taken from each lung. Liver samples were collected from the right and left lobes. Samples were sliced into different pieces to be studied by LM and transmission electron microscopy TEM.

A comprehensive methodological description for such methodologies has been described elsewhere [ 47 ]. Samples were then embedded in paraffin to be studied by LM and to perform immunohistochemistry and morphometric analyses.

A comprehensive description of the protocol has been described elsewhere [ 47 ]. To study SARS-CoV-2 presence in VAT, we used the SARS-CoV-2 nucleocapsid Invitrogen MA and spike protein Sino Biological T62 antibodies at different dilutions. The same antibodies were used to detect the virus on infected VeroE6 at dilution: for nucleocapsid protein and for the spike protein.

Negative control in which primary antibody was omitted were always included in each set of reactions to assess antibody specificity.

Spot exercising, such as doing sit-ups, can tighten abdominal muscles, but it won't get at visceral fat. Diet is also important. Pay attention to portion size, and emphasize complex carbohydrates fruits, vegetables, and whole grains and lean protein over simple carbohydrates such as white bread, refined-grain pasta, and sugary drinks.

Replacing saturated fats and trans fats with polyunsaturated fats can also help. Scientists hope to develop drug treatments that target abdominal fat.

For now, experts stress that lifestyle, especially exercise, is the very best way to fight visceral fat. As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

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Can watching sports be bad for your health? To explore brain effects, the scientists knocked NLRP3 out of mice and found the mice were protected against obesity-induced inflammation of the brain and the cognitive problems that can result.

They also transplanted visceral adipose tissue from obese mice and obese mice missing NLRP3 into lean mice recipients and found the transplant from the NLRP3 knockout mouse had essentially no effect.

But the transplant from the obese but genetically intact mice increased levels of interleukin-1 beta in the hippocampus, a center of learning and memory in the brain, and impaired cognition. They looked further and found that just transplanting the visceral fat caused essentially the same impact as obesity resulting from a high-fat diet, including significantly increasing brain levels of interleukin-1 beta and activating microglia.

Mice missing interleukin-1 beta's receptor on the microglia also were protected from these brain ravages. Their findings enabled the scientists to start putting together the pieces that NLRP3 was working through interleukin-1 beta, which led them to also knock out the receptor for interleukin-1 beta on microglia and confirm that action in the brain.

Microglia typically function as watchdogs, constantly surveilling and roaming the brain, eliminating dead cells and other debris as well as a myriad of other tasks like forming and pruning connections between neurons.

Microglia also have receptors for interleukin-1 beta, and the protein, whose many actions include promoting inflammation, easily passes through the protective blood brain barrier. In the absence of disease, microglia also are known to embrace synapses but to release good things like brain-derived neurotrophic factor, which is like fertilizer for these invaluable connections.

Happy microglia also have long processes that enable them to reach out and do their many tasks; and inflammation retracts those processes. The scientists found much shorter processes and less complex microglia in mice on a high-fat diet, more changes that didn't happen when NLRP3 was knocked out.

To measure cognitive ability, the scientists looked at mice's ability to navigate a water maze after 12 weeks on a high- or low-fat diet. They found it took the normal, or wild type, mice consuming the higher fat diet as well as the visceral transplant recipients with NLRP3 intact longer to negotiate the water maze.

Quit smoking. Smoking causes inflammation in your body, and swearing off tobacco can improve your health within days.

Roy Buchinsky, MD is an internal medicine specialist and the director of wellness at University Hospitals Cleveland Medical Center.

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