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Rubber Banding” or The Fat “Yo-Yo” or Relapse-Induced Hyperplasia of Adipose Tissue

Why we regain weight after weight loss regains more than we lost.

Each time you lose weight it becomes more difficult . “rubber banding” or the fat “yo-yo” or relapse-induced hyperplasia of adipose tissue.

Weight loss awakens the body’s defense system which is focused on the objective of restoring the body’s depleted energy reserves.

• Adipocytes shrink during weight loss, but there is no discernible change in the number of adipocytes in adipose tissue.
• But when you regain the weight, they don’t just grow back to normal size, they actually multiply. Metabolic conditions during the relapse to obesity may provide the conditions that promote hyperplasia
• This increase in cell number persisted throughout the relapse process as all of the adipocytes became larger. This increased cell number partially explains animals surpassing their pre-weight loss weight following relapse.

Obes Rev. 2015 Feb; 16(Suppl 1): 45–54.
Published online 2015 Jan 22. DOI: 10.1111/obr.12255

The interplay between immunity, inflammation, and metabolic changes is a growing field of research. Exciting new evidence is emerging with regard to their role in the regulation of metabolism and the activation of inflammatory pathways during the progression of metabolic disorders such as Type 2 Diabetes and Atherosclerosis.

  1. The innate immune system

The innate immune system is an evolutionarily conserved system that senses and defends against infection and irritation. Innate immune signaling is a complex cascade that quickly recognizes infectious threats through multiple germline-encoded cell surface or cytoplasmic receptors and transmits signals for the deployment of proper countermeasures through adaptors, kinases, and transcription factors, resulting in the production of cytokines.

As the first response of the innate immune system to pathogenic signals, inflammatory responses must be rapid and specific to establish a physical barrier against the spread of infection and must subsequently be terminated once the pathogens have been cleared. Long-lasting and low-grade chronic inflammation is a distinguishing feature of type 2 diabetes and cardiovascular diseases, which are currently major public health problems.

  1. How does the innate immune system work?

The ability of organisms to mount a response to infectious challenge without prior exposure is regulated by the coordinated interaction of components of the innate immune system. This preformed system is important to respond to exogenous stimuli such as bacterial, viral, and fungal infections. Beyond the initial response to a stressor, the innate immune system coordinates the resolution of inflammation, tissue repair, and the activation of the adaptive immune system to provide memory for future challenges.

While much of our understanding of innate immunity comes from models of infection, it is also clear that immune responses can be triggered by endogenous stimuli. Such mechanisms play a wide role in health and disease from the response to tissue injury, the direction of tissue remodeling, and the response to tumors.

  1. The Innate Immune Response to Obesity

The increased prevalence of obesity and overweight in adults continues to rise and contributes to morbidity and mortality that is estimated to cost $147 billion dollars a year in the U.S. (Finkelstein et al., 2009) and up to 0.6% of the gross domestic product of European countries (Muller-Riemenschneider et al., 2008). More ominous is the high rates of childhood obesity which is a strong predictor of adult obesity (Lee et al., 2009). This has also shifted the prevalence of adult diseases such as type 2 diabetes and pre-diabetes into childhood and has generated new treatment and prevention challenges (Lee, 2006; Lee et al., 2006). Relevant to this review, increases in inflammatory biomarkers such as C-reactive Protein (CRP) and neutrophilia are seen in obese children as young as 3 years of age (Skinner et al., 2010). This indicates that many of the origins of obesity-induced inflammation may actually be initiated during childhood. Therefore, many people will face a lifetime threat to health from obesity.

The long term duration of obesity-induced inflammation makes it challenging to describe this unique type of inflammatory activation based on classical models of innate immunity. Applying such models may be inaccurate and insufficient to encompass the events that are triggered by obesity in metabolic tissues such as fat. Furthermore, it is clear that the inflammation generated by obesity is not as high in amplitude as those seen in acute infectious settings (Hotamisligil, 2006). These unique challenges have led to the coining of the term “metal inflammation” to describe the chronic low-grade inflammatory events that occur in obesity and its associated diseases.

A frequently asked question is why would obesity trigger an immune response? For the most part, this question remains unanswered, but one answer to this may lie in the fact that many of the key regulators of metabolism also play critical roles in regulating inflammatory responses.

  1. Inflammation as a link between obesity and disease

The interest in obesity-induced inflammation relates to the understanding that inflammatory mechanisms are central to the pathogenesis of diseases such as heart disease that is modified by obesity.

It is impossible to cover the scope of all of these diseases so we will focus our attention on the inflammatory mechanisms of fatty liver disease and Type 2 Diabetes-related diseases with fundamental alterations in nutrient control derived from pro-inflammatory inputs. This will set the stage for future discussion of the innate immune components activated in obesity. I will highlight both clinical and pre-clinical studies in animal models of obesity that have built our understanding of the mechanisms that drive obesity-associated diseases.

4.1 Non-alcoholic Fatty Liver Disease (NAFLD)

The liver plays a critical role in the regulation of glucose and lipids levels in the blood. Obesity generates a number of physiologic changes in hepatocyte glucose production as well as lipid oxidation and storage. Unusual hepatic lipid accumulation is connected to many obesity-associated illnesses that include non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome. The metabolic changes that occur with hepatic lipid accumulation include hepatic insulin resistance which is related to inflammatory cytokine signals.

4.2 Type 2 Diabetes (T2D)

The regulation of glucose metabolism is securely coordinated between nutrient inputs regulated by the liver and gut, nutrient utilization and storage in muscle and fat, insulin secretion by the pancreas, and central signals from the hypothalamus that coordinate these responses. The dysregulation of almost all of these processes with obesity is now known to be associated with the activation of innate pro-inflammatory pathways. The net result of this is the generation of systemic insulin resistance and hyperglycemia.

  1. Why obesity affects the innate immune system

The blend of a sedentary lifestyle and surplus energy intake has led to an increased occurrence of obesity which constitutes a major risk factor for several comorbidities including type 2 diabetes and cardiovascular diseases. Intensive research during the last two decades has revealed that a characteristic feature of obesity linking it to insulin resistance is the presence of chronic low-grade inflammation being indicative of activation of the innate immune system.

Recent evidence suggests that activation of the innate immune system in the course of obesity is mediated by metabolic signals, such as free fatty acids (FFAs), being elevated in many obese subjects, through activation of pattern recognition receptors thereby leading to stimulation of critical inflammatory signaling cascades, like IκBα kinase/nuclear factor-κB (IKK/NF- κB), endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and NOD-like receptor P3 (NLRP3) inflammasome pathway, that interfere with insulin signaling.

Exercise is one of the main prescribed interventions in obesity management improving insulin sensitivity and reducing obesity-induced chronic inflammation. A deeper understanding of the effects of exercise on inflammatory signaling pathways in obesity is useful to optimize preventive and therapeutic strategies to combat the increasing incidence of obesity and its comorbidities.

References:

  1. Journal of Biological Chemistry (2013): How Metabolism Generates Signals during Innate Immunity and Inflammation. Retrieved from http://www.jbc.org/content/288/32/22893.full.html
  2. Physiological Reviews (2018): Innate Immune Signaling and Its Role in Metabolic and Cardiovascular Diseases. Retrieved from https://www.physiology.org/doi/abs/10.1152/physrev.00065.2017
  3. NCBI (2012): Innate Immune Activation in Obesity. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888776/
  4. NCBI (2015): Metabolic signals and innate immune activation in obesity and exercise. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/25825956

Obesity is a disease that has plagued the modern-day man in recent times. Access to highly processed foods and a decrease in physical activity are key contributors to this ailment. Researchers are hard at work looking into what other underlying factors lead to obesity, especially given its relationship with the onset of Type 2 Diabetes, Cardiovascular diseases, and liver disease. We will take an in-depth look at metabolic inflammation and its role in the onset of obesity in this article. Let’s dive in.

  1. What is obesity?

Obesity is characterized by a low-grade chronic state of inflammation in which the level of pro-inflammatory cytokines such as TNF-α, IL-6, and CRP are increased. It is a state in which there is an over-accumulation of subcutaneous and/or abdominal adipose tissue. This adipose tissue is no longer considered inert and mainly devoted to storing energy; it is emerging as an active tissue in the regulation of physiological and pathological processes, including immunity and inflammation.

Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To determine your body mass index, divide your weight in pounds by your height in inches squared and multiply by 703. Or divide your weight in kilograms by your height in meters squared.

BMI Weight status
Below 18.5 Underweight
18.5-24.9 Normal
25.0-29.9 Overweight
30.0 and higher Obesity

For most people, BMI provides a reasonable estimate of body fat. However, BMI doesn’t directly measure body fat, so some people, such as muscular athletes, may have a BMI in the obesity category even though they don’t have excess body fat.

  1. What is Diabesity?

‘Diabesity’ is the term for diabetes occurring in the context of obesity. This form of obesity-dependent diabetes has emerged as a major public health problem in recent times. Though it is basically explained by insulin resistance and pancreatic beta-cell dysfunction, new patterns have evolved to explain these modifications in the context of the modern spates of obesity and diabetes.

  1. Is obesity an inflammatory condition?

The connection between obesity and inflammation has been often come up in debate in the recent past. Unbeknownst to many, the link between these conditions was made decades ago. Over a century ago, high doses of a class of anti-inflammatory compounds including aspirin called salicylates were used to treat Type 2 diabetes. In some cases, the symptoms of diabetes totally disappeared. Unfortunately, this treatment was discontinued due to the serious side effects caused by the high doses of salicylates.

We will now look at the questions of our topic today in-depth; Does obesity cause inflammation, or is inflammation caused by something secondary to obesity (like high blood sugar or triglycerides)? How about diabesity? Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body initiate an inflammatory response to diabesity? Let us tackle each item separately.

  1. How does Inflammation Cause Diabesity?

We look at some lines of evidence that show that inflammation directly causes obesity and diabesity.

  • The development of diabesity has been shown to follow inflammation. Raised levels of inflammatory cytokines predict impending weight gain. In a study carried out, the infusion of inflammatory cytokines into healthy, normal-weight mice caused insulin resistance. This concept is also illustrated by the fact that people with other chronic inflammatory conditions are at higher risk of developing Type2 Diabetes, for example, about one-third of chronic Hepatitis C patients develop T2DM, and those with rheumatoid arthritis are also at higher risk.
  • In obesity, inflammation has been noted to start in the fat cells themselves. As fat mass expands, inflammation increases. An explanation for this may be the dysfunction of the mitochondria (the “power plant” of our cells) caused by the increased stress obesity puts on cellular function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they produce an excess of reactive oxygen species (ROS) which in turn starts an inflammatory cascade within the cell.
  • Further, inflammation of the fat tissue causes insulin resistance, which is the primary feature of T2DM. TNF-α, a cytokine (small protein) released during the inflammatory response, has been repeatedly shown to cause insulin resistance. Several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein, have also been shown to cause insulin resistance.
  • Also, inflammation of the brain (specifically the hypothalamus) causes leptin resistance, which often precedes and accompanies insulin resistance and T2DM. Leptin is a hormone that regulates appetite and metabolism. It does this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolism are impaired and weight gain and insulin resistance result.
  • When there is inflammation of the gut, there arises leptin and insulin resistance. This may occur via an increase in lipopolysaccharide (LPS), an endotoxin produced by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver and weight gain.
  1. How does Diabesity Cause Inflammation?

In the past, fat was considered an inactive tissue with no biological action. It wasn’t considered for much other than storing energy. It has now emerged that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. This metabolic activity of fat is the key to understanding its role in diabesity.

  1. Why would obesity cause inflammation?

The first theory is that obesity-induced inflammation a protective mechanism that prevents the body from losing mobility or fitness. Fat storage is an anabolic process, which means it builds up the organs and tissues. Inflammation, on the other hand, is a catabolic process. Catabolism breaks down organs and tissues. It’s possible that the activation of catabolism via inflammation is the body’s attempt to keep weight within acceptable bounds. Evidence that experimentally induced local inflammation in fat tissue improves insulin resistance and causes weight loss supports this theory.

The second theory is that obesity-induced inflammation is simply a malfunction that was never selected against human evolution. Obesity and its related disorders have been extremely rare throughout human history, and have only become common in the past 40 years. The surplus of modern, processed foods that accompanies diabesity is also a relatively new phenomenon. It’s possible that the stresses of obesity are similar enough to the stresses of an infection that the body reacts to obesity in the same way it would to an infection: via inflammation. Supporting this theory is evidence that the same intracellular, inflammatory stress pathways are activated in both obesity and infection.

  1. Tackling Inflammation in the control of diabesity

We can, therefore, conclude that inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.
Reduction of inflammation is a major key in preventing and treating diabesity. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.

References

1.    NCBI (2003): Diabesity: an inflammatory metabolic condition. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/14598860

2.    NCBI (2013): Obesity, Inflammation, and Diet. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819692/

3.    NCBI(2006): Inflammation and insulin resistance. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1483173/

4.    Chris Kessler (2019): How Inflammation Makes You Fat and Diabetic (And Vice Versa). Retrieved from https://chriskresser.com/how-inflammation-makes-you-fat-and-diabetic-and-vice-versa/

Adipose tissue-derived proteins known to affect inflammation

TNF-α
IL-6
IL-1β
Leptin
Adiponectin
Resistin
Acylation-stimulating protein
SAA3
α1 acid glycoprotein
Pentraxin-3
IL-1 receptor antagonist
Macrophage migration inhibitory factor.

Sugar has been vilified over the years with claims of its disastrous effects on our health. Are these claims true? Does taken a soda a day guarantee one ill health? What of the effects of excess sugar on obesity? In this article, we will explore these claims and determine whether indeed excessive sugar intake leads to obesity.

1. What is obesity?

Obesity rates have skyrocketed over the past century. In 1962, 46 percent of adults in the U.S. were considered overweight or obese. By 2010,that figure had jumped to 75 percent.

So, what exactly is obesity……

Obesity is a complex disease involving an excessive amount of body fat. Obesity isn’t just a cosmetic concern. It is a medical problem that increases your risk of other diseases and health problems, such as heart disease, diabetes, high blood pressure and certain cancers.

Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To determine your body mass index, divide your weight in pounds by your height in inches squared and multiply by 703. Or divide your weight in kilograms by your height in meters squared.

BMI Weight status
Below 18.5 Underweight
18.5-24.9 Normal
25.0-29.9 Overweight
30.0 and higher Obesity

For most people, BMI provides a reasonable estimate of body fat. However, BMI doesn’t directly measure body fat, so some people, such as muscular athletes, may have a BMI in the obesity category even though they don’t have excess body fat.

2. Sugar and obesity

Obesity is a complex problem with multiple causes. But among the likely suspects, sugar is a top favorite. As sugar consumption has increased, so too has the size of our waistlines.

Added sugars are a controversial and hotly debated topic. Consumption of added sugars has been implicated in increased risk of a variety of chronic diseases including obesity, cardiovascular disease, diabetes and non-alcoholic fatty liver disease (NAFLD) as well as cognitive decline and even some cancers. Support for these putative associations has been challenged, however, on a variety of fronts.

The sugars in your diet can be eithernaturally occurring or added. Naturally occurring sugars are found naturally in foods such as fruit (fructose) and milk (lactose). Added sugars are sugars and syrups put in foods during preparation or processing, or added at the table.

Numerous dietary and lifestyle habits can lead to weight gain and cause you to put on excess body fat.Consuming a diet high in added sugars, such as those found in sweetened beverages, candy, baked goods, and sugary cereals, is a contributing factor in weight gain and chronic health conditions, including obesity, heart disease, and diabetes.

Many people consume more sugar than they realize. It’s important to be aware of how much sugar you consume because our bodies don’t need sugar to function properly. Added sugars contribute zero nutrients but many added calories, which can lead to extra pounds or even obesity, thereby reducing impacting our health.

The ways in which added sugar intake leads to weight gain and increased body fat are complex and involve many factors.

3. Some ways why added sugar is fattening….

  1. It is high in empty calories
    Added sugars are sweeteners added to foods and beverages to improve taste. Common types of added sugar include fructose, corn syrup, cane sugar, and agave.Excess sugar may cause you to pack on weight because it’s high in calories while offering few other nutrients.Though using small amounts of added sugar is unlikely to cause weight gain, regularly indulging in foods high in added sugars may cause you to gain excess body fat quicker and more drastically.

    1. Impacts blood sugar and hormone levels

    It’s well known that eating sugary foods significantly raises your blood sugar levels.Though enjoying a sweet food infrequently isn’t likely to harm health, daily consumption of large amounts of added sugar can lead to chronically elevated blood sugar levels.

    Prolonged elevated blood sugar — known as hyperglycemia — can cause serious harm to your body, by causing insulin resistance and resulting including weight gain.

    1. May lead to overeating

    Foods high in added sugars tend to be less filling. Eating foods rich in carbs — particularly refined carbs high in added sugars — yet low in protein can negatively impact fullness and may lead to weight gain by causing you to eat more at subsequent meals throughout the day or overeat at any one particular seating.

    Animal studies indicate that fructose impacts signaling systems in your hypothalamus, increasing levels of hunger-stimulating neuropeptides — molecules that communicate with one another, influencing brain activity — while decreasing fullness signals. Additionally, your body is predisposed to crave sweetness. In fact, research shows that sugar consumption is driven by the pleasure derived from the sweet taste of sugary drinks and foods.

    1. Linked to obesity and chronic disease

    Numerous studies have linked high intake of added sugars to weight gain and chronic conditions, such as obesity, heart disease, and diabetes.This effect has been observed both in adults and in children. Recently, a review of 30 studies in more than 242,000 adults and children found a significant link between sugar-sweetened beverages and obesity.

    4. What are some of the health problems associated with obesity?

    People with obesity are more likely to develop a number of potentially serious health problems, including:

    • Heart disease and strokes. Obesity makes you more likely to have high blood pressure and abnormal cholesterol levels, which are risk factors for heart disease and strokes.
    • Type 2 diabetes. Obesity can affect the way your body uses insulin to control blood sugar levels. This raises your risk of insulin resistance and diabetes.
    • Certain cancers. Obesity may increase your risk of cancer of the uterus, cervix, endometrium, ovary, breast, colon, rectum, esophagus, liver, gallbladder, pancreas, kidney and prostate.
    • Digestive problems. Obesity increases the likelihood that you’ll develop heartburn, gallbladder disease and liver problems.
    • Gynecological and sexual problems. Obesity may cause infertility and irregular periods in women. Obesity also can cause erectile dysfunction in men.
    • Sleep apnea. People with obesity are more likely to have sleep apnea, a potentially serious disorder in which breathing repeatedly stops and starts during sleep.
    • Osteoarthritis. Obesity increases the stress placed on weight-bearing joints, in addition to promoting inflammation within the body. These factors may lead to complications such as osteoarthritis.

    5. How can obesity affect your quality of life?

    People who are obese often find themselves struggling with some issues that might diminish their overall quality of life. Some of these issues might include:

    • Depression
    • Disability
    • Sexual problems
    • Shame and guilt
    • Social isolation
    • Lower work achievement

    6. How can you keep yourself from getting obese?

    Whether you’re at risk of obesity, currently overweight or at a healthy weight, you can take steps to prevent unhealthy weight gain and related health problems.

    • Exercise regularly. You need to get 150 to 300 minutes of moderate-intensity activity a week to prevent weight gain. Moderately intense physical activities include fast walking and swimming.
    • Follow a healthy-eating plan. Focus on low-calorie, nutrient-dense foods, such as fruits, vegetables and whole grains. Avoid saturated fat and limit sweets and alcohol. Eat three regular meals a day with limited snacking. You can still enjoy small amounts of high-fat, high-calorie foods as an infrequent treat.
    • Know and avoid the food traps that cause you to eat. Identify situations that trigger out-of-control eating. Try keeping a journal and write down what you eat, how much you eat, when you eat, how you’re feeling and how hungry you are, stay in control of your eating behaviors.
    • Monitor your weight regularly. People who weigh themselves at least once a week are more successful in keeping off excess pounds.
    • Be consistent. Sticking to your healthy-weight plan all the time

      7. So, is sugar friend or foe?

      Interfering with your hormones, increasing hunger, and displacing healthy foods are just a few of the ways that added sugars can lead to weight gain.Aside from causing you to put on excess body fat, eating too much added sugar can significantly increase your risk of chronic conditions, such as obesity, heart disease, and diabetes. It is thus wise to consume added sugars with caution because a stitch in time save nine.

      References

      1. Endocrineweb(2018):Insulin Resistance Causes and Symptoms, Retrieved from

      https://www.endocrineweb.com/conditions/type-2-diabetes/insulin-resistance-causes-symptoms

      1. Healthline (2019):6 Ways Added Sugar Is Fattening. Retrieved from

      https://www.healthline.com/nutrition/does-sugar-make-you-fat#section1

      1. American Heart Association (2018): Added Sugars. Retrieved from

      https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/sugar/added-sugars

      1. NCBI (2016): Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding. Retrieved from

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133084/

      1. John Hopkins Medicine (2019): Obesity, Sugar and Heart Health. Retrieved from

      https://www.hopkinsmedicine.org/health/wellness-and-prevention/obesity-sugar-and-heart-health

      1. Mayo Clinic: Retrieved from

      https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742

It is estimated that by 2020, two-thirds of the global burden of disease will be due to chronic non-communicable diseases, most of which are associated with diet. While hunger is a tremendous global health concern that cannot be minimized, overnutrition should similarly be given concentrated attention. Malnutrition affects up-to 1 billion people. Even though undernutrition is the main cause of malnutrition, people who are overweight could also be malnourished.

The “dual burden of malnutrition” is a term coined by the World Health Organization (WHO) to describe a situation which is characterized by “the coexistence of undernutrition along with overweight and obesity, or diet-related non-communicable diseases, within individuals, households and populations, and across the life course. Globally, the problem is not the availability of food resources, but the allocation and consumption of food.

Despite it being an essential response to infection and tissue injury, inflammation has also been associated with several pathological processes. Excessive acute inflammation causes tissue damage and non-resolving inflammation leads to chronic tissue malfunction, suggesting a delicate balance between the rapid and effective response to distresses in tissue homeostasis and the collateral damage on tissue function.

As a cluster, obesity, raised fasting plasma glucose, high cholesterol and hypertension comprise the metabolic syndrome.

Heart disease is currently one of the major causes of morbidity and correlates closely with the global incidence of obesity and type 2 diabetes.

Recently, there is an increasing focus on metainflammation as the primary pathophysiology.

Recent studies implicate early metabolic abnormalities (weight gain, insulin resistance, and prehypertension, and irregular blood lipid levels). A basic description would be that inflammation is secondary to insulin resistance, which in turn leads to obesity which increases the chances of diabetes, high blood pressure, prothrombotic state, and abnormal lipid presence.

Despite it being an essential response to infection and tissue injury, inflammation has also been associated with several pathological processes. Excessive acute inflammation causes tissue damage and non-resolving inflammation leads to chronic tissue malfunction, suggesting a delicate balance between the rapid and effective response to distresses in tissue homeostasis and the collateral damage on tissue function.

As a cluster, obesity, raised fasting plasma glucose, high cholesterol and hypertension comprise the metabolic syndrome.

Obesity is characterized by a low-grade chronic state of inflammation in which the level of pro-inflammatory cytokines such as TNF-α, IL-6, and CRP are increased. It is a state in which there is an over-accumulation of subcutaneous and/or abdominal adipose tissue.

This adipose tissue is no longer considered inert and mainly devoted to storing energy; it is emerging as an active tissue in the regulation of physiological and pathological processes, including immunity and inflammation. Adipose tissue is also implicated in the development of chronic metabolic diseases such as type 2 diabetes mellitus or cardiovascular disease.

Obesity can therefore be caused by inflammatory and metabolic diseases. Diet or dietary patterns as well play critical roles in obesity and other pathophysiological conditions. It is therefore recommended for one to have a healthy diet and other nutrients that are generally considered to be beneficial.