*2.2.2 Obesity and asthma*

The relationship between obesity and asthma has been established by a meta-analysis involving more than 300,000 adults [25]. The expression of adipokines secreted by adipose tissue is different in persons with obesity. Decreased expression of adiponectin (anti-inflammatory adipokine) and increased expression of leptin (pro-inflammatory adipokine) have been reported in asthmatic patients with obesity [26]. Leptin, an anorexigenic hormone, increases metabolic rate and is involved in surfactant production and neonatal lung development [27]. Sood et al. [28] have reported a strong association between high BMI and high levels of serum leptin with asthma in adults.

Inflammatory cytokines such as TNF-α, IL-8, and monocyte chemoattractant protein-1 (MCP-1) have also been reported to be raised in persons with obesity. However, their role in asthma associated with obesity is not clear [29]. In older patients, abdominal obesity and metabolic syndrome have been reported to be associated with restrictive lung disease [30].

### *2.2.3 Obstructive sleep apnea (OSA)*

The prevalence of obstructive sleep apnea in adult persons with obesity is about 45%, compared with 25% in persons with normal weight [31]. Increased fat deposit in tissues surrounding the upper airway decreases the size of lumen and increases collapsibility of the upper airway. OSA may cause sleep fragmentation, which may lead to sleep deprivation [32]. Since experimental sleep deprivation and self-reported short sleep have been linked with metabolic dysregulation, it is possible that OSA may also be a contributing factor in metabolic dysregulation associated with obesity.

### **2.3 Lower limb venous diseases**

Venous diseases (blood clots, deep vein thrombosis, superficial venous thrombosis or phlebitis, chronic venous insufficiency or CVI, varicose and spider veins, and venous stasis ulcers) may be caused by one or more of the following factors: immobility (as in bed-ridden patients) leading to stagnation of blood), blood vessel injury caused by trauma/needles/intravenous catheters/infections, central venous hypertension, conditions that increase the blood coagulation, and pregnancy. Different cancers are associated with deep vein thrombosis.

Varicose veins and chronic venous insufficiency are more common in aged women compared with men. Obesity has been found to be associated with all types of lower limb venous diseases (**Figure 3**). Willenberg et al. [33] showed that lower limb venous flow parameters are different in healthy persons with and without obesity. Various

**Figure 3.** *Obesity as a cause of lower limb venous diseases.*

### *The Multiple Consequences of Obesity DOI: http://dx.doi.org/10.5772/intechopen.104764*

epidemiological studies show that obesity is associated with chronic venous disease, phlebitis, and thromboembolism [34–37]. Untreated CVI results in increased pressure and swelling leading to rupture of capillaries. The skin may appear reddish-brown and becomes sensitive to bumps and scratches. Burst capillaries may lead to inflammation and even ulcers.

Increased intra-abdominal pressure caused by central obesity is transmitted to the extremities via femoral veins leading to resistance to venous return, producing venous valvular insufficiency. The self-perpetuating cycle of worsening venous insufficiency causes venous stasis and distension of veins in the lower limb. Obesity produces a chronic low-grade inflammation, which damages the affected veins and increases the risk of thromboembolism [33].
