INTRODUCTION

This article will discuss diabetes, the pathophysiology of the disease, types, autoimmune correlation, genetic predisposition, lifestyle, management and complications as well as the role of sugar consumption in the sequelae of the disease.

PREAMBLE

What if I tell you sugar does not cause diabetes! Many years of misconceptions have made believe that sugar consumption is the single most important cause of diabetes, if this rhetoric holds true then the only tangible conclusion would be that majority of children willhave diabetes, as children remain the most consumers of sweets. So, why is there no direct correlation between how much sugar is consumed by children and diabetes mellitus? Considering these facts,it should be reasonable to concluded that sugar consumption does not contribute to the etiology of the disease and even if it does, the notion wouldn’t hold in the pediatric population.

PANCREAS; THE CULPRIT ORGAN

The fundamental organ related problem in diabetes lies within the pancreas, an endocrine organ that also serves some exocrine functionsimportant for the digestive system. However, the pathophysiology of diabetes lies within the endocrine functions of the pancreas. The pancreas has many endocrine cells such as alpha, beta, delta, gamma and epsilon cells. All the cells have endocrine functions and found in pancreatic Islets of Langerhans, some have dual functions withexocrine functions found in pancreatic acinus and ducts.

Alpha cells secret glucagon, a stress hormone and an insulin buffer. The beta cells secret insulin which is a counter regulatory hormone for glucose, secreted in abundance in the fed state and the main culprit for diabetes mellitus. Delta cells secret somatostatins which help in maintaining balance between insulin and glucagon, there are also gamma cells (PP cells) which secret polypeptides that help regulate both endocrine and exocrine functions of the pancreas that affect appetite. Epsilon cells are the least mentioned but secrets ghrelin thehormone responsible for hunger and plays a major role in the sensation of hunger, and also responsible for obesity.

For the purpose of this discussion, we are going to focus on insulin and the pathophysiology of diabetes and its relationship with sugar consumption. Insulin is a growth hormone and the most important counter regulatory hormone against glucose. The fed state and digestion produce a lot of glucose so our maker in his infinite wisdom made insulin to be released in larger quantities when we eat. The goal is to calm the effects of an overwhelming glucose load on the body;so, under normal circumstances the body should always be in homeostasis (equilibrium) no matter how much sugar we consume. This is the main reason why most children are not suffering from diabetes. Insulin does not only buffer glucose but plays a permissive role in various electrolytes and glucose transportation into various tissues such as muscles and adipose via various transporters called GLUT for metabolic uses.

Glucose is an important source of energy for major organs and tissues, and for this reason the kidneys reabsorb any amount of glucose introduced into the body. The brain alone consumes 20-50% of total body glucose at rest for brain cell (neuron) survival. Skeletal muscles require 30% of total body glucose at rest and even more during aerobic exercise whilst the rest is shared amongst the liver, heart and kidneys. Glucose is so important to the body in such that it converts almost anything we eat into some form of glucose or something that eventually convert to glucose, and in prolonged starvation the body generates the chemical ketones in place of glucose for brain cellsurvival. As a matter of fact, there are diseases such as McArdle’s disease caused by deficient enzymes that prevent skeletal muscles from breaking down stored glycogen into energy, resulting in exercise intolerance.

PATHOPHYSIOLOGY OF DIABETES

There is no single pathophysiology that explains the cause of diabetes owing to the different types of the disease. However, they share a common denominator of high blood glucose (hyperglycemia). To understand the topic better it will be imperative to approach from the different types of diabetes as the various types have different pathogenic etiologies such as autoimmunity, lifestyle and various genetic predispositions, so for the purpose of this discussion, we will focus mainly on type I and type II diabetes even though there’s gestational as well as maturity onset diabetes of the young (MODY).

TYPE I DIABETES

Type I diabetes has a unique etiology that cannot be traced to lifestyle,and less likely to be caused by a genetic predisposition. The condition is caused by an autoimmune destruction of the pancreatic islet beta cells that result in insulin deficiency with consequent hyperglycemia. This means that a person who has type I diabetes couldn’t have lived a preventative life from the disease as the insulin deficiency is caused by an autoimmune destruction of the cells that produce insulin in comparison to hyperinsulinemia (high levels of insulin), which is the hallmark of type II diabetes with a high lifestyle and genetic predisposition, taking into consideration that both conditions lead to hyperglycemia.

TYPE II DIABETES

Unlike type I diabetes, type II diabetes is associated with hyperinsulinemia rather than insulin deficiency. In this scenario, if insulin is indeed a counter-regulatory hormone to glucose why shouldthere be hyperglycemia in the midst of high insulin levels. This is explained by insulin receptor malfunction and glucose transporter down regulation in type II diabetes that deregulates glucose uptake and usage by important cells and tissues (muscles, adipose, neurons etc.) with resultant hyperglycemia and glycation of different cells of the body causing serious complications.

There are various glucose transporters (GLUTS) in the body, howeverthe most important for this discussion will be GLUT 1-5. These transporters move glucose from blood into cells of various tissues to serve as fuel for metabolism; an action that reduces ambient blood glucose levels. Insulin is a growth hormone that plays a permissive role for various GLUTS in moving glucose to various tissues for metabolism. GLUT-4 is insulin dependent and a key culprit in type II diabetes. Certain modifications in glucose transporters by poisonssuch as alcohol and inflammation has led to defective and deficient glucose transport and disposal leading to hyperglycemia in the midst of high levels of insulin.

Excess abdominal visceral fat has been linked to sedentary lifestyle and studies have shown that the collection of visceral fat elicits inflammatory products that interfere with insulin function at the receptor / molecular level, which goes further to affect liver metabolism of glucose which in turn leads to hyperglycemia. This is the most direct linkage between lifestyle and type II diabetes. In addition to lifestyle, the American diabetic association has supported studies (Dean, et.al. 2004) that associate strong genetic predispositionfrom family history of type II diabetes to support that individuals with a family history of type II diabetes may store glucose differently in adipose tissues and have altered insulin sensitivities and resistance thatcan predispose them to type II diabetes even before symptoms appear.

DIABETES; WHEN SUGAR BECOMES A PROBLEM

This paragraph will discuss complications of diabetes mellitus and the reason why diabetes is arguably the most dangerous chronic disease in life. Let’s take a head-to-toe organ approach in discussing the various complications of the disease.

THE HEAD REGION

Diabetes is amongst the leading causes of blindness worldwide andthe most important cause of blindness in diabetics; it is also animportant risk factor for cerebrovascular accidents (stroke). Diabetes eye disease (retinopathy) is the lead cause of blindness in diabetics worldwide, this is as a result of thickening of the basement membrane of the small blood vessels of the retina as well as sorbitol accumulation in the eye. High blood glucose is converted to sorbitol by an enzyme in the body called aldose reductase. Sorbitol interacts with the lens of the eyes causing lens opacification (cataracts), blurring of vision and eventual blindness. Diabetes is also a blood vessel disease that causes decreased vascular capacitance and increased intravascular resistance, elevated blood pressure and eventual stroke by ischemia or hemorrhage.

THE THORAX (CHEST)

The chest houses important organs such as the heart and lungs. Poorly controlled diabetes downregulates the immune system predisposing the individual to infections including mucormycosis, a fungal upper respiratory tract infection from the Rhizopus species susceptible in diabetics with ketoacidosis (a metabolic complication in diabetes).

The heart is the final hub that connects all the blood vessels in the body, and blood pressure itself is generated from the heart. Insulin is a growth hormone so hyperinsulinemia promotes lipogenesis (fat formation) and obesity which is a major risk factor for cardiovascular disease. Ambient blood glucose levels in diabetes cause arteriosclerosis (hardening) of blood vessels of the heart which leads to hypertension, this occurs in conjunction with plaque buildup (atherosclerosis) within the vessels causing narrowing and eventual rupture of plaques that result in total occlusion and infarction (heart attack).

Diabetes does not only affect the vessels of the heart but also the nerves that control the heart causing autonomic dysfunction. There is no wonder that people with type II diabetes are twice as likely to suffer a cardiovascular related death and stroke than the general population (cdc.gov 2024).

THE ABDOMEN

The abdomen is where everything occurs, it houses the stomach and liver and within its retroperitoneal space lies the kidneys and the pancreas itself. Within the abdomen lies a very rich architecture of blood vessels incorporated in intraabdominal fat (omentum) to supply the visceral organs of the abdomen. Autonomic neuropathy of diabetes causes gastropathy, a condition that slows and in severe cases shuts down gastric emptying in a condition called gastroparesis leading to bloating and GI obstruction. Today diabetes is a leading cause of chronic kidney disease and the main culprit of end stage kidney disease and need for dialysis. Non-alcoholic fatty liver disease has a strong association with type II diabetes which in turn affect liver metabolism of glucose.

THE PELVIS

The pelvis lies the powerhouse of intimate pleasure. Diabetic neuropathy is a leading cause of erectile dysfunction in men causingaccelerated atherosclerosis and endothelial damage of penile vessels that impede nitric oxide flow needed for adequate erection; this occurs in conjunction with the nerves that supply the erectile tissue. Studies have shown that diabetes promotes UTI in women together with some gynecological infections such as yeast infection (candidiasis) as glucose in urine serves as a nidus for bacteria growth. Autonomic neuropathy of diabetes can cause bladder nerve damage leading to incomplete bladder emptying accompanied by glucosuria and a breeding ground for bacteria growth.

THE LOWER LIMB AND SKIN

Peripheral neuropathy is the underlying hallmark of diabetic foot ulcer. Peripheral neuropathy produces a mixture of symptoms from symmetric numbness, tingling sensation as well as sharp pains described as pins and needles yet difficult to explain as accompanied by loss of sensation to pain and temperature in the feet. The condition poses risks for injuries such as nails getting caught up in foot without knowing. This condition can also cause balance derangements that lead to Charcot’s arthropathy characterized by microfractures, bone deformity and eventual joint collapse. Frequent injuries lead to diabetic foot ulceration and deep bone infections (osteomyelitis) that is often difficult to treat due to nutrient vascular damage caused by persistent hyperglycemia. The eventual outcome is limb amputation and devastating disability, poor quality of life and depression. Skin conditions such as acanthosis nigricans (hyperpigmented leathery skin around neck) and spontaneous skin tag (acrochordons) development in visible areas on the skin.

MANAGEMENT

The best management of diabetes is awareness of uncontrollable risks such as age and genetic predispositions. Lifestyle modification often help in Type II diabetes, so it is worth considering weight loss programs with diet and exercise, avoidance of alcohol and cigarette smoking as well as keeping up with physician appointments. In severe cases when the above has failed and the diagnosis is made, one must stay compliant with oral antidiabetics, insulin and other injectables. Look out for cardinal signs of worsening diabetes such as polydipsia, polyuria and polyphagia i.e. frequent thirst, urination and hunger respectively. Polyuria and micro albuminuria (a special protein) can be the first sign of diabetic kidney disease, blur vision is also common in poorly controlled cases. The condition requires aggressive attention and can be very expensive as it requires a multi-faceted managementapproach from ophthalmologist (eye doctor), cardiologist, endocrinologist, nephrologist (kidney doctor), dermatologist, all the way to podiatrist.

CONCLUSION

The above discussed literature shows clearly that it is not the sugar that causes the diabetes but rather an autoimmune destruction of the cells that produce counter-regulatory hormone insulin in type I diabetes, and in type II diabetes, defects in glucose transportation into cells as well as insulin resistance due to receptor abnormality making it difficult for cellular uptake and clearance of ambient glucose levels.Even in extreme scenarios to stretch the topic to say that glucose is converted to fat which elicits inflammatory products that destroy insulin receptors and glucose transporters to cause type II diabetes, it will still fall back on the permissive action of the growth hormone insulin for the fat to be synthesized and stored, where the same insulinprevents lipolysis (the breakdown of fat).

In conclusion, once the diagnosis of diabetes is made, sugar becomes adangerous chemical in the body that destroys tissues and organs, so in a nutshell whether sugar causes diabetes or not it topples insulin as the cardinal feature of the disease, yet the importance of glucose cannot be overruled as it remains the single most important fuel for energy in the body other than oxygen, and as badly as labeled it produces a more indolent and longer-term complications when compared to insulin thatcauses both acute and chronic complications. Patients taking oral antidiabetics such as sulfonylureas and insulin will require close monitoring to avoid fatal hypoglycemia.

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