The Immunity Link to Obesity

American Medical Holdings’ Dr. Vladimir Badmaev breaks down this heavy revelation.

Vladimir Badmaev

May 8, 2015

3 Min Read
The Immunity Link to Obesity

When formulating immune-support supplements, have you thought about how status of obesity or overweight can suppress immune functions, and how in turn chronic inflammation can fuel the obesity? There is an interesting link that is worthwhile to consider for this population.

Adipose tissue is considered not only a form of storage energy source but an active immunological organ in the body that is capable of modifying whole-body metabolism and the immunological response. The immune cells (white blood cells) including B cells (lymphocytes), T cells (lymphocytes), macrophages, and neutrophils, all have been identified in adipose tissue, especially in obese individuals, establishing a link between obesity and inflammation.

Obesity-associated inflammation is characterized by an increased abundance of inflammatory cells (white blood cells) in adipose tissue along with production of inflammatory cytokines (messengers of inflammation). It is now broadly accepted that low-grade chronic inflammation is associated with obesity. Therefore obesity fuels pro-inflammatory processes in the body and inflammation contributes to obesity. The emerging target in the mechanism of obesity is the endocannabinoid system and its role regulating metabolic and immunological functions. Arguably the overload of the liver with dietary fatty acids leads to an overactive endocannabinoid system, which upregulates the immunological reactions, generating inflammatory cells and the pro-inflammatory cytokines that contribute to obesity.

The cross-talk between the white blood cells infiltrating adipose tissue and adipocytes (fat cells), may decide on the pathways in obesity and inflammatory processes in the body. Recent evidence suggests that obesity is mediated by cytokines from white blood cells infiltrating adipose tissue, including TNF-alpha (tumor necrosis factor alpha) and IL-6 (interleukin 6), and adipocyte-derived adipokines (hormones regulating adipose tissue), leptin, and adiponectin.

In obese individuals, TNF-alpha and IL-6 are overproduced in adipose tissue and contribute to insulin resistance. Leptin has opposite effects on inflammation and insulin resistance to those of adiponectin. The ratio of leptin to adiponectin increases in metabolic decline and obesity. Leptin upregulates pro-inflammatory cytokines (such as TNF-alpha and IL-6,) while adiponectin has anti-inflammatory properties and down-regulates pro-inflammatory cytokines. Adiponectin, unlike leptin, improves insulin resistance and promotes fatty acid oxidation for energy. In addition, adiponectin counteracts the pro-inflammatory effects of TNF-alpha on the arterial wall and probably protects against the development of arteriosclerosis. The elevated levels of leptin in obese individuals may contribute to the low-grade, chronic inflammation increasing risk of developing cardiovascular diseases, diabetes, or degenerative disease—including autoimmune conditions.

Increasing knowledge of the mechanisms linking obesity with immunological functions and chronic inflammation provides meaningful solutions in weight and fat management. The shift from sedentary to active lifestyle by incorporating aerobic exercise improves insulin sensitivity, reducing obesity and obesity-induced chronic inflammation. In addition, dietary and drug intervention provide helpful support of the immune and metabolic systems.  Supplementation with plant polyphenols (turmeric) and triterpenoids (boswellia), both recognized for their NSAID-like properties, has been known to significantly reduce macrophage infiltration of adipose tissue, increase production of adiponectin, and decrease biomarkers of inflammation in the liver, i.e. decrease nuclear factor-kappaB activity.

Another useful polyphenol derived from Salacia reticulata, which is sometimes called a “metabolic adaptogen,” may improve multiple metabolic and immune targets, including inhibition of lipogenic gene transcription (preventing adipose tissue build-up), angiotensin II/angiotensin II type 1 receptor (lowering blood pressure), alpha-glucosidase (preventing dietary sugar absorption), aldose reductase (preventing advanced glycation end-products), and pancreatic lipase (preventing excess dietary fat absorption).

Salacia’s principle of metabolic adaptogen is a backbone of a novel approach to prevent excessive absorption of dietary fat in a formula called FB3®Fusion Ingredient  that also includes Coleus forskohlii and Sesamum indicum. It has also been suggested that the improved glucose tolerance observed in the presence of thiazolidinediones (oral antidiabetic drugs) or statins (cholesterol-lowering class of drugs) is likely due to their anti-inflammatory and immunoregulatory properties.

The lifestyle and age-related metabolic deterioration and resulting obesity may require a multiple-target strategy. Therefore, in addition to lifestyle modification and low-fat diet the supportive line of defense in combating obesity should consider functional foods, food supplements, and certain drug compounds that modify and support the immune system, preventing oxidative stress and inflammation.

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