Inflammation has always been viewed as a positive occurrence for human healing. Inflammation seals wounds and fights bacteria. This shows an active immune system. However, an overly active immune system has its flipside. Chronic inflammation, which arises from disorders such as autoimmune disease, arthritis, asthma, depression, digestion and sinus disorders, has been recognized as the cause of weight gain and diseases associated with aging. Studies have established that inflammation and excess insulin are the leading cause of type 2 diabetes and the increasing weight issues in global populations. Experiments are just beginning to uncover the connection between inflammation and weight gain.
The first explanation is the interaction between inflammation and the microbiome. The microbiome consists of bacteria that assist in the processing of calories. Some utilise these calories and thus contribute to the overall metabolism of losing weight. Inflammatory conditions often alter microbiome compositions. These changes are often noted at the onset of disease (Strohacker & McFarlin, 2009). Patients with type 2 diabetes and cardiovascular disease show reduced amounts of bacteria that promote weight loss. Therefore, inflammation hinders all processes by the microbiota to lose the excess calories. These processes include the transformation of polysaccharides into digestible foods, development of the gut epithelium, inhibiting lipoprotein lipase in adipose tissue and increasing lipogenesis.
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Contrary to common knowledge, adipose tissue contains metabolically active cells and not simply storage space for fat. Among other constituents, adipose tissue contains macrophages. The macrophage is a major contributor to inflammation. The main structural components of adipose tissue (adipocytes) also show great intrinsic inflammatory properties (Paresh, et al, 2004). Adipose tissue also contains resident immune cells, which help in maintaining tissue homeostasis. However, increased storage of fat results in significant changes in the number and function of these cells. It leads to increased production of some while suppressing others. This imbalance is the sole cause of local and systemic inflammation linked to obesity.
Chronic inflammation is also associated with insulin resistance. Insulin helps regulate blood glucose levels and allows it to be stored as fat. Chronic inflammation leads to a surge in production of insulin. This goes to a point where the individual is insulin resistant, the cells do not actively utilise it, and therefore the pancreas secretes more insulin (Daniel et al, 2004). Elevated levels of insulin encourage the body to store excess glucose as fat to be used as fuel. Low insulin sensitivity signifies hyperinsulinemia, which is a precursor to type 2 diabetes. Living a sedentary lifestyle and being overweight significantly increases the chances of one becoming insulin resistant. More current research shows that hypothalamic–pituitary– adrenal axis dysfunction plays a role in metabolic disease. Pro-inflammatory cytokines can stimulate the HPA axis; on the other hand, cortisol decreases the production of cytokines and other inflammatory mediators. Hence, it is evident that there exists a disturbance between the HPA axis and the inflammatory response. In terms of tissue-specific cortisol metabolism, it is said that the enzyme 11 beta – hydroxysteroid dehydrogenase type 1 (11B-HSD1) is relevant in HPA axis activity, regenerating active cortisol from its inactive forms intracellularly. Adipose tissue expression of 11B-HSD1 and regulation of local cortisol levels play a role in the development of obesity.
The physiology of obesity and inflammation is multi-faceted, it is encouraged that those who present with these conditions investigate and address the body root causes rather than just working towards treating the symptoms.
• Drink plenty of water, which reduces cases of inflammation arising from dehydration.
• Exercising in moderation promotes beneficial inflammation while avoiding chronic inflammation (Lourdes, et al, 2006). The reason for this is that enlarged fat cells are reduced to fewer pro-inflammatory messengers such as tumor necrosis factor alpha (TNF-a) and interleukin 6 (IL-6) are released.
• 7 to 9 hours of sleep daily, as sleep deprivation promotes the secretion of inflammatory hormones which lead to obesity.
• Supplements that help fight inflammation
• Curcumin with Piperine to increase absorption by 2000%,
• Omega 3’s, such as Cod Liver oil
• Melatonin which protects against oxidative and mitochondrial stressors that are induced by excess cortisol
• A proper diet that contains antioxidants, polyphenols and essential fats also reduce inflammation resulting from 'free radicals'.
• Finally, patients are urged to reduce stress, as the stress hormone cortisol controls the immune response. Incorporating a daily mindfulness practice starting with 5 to 10 minutes daily, and increasing to 20 to 60 minutes daily such as meditation, yoga, and Qi Gong, which have been shown to greatly reduce stress.
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2. Dandona, Paresh, Ahmad Aljada, and Arindam Bandyopadhyay. "Inflammation: the link between insulin resistance, obesity and diabetes."Trends in immunology 25.1 (2004): 4-7.
3. Cottam, Daniel R., et al. "The chronic inflammatory hypothesis for the morbidity associated with morbid obesity: implications and effects of weight loss." Obesity surgery 14.5 (2004): 589-600.
4. Ibáñez, Lourdes, et al. "Early development of adiposity and insulin resistance after catch-up weight gain in small-for-gestational-age children."The Journal of Clinical Endocrinology & Metabolism 91.6 (2006): 2153-2158.
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