Obesity and Diabetes: The Enemies Within

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Table of Contents

Introduction
Statistics on Diabetes
Relationship between Obesity and Diabetes
Implications of Diabetes
Possible Solutions to the Problem
Conclusion
References

Introduction

The world is in a perpetual state of change and so are diseases. Obesity and diabetes are examples of emergent epidemics unheard of in the past. The diseases are currently household names and scourges in the waiting. Obesity is believed to be among the causal factors for diabetes. There is proof beyond reproach that obese people are at a risk of developing type 2 diabetes (insulin-resistant diabetes).

An appalling number of diabetes victims are a product of the last two decades (Pollock & Favret n.d.). The number is postulated to double in the coming years. A combination of type 2 diabetes and obesity is the notorious ‘diabesity.’ Recent worldwide predictions indicate that there are 285 million people with diabetes. Acknowledging the atrociousness of the circumstances, the United Nations General Assembly has resolved to declare diabetes an international public health issue.

Diabetes is the second disease after HIV/AIDS to receive such attention. Indeed, not for absence of better terms, but for the gravity of the issue at hand diabetes suffices to be termed “the enemy within.” A chronic disease can have adverse implications to an individual’s wellbeing. The disease compromises one’s quality of life, as well as exposing them to undue suffering and early deaths. It is saddening that the disease not only affects the individual, but their families and the economy of a nation, as well (Knutsona & Van Cauter 2008). Diabetes affects people of all ages hence those in the workforce are not immune.

Diabetes is typified by elevated blood glucose (sugar) levels. It is an outcome of lack of the hormone insulin. Insulin regulates blood glucose levels. The failure of the body’s tissues to respond suitably to insulin (a state called insulin resistance) also characterizes diabetes. Type 2 diabetes is the most common type of diabetes. Its victims form 90% of all people with diabetes (World Health Organization 2005).

Statistics on Diabetes

The astounding statistics on people living with diabetes leaves a lot to ponder. Diabetes was a relatively low high-risk disease in the past years hence there must be a clear explanation on the reasons for the escalation of the disease. Research cited by Barnett and Kumar indicates that there is a 9% risk of developing diabetes for every kilogram of weight gained (2009). According to a study done among Pima Indians of Arizona Micronesian, Nauruan islanders formerly lean groups, are now obese diabetics due to lifestyle change. Only an estimated 20% of Pima adults are safe from obesity.

An outstanding 40% of the obese population are diagnosed with type 2 diabetes. In an almost identical population of lean subjects, there is almost a zero chance of developing diabetes. A strong correlation with obesity is evident as four fifths of diabetics frequenting the clinic in Dundee border on obesity (Barnett & Kumar 2009). According to Yach, Stuckler and Brownwel, 60% of people in the world with diabetes directly attribute it to obesity (2006).

Statistics also indicate diabetes is no longer an adult’s disease. In some countries up to 80% of the cases are children, a great contrast to two decades ago where only 2% of the diabetic patients were children. Universal mortality ascribed to diabetes in the year 2000 is estimated to be 2.9 million deaths, which is 5.2% of all deaths. Diabetes is responsible for 2–3% of deaths in the poorest countries. It accounts for about 27% of deaths among people aged 35 to 64 (Roglic et al. 2005).

Relationship between Obesity and Diabetes

There is evidence to support the notion that diabetes is among the resultant diseases of obesity (Lois & Kumar 2009). On the other hand, the interplay between genetic, cultural and environmental factors with relative impact put into consideration are said to be the causes of obesity. The thrifty gene hypothesis is a proposal of one James Neel, an American geneticist. He suggests that the existence of the gene for type 2 diabetes is a survival benefit to early hunter-gatherer and agricultural societies (Lazar 2005; Stoger 2008). Experiences of nutritional hardship are said to be characteristic of such societies.

Presence of the thrifty gene hence is so crucial for survival in such situations. In times of plenty food, the thrifty gene stimulates fat accumulation in the body. Consequently, this fat provides a means for survival in times of food scarcity. In modern sedentary life, there is sufficient food hence the gene poses a shortcoming as it predisposes people to the development of obesity and diabetes.

An analysis by Lazar confirms that biological factors can be part of the causes of diabetes (2005). He argues that leptin levels are higher than usual in a diabetic person apart from a few rare cases where the leptin gene is defective. Insulin resistance at the cellular level can be related to the resistance to the actions of leptin (Stöger 2008). Other factors too may result in a similar scenario. Adipocyte-derived elements play a significant part in insulin resistance. One such element is increased levels of adipocyte-derived free fatty acids that trigger insulin resistance in the liver and muscle in obesity. Adipose tissue secretes numerous proteins over and above leptin that alter glucose metabolism and insulin action.

Lois and Kumar observe that, for such a long time, adipose tissues are considered the only fat storage tissues in the human body (2009). However, studies indicate that due to increasing diet-derived fat intake, fat storage takes place in other tissues and organs. This can include skeletal muscle, the liver and pancreatic β-cells. The result is excess mitochondrial production of toxic, reactive lipid varieties that cause organ-specific oxidative destruction and cellular malfunction. This eventually leads to the development of impaired glucose metabolism ultimately causing diabetes. Accumulation of lethal metabolites within the pancreatic islet β-cells affects insulin secretion and enhances β-cell apoptosis eventually leading to the development of overt diabetes (Hummasti & Hotamisligil 2010).

The causal function of numerous proteins in insulin resistance and diabetes is ascertained through studies of mouse genetic models. Studies carried out on human beings indicate that circulating levels of proteins are higher in people with type 2 diabetes (Lazar 2005). However, adiponectin protein is an exception since it heightens insulin action yet circulates at reduced levels in obesity (Irwin & Flatt 2009).

Each of these proteins comprises a potential target for therapies designed to separate insulin resistance from obesity. Adipose-derived proteins have a role in innate immunity, which is a moderate defence mechanism against infection, unlike the adipose-specific proteins (Sundell 2005). Certain cytokines such as the tumour necrosis factor are produced by macrophages. Besides acting on adipocytes, these cytokines act directly on inflammatory cells and impact inflammation indirectly to the liver leading to the generation acute phase proteins (Weyer, Gautie & Danforth 1999).

Additionally, cytokines induce suppressor of cytokine signaling-3 (SOCS-3) an intracellular signalling molecule that consequently damages the signalling of leptin and insulin. SOCS-3 levels are high in obesity hence can represent a joint pathway of obesity-associated resistance to the activities of leptin and insulin (Jia et al. 2010). The extent to which macrophages and adipocytes are similar exceeds cytokine production. The two cell types indicate peroxisome proliferator-activated receptor, an element that is the target of insulin sensitizing therapies labelled ‘‘the ultimate thrifty gene’’ due to its function in lipid accumulation.

It is unmistakable that macrophage infiltration of adipose tissue is typical of obesity even though the pathophysiological significant outcomes are obscure. Anatomic blurring of the line between adipocytes and macrophages is analogous and corresponds to the tissue expression of the polypeptide hormone resisting (Schwartz & Porte 2005). Indeed, polypeptide concentration increases in insulin resistant mice and humans (Cani et al. 2008).

In mice, insulin resistance is only seen in adipocytes, whereas insulin resistance is prevalent in human macrophages. Evolutionary and functional connotations of this are still undetermined. There are speculations that the harmonies of adipocyte and macrophage function are the remains of an ancestral evolutionary adaptation (Jia et al. 2009). Intriguingly, invertebrates concentrate endocrine and immune functions in an individual cell type akin to the macrophage.

Obesity is an inflammatory state and inflammation causes diabetes (Lazar 2005; Lois and Kumar 2009). The response to infection is more effective when glucose is pushed from muscles to the inflammatory cells concerned with the immune response and tissue repair. The body’s resilience in cases of major stress including times of infection and hunger is enhanced by marginal insulin resistance. The resistance conserves the brain’s glucose source (Sein, Shibasaki & Minami 2011; Black 2003).

This is a hypothesis that explains why the key stress hormone known as cortisol causes insulin resistance. This state of resistance in turn accelerates the innate immune response. However, recurring cortisol disclosure is anti-inflammatory because of down-regulation of the attained immune response (Keller 2006; Reynolds 2010). The stress connection extends to individual cells as there is evidence that intracellular stress induces insulin resistance in a way that is impaired by obesity, possibly across adipocyte-secreted factors (Cani et al. 2008; Minton et al. 2006). Oxidative stress is often linked to inflammation, and metabolic malfunction in adipose depots. Likewise, chronic metabolic stress weakens the ability of pancreatic beta cells to emit sufficient insulin to overcome insulin resistance, the hallmark of type 2 diabetes (Kahn, Hull & Utzschneider 2006).

Lois and Kumar seem to hold a similar opinion albeit with a slight difference (2003). Unlike the studies mentioned earlier, their correlation of inflammatory cells is considered weak. They term obesity as a low-grade inflammatory condition in which there is higher plasma circulating mononuclear cells and lymphocytes in obese people than in lean individuals. In addition, obese people have more adipose tissue, and there is increased intensity of creative protein tumour necrosis component in the entire body (Hotamisligil 2008). Adipose tissue is regarded as the initial site of the pro-inflammatory state generation that eventually spreads out to the entire body (Lois & Kumar 2009; Nguyen, Nguyen & Wang 2011).

Visceral fat seems to produce pro-inflammatory markers more vigorously than subcutaneous adipose tissue, validating the crucial function of central obesity in the pathogenesis of the obesity-associated illnesses. The proposed illness mechanisms consist of numerous heterogeneous factors in the production of inflammation within the adipose tissue.

There is an association between short sleep and increased risk of obesity and diabetes as discussed by Knutsona and Van Cauter (2008). They explore supposed causal mechanisms of diabetes and obesity in relation to short hours of sleep. Short sleep can be defined as less than seven hours of sleep per night (Punjabi et al. 2004). On the other hand, there is proof to confirm the relationship between long hours of sleep and decreased morbidity and mortality (Wiedmer et al. 2007).

The research by Knutsona and Van Cauter suggests that chronic partial sleep loss can heighten the risk of obesity and diabetes through several ways (2008). This can be inclusive of an adverse effect on issues of glucose regulation, a deregulation of the neuroendocrine appetite regulator thus resulting in excessive food intake and reduced energy expenditure. Chronic partial sleep restriction, a unique behaviour that appears to have developed with the dawn of a 24-hour society, calls for quick behavioural intervention.

Besides biological factors, environmental and social factors are speculated to cause obesity that in turn leads to the development of diabetes. There are profound changes in the dieting habits of people. These changes coupled with a decrease in physical actions lead to the development of diabetes and related complications (Yach, Stuckler & Brownwel 2006). Diabetes trends are also strongly attributed to environmental factors existent at birth.

The factors are the mother’s body mass index, the weight of the child at birth, growth trajectories of the child in early life, later eating traditions, activities in adulthood, and other complications (Yach, Stuckler & Brownwel 2006). Children with overweight or diabetic mothers are more liable to acquire the condition than those with lean mothers (Dabelea 2007).

Implications of Diabetes

Diabetes has several implications on the economy. As Yach et al. discuss, diabetes is an economic issue as much as it is a health issue (2006). Diabetes has glaring repercussions on the economy. It is also an indicator of the changing socio economic times. Part of the visible implications include the enlargement of labour market and opportunities for women, increasing costs of healthy foods, jobs that limit physical activities, increased food intake away from home, and a growing quantity of caloric ingestion with decreasing overall food prices. The treatment of these conditions siphons a huge chunk of money from the health system. It is a burden to the society as the resources channelled towards diabetes can be useful elsewhere.

A case of America demonstrates an explosive rate of uncontainable diabetes. The amount of money used to manage the disease is an equivalent to that used in twenty years of natural aging (American Diabetes Association 2003). Unfortunately, despite all the resources channelled towards diabetes the public does not still receive the right amount of care needed. The situation is worse for individuals in developing countries as they foot their own medical bills. In countries like India, a diabetic needs to spend fifteen to twenty five per cent of their household income for treatment. In Tanzania, it is 25% of total wage or 20% per capita health expenditure.

The burden on health systems appears to be a tip of the iceberg. Individuals cover accrued costs as they have to contend with decreased household income, premature retirements, unemployment in some instances, and overdependence on welfare and charity, which at times lower returns on education (Hogan, Dall & Nikolov 2003). The society has its fair share as the burden of obesity spills over to the non-obese through cross subsidization of commodities.

Diabetes has negative implications on pregnant women and their foetuses because they stand high chances of undergoing caesarean section. Notably, careful monitoring of diabetic pregnant women can enhance safe pregnancy and natural childbirth. Nevertheless, long-term public health goal ought to eradicate type 2 diabetes and gestational diabetes by regulating women’s weight in their lifetimes (Rosenberg et al. 2005; Lawrence, Lukacz, Liu, Nager & Luber 2007). Pregnancy and the postnatal period can be an opportunity during which women are more open to counselling concerning the risks of obesity and more likely to make behavioural changes that enhance their health in the long run (Yogeva & Visser 2009).

Possible Solutions to the Problem

Approaches aimed at decreasing fat mass are the cornerstones for the prevention and treatment of obesity (Lois and Kumar 2009). Physical activities alongside a healthy diet with a controlled calorie intake remain the best and affordable treatments there can ever be. Anti-obesity drugs and bariatric surgery are also useful in achieving similar results (Dixon 2009).

Prevention and intervention approaches ought to focus on detailed knowledge of causes of diabesity (Zindah et al. 2008). Failure to do so results in scattered efforts and poor assessment of the situation. Adverse effects on public health eventually ensue (Yach, Stuckler & Brownwel 2006). There needs to be clear definitions of the conditions at all levels for the development of comprehensive intervention plans. One such approach that works for many countries is the increasing of taxes on tobacco products to discourage misuse.

Research on cost effective plans to fill the causal niche ought to be conducted regionally (Ludwig et al. 2011; Naser, Gruber & Thomson 2006). This results in tailor-made approaches that are well suited for environmental and economic situations at hand (Fisher-Hoch et al. 2010).

One other viable solution is the control of certain types of foods in the market. Foods with high calorie content should be sold in small quantities. Markets in Africa are currently flooded with cheap foods that have a high content of refined oil (Prentice 2006). Controlling the quality of food available for consumption goes a long way in helping solve the situation that is already out of hand (Hjartåker, Langseth & Weiderpass 2008).

Psycho education is quite a useful tool. Information can be extremely powerful when well used. Prevention is better than cure. It is vital that the widespread, chronic diseases are well known, comprehended and acted on instantly (World Health Organization 2005).

Conclusion

The bitter truth remains that obesity and diabetes are ‘enemies within.’ They eat up the society bit by bit and have massive implications on their victims. Diabetes affects people directly or indirectly. Consequently, many governments channel resources towards curbing the disease and impose heavy taxes on their citizens to cater for national medical cover. Despite the looming bleak future of the diseases, there are several potential solutions to the stalemate. Most of the causal factors are within control. I dare say the enemy within can be approached without fear and tackled efficiently.

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