The moment we hear someone we know just diagnosed with PCOD, it’s a gut-wrenching feeling. It’s something you wish your loved ones never have to go through. Unfortunately, as I have noticed this trend is only climbing & affecting more younger populations with each passing day.

All this got me thinking. What is a PCOD? How bad is it? Is there a way to prevent it? Or are we all resigned to the fate of rapidly increasing such disorders? So many questions to answer, so I am sharing my research and I hope it will add some value to your lives.


**This is not a medically accurate article. If you are experiencing any symptoms contact your doctor immediately.


What is diabetes?

metabolic disorder of multiple etiology characterized by chronic hyperglycemia with disturbances of carbohydrate, fat (dyslipidemia), and protein metabolism resulting from defects in insulin secretion, insulin action, or both. i.e having a blood glucose level of 126 milligrams per deciliter (mg/dL) or more after an overnight fast (not eating anything).  Normally, the pancreas (an organ behind the stomach) releases insulin to help the body store and use the sugar and fat from the food we eat. Diabetes occurs when one of the following occurs:

  • When the pancreas does not produce any insulin
  • When the pancreas produces very little insulin
  • When the body does not respond appropriately to insulin, a condition called “insulin resistance”

Diabetes is a lifelong disease. Approximately 18.2 million Americans have the disease and almost one-third (or approximately 5.2 million) are unaware that they have it. An additional 41 million people have pre-diabetes. As yet, there is no cure. People with diabetes need to manage their disease to stay healthy.



Type 1 Diabetes

Type 1 diabetes is also called insulin-dependent diabetes. It used to be called juvenile-onset diabetes because it often begins in childhood. It is an autoimmune condition. It happens when the body attacks the pancreas with antibodies. The organ is damaged and doesn’t make insulin. Genes might cause this type of diabetes. It could also happen because of problems with cells in the pancreas that make insulin.

Many of the health problems that can come with type 1 happen because of damage to tiny blood vessels

Type 2 Diabetes

Type 2 diabetes used to be called non-insulin-dependent or adult-onset diabetes. But it’s become more common in children and teens over the past 20 years, largely because more young people are overweight or obese. About 90% of people with diabetes have type 2. 

It involves a more insidious onset where an imbalance between insulin levels and insulin sensitivity (Insulin resistance) causes a functional deficit of insulin. The pancreas usually creates some insulin. But either it’s not enough or the body doesn’t use it as it should. 

It is often milder than type 1. But it can still cause major health complications like type 1. People who are obese — more than 20% over their target body weight for their height — have an especially high risk of type 2 diabetes and the health problems that can follow. Obesity and an inactive lifestyle often cause insulin resistance. Although not everyone with type 2 diabetes is overweight. These things are responsible for about 90% to 95% of diabetes cases in the United States.

The Role of Pancreas in Diabetes

After eating, food travels to the stomach and small intestines, where it’s broken down into nutrients that include glucose. The nutrients are absorbed and distributed via the bloodstream. The pancreas is a gland located behind the stomach that performs an essential role in the digestion process. It creates enzymes that break down the fat, starches, and sugar in the food. It also contains:

  • Beta cells 
  • Alpha cells. 

Beta cells produce Insulin hormone: When we eat food, glucose is absorbed from our gut into the bloodstream, raising blood glucose levels. This rise in blood glucose causes insulin to be released from these cells so glucose can move inside the cells and be used. As glucose moves inside the cells, the amount of glucose in the bloodstream returns to normal and insulin release slows down.

Alpha cells release Glucagon: It is released in response to a drop in blood sugar, prolonged fasting, exercise, and protein-rich meals.

Beta and alpha cells are continually changing their levels of hormone secretions based on the glucose environment. Without the balance between insulin and glucagon, the glucose levels become inappropriately skewed. People with diabetes either don’t make insulin or their body’s cells are resistant to insulin (Insulin resistance), leading to high levels of sugar circulating in the blood, called simply high blood sugar (hyperglycemia).

Insulin role

The function of insulin is to help transform glucose into energy and distribute it throughout your body, including the central nervous system and cardiovascular system. Without insulin, cells are starved for energy and must seek an alternative source. This can lead to life-threatening complications. It is a key player in developing type 2 diabetes. Here are the high points:

  • The food you eat is broken down into blood sugar.
  • Blood sugar enters your bloodstream, which signals the pancreas to release insulin.
  • Insulin helps blood sugar enter the body’s cells so it can be used for energy.
  • Insulin also signals the liver to store blood sugar for later use.
  • Blood sugar enters cells, and levels in the bloodstream decrease, signaling insulin to decrease too.
  • Lower insulin levels alert the liver to release stored blood sugar so energy is always available, even if you haven’t eaten for a while.

The major effects of insulin on muscle and adipose tissue are: 

  • Carbohydrate metabolism: 
  1. It increases the rate of glucose transport across the cell membrane, (b) it increases the rate of glycolysis by increasing hexokinase and 6-phosphofructokinase activity, and (c) it stimulates the rate of glycogen synthesis and decreases the rate of glycogen breakdown. (2) Lipid metabolism: (a) it decreases the rate of lipolysis in adipose tissue and hence lowers the plasma fatty acid level, (b) it stimulates fatty acid and triacylglycerol synthesis in tissues, (c) it increases the uptake of triglycerides from the blood into adipose tissue and muscle, (d) it decreases the rate of fatty acid oxidation in muscle and liver. (3) Protein metabolism: (a) it increases the rate of transport of some amino acids into tissues, (b) it increases the rate of protein synthesis in muscle, adipose tissue, liver, and other tissues, (c) it decreases the rate of protein degradation in muscle (and perhaps other tissues). These insulin effects serve to encourage the synthesis of carbohydrates, fat, and protein, therefore, insulin can be considered to be an anabolic hormone. 
  • Carbohydrate Metabolism: Insulin acts at multiple steps in carbohydrate metabolism. Its effect on facilitated transport of glucose into fat and muscle cells via modulation of GLUT 4 translocation.
  • Lipid Metabolism: It is estimated that adipose tissue accounts for about 10% of insulin-stimulated whole-body glucose uptake. Insulin stimulates:
  1. Fatty acid synthesis in adipose tissue, liver, and lactating mammary glands along with 
  2. Formation and storage of triglycerides in adipose tissue and liver. 
  3. Intracellular glucose transport into adipocytes in the postprandial state is insulin-dependent via GLUT 4.
  • Muscle: Muscle accounts for about 60–70% of whole-body insulin-mediated uptake. Insulin promotes:
  1. Protein synthesis in a range of tissues. 
  2. Glucose uptake into muscle is essentially insulin-dependent via GLUT 4. Glucose entry enables glycogen to be synthesized and stored, and carbohydrates, rather than fatty acids or amino acids to be utilized as the immediately available energy source for muscle contraction. Insulin, therefore, promotes glycogen and lipid synthesis in muscle cells, while suppressing lipolysis and gluconeogenesis from muscle amino acids. In starvation, protein synthesis is reduced by 50%. 
  • Liver: While glucose uptake into the liver is not insulin-dependent, it accounts for about 30% of whole-body insulin-mediated glucose disposal, with insulin being needed to facilitate key metabolic processes. Through intracellular signaling described above, glycogen synthesis is stimulated while protein synthesis and lipoprotein metabolism are modulated. 
  • Endothelium and Vasculature: Insulin and its actions play an important role in various aspects of endothelial function. The functions of vascular endothelial cells are critical to many aspects of cardiovascular biology, with endothelial dysfunction being seen at a very early stage of atherosclerosis and its associated clinical risk factors. Endothelial cells not only provide the physical lining of the blood vessels but secrete various factors influencing vessel tone, platelet function, coagulation, and fibrinolysis. Clinical problems develop when these processes are imbalanced.
  • Brain: Insulin appears to act through other appetite-regulating neurotransmitters and peptides. Leptin and insulin appear to share a common signaling pathway in the hypothalamus. There is a suggestion of a potential link to Alzheimer’s disease, given insulin’s role in normal cognitive functioning and in the regulation of amyloid precursor protein and beta-amyloid itself. The possibility that syndromes associated with insulin resistance in the periphery, such as obesity and type 2 diabetes, may also be associated with insulin resistance in the brain, with dysregulation of appetite and body weight, is intriguing.
  • Pancreas: Pancreatic β cells possess receptors for both insulin and IGF-1. Insulin may have a role in regulating glucose-stimulated insulin secretion.
  • Pituitary: Insulin acts in concert with other hormones. Insulin stimulates growth hormone production from the pituitary gland, which in turn promotes IGF-1 production by the liver.
  • Kidney: Insulin regulates mineral transport and gluconeogenesis in the kidney and reduces urinary sodium excretion.
  • Gonads: Insulin receptors are found in the ovary and appear to have a role in enhancing estrogen and androgen production 
  • Bone: Insulin appears to be anabolic in bone. Insulin receptors are found in osteoblasts and osteoclasts. Insulin stimulates bone formation by osteoblasts and is also reported to suppress osteoclast function.

Commonly asked questions

What is insulin resistance?

Insulin resistance, also known as impaired insulin sensitivity, happens when cells in muscles, fat, and liver don’t respond as they should to insulin, which means they can’t efficiently take up glucose from blood or store it. Insulin resistance can be temporary or chronic and is treatable in some cases.

Under normal circumstances, insulin functions in the following steps:

  • The body breaks down the food you eat into glucose (sugar), which is your body’s main source of energy.
  • Glucose enters your bloodstream, which signals your pancreas to release insulin.
  • Insulin helps glucose in your blood enter your muscle, fat, and liver cells so they can use it for energy or store it for later use.
  • When glucose enters your cells and the levels in your bloodstream decrease, it signals your pancreas to stop producing insulin.

As long as the pancreas can make enough insulin to overcome cells’ weak response to insulin, blood sugar levels will stay in a healthy range. If cells become too resistant to insulin, it leads to: 

In addition to Type 2 diabetes, insulin resistance is associated with several other conditions, including:

What is the difference between insulin resistance and diabetes?

Anyone can develop insulin resistance — temporarily or chronically. Over time, chronic insulin resistance can lead to pre-diabetes and then Type 2 diabetes if it’s not treated or able to be treated. Prediabetes happens when blood glucose levels are higher than normal, but not high enough to be diagnosed as diabetes. Prediabetes usually occurs in people who already have some insulin resistance. Prediabetes can lead to Type 2 diabetes (T2D), the most common type of diabetes. T2D happens when your pancreas doesn’t make enough insulin or your body doesn’t use insulin well (insulin resistance), resulting in high blood glucose levels.

Type 1 diabetes (T1D) happens when your body’s immune system attacks and destroys the insulin-producing cells in your pancreas for an unknown reason. It is an autoimmune and chronic disease, and people with this condition have to inject synthetic insulin to live and be healthy. While it is not caused by insulin resistance, people can experience levels of insulin resistance in which their cells don’t respond well to the insulin they inject.

Type 2 diabetes happens when one or more of the following occurs:

  • Your pancreas doesn’t make any insulin.
  • Your pancreas makes very little insulin.
  • Your body doesn’t respond the way it should to insulin

Unlike people with type 1 diabetes, people with type 2 diabetes make insulin. But the insulin their pancreas releases isn’t enough, or their body can’t recognize the insulin and use it properly. (Doctors call this insulin resistance). When there isn’t enough insulin or the insulin isn’t used as it should be, glucose (sugar) can’t get into your cells. It builds up in your bloodstream instead. This can damage many areas of the body. Also, since cells aren’t getting the glucose they need, they don’t work the way they should.

Gestational diabetes is a temporary form of diabetes that can happen during pregnancy. It’s caused by insulin resistance that’s due to the hormones the placenta makes. Gestational diabetes goes away once you deliver your baby. Approximately 3% to 8% of all people who are pregnant people in the United States are diagnosed with gestational diabetes.

Healthcare providers often use a blood test called glycated hemoglobin (A1c) to diagnose diabetes. It shows your average blood sugar level for the past three months. In general:

  • An A1c level below 5.7% is considered normal.
  • An A1c level between 5.7% and 6.4% is considered prediabetes.
  • An A1c level of 6.5% or higher on two separate tests indicates type 2 diabetes.

People with Type 1 diabetes usually have a very high A1C and very high blood glucose levels upon diagnosis because their pancreas is producing very little or no insulin.

Who does insulin resistance affect?

Insulin resistance can affect anyone — you don’t have to have diabetes — and it can be temporary (for example, using steroid medication for a brief period causes insulin resistance) or chronic. The two main factors that seem to contribute to insulin resistance are excess body fat, especially around your belly, and a lack of physical activity. People who have prediabetes and Type 2 diabetes usually have some level of insulin resistance. People with Type 1 diabetes can also experience insulin resistance.

How common is insulin resistance?

Since there aren’t any common tests to check for insulin resistance and there aren’t any symptoms until it turns into prediabetes or Type 2 diabetes, the best way to measure the prevalence of insulin resistance is through the number of prediabetes cases. More than 84 million adults in the United States have prediabetes. That’s about 1 out of every 3 adults.

How does insulin resistance affect my body?


The development of insulin resistance typically increases insulin production (hyperinsulinemia) so your body can maintain healthy blood sugar levels. Elevated levels of insulin can result in weight gain, which, in turn, makes insulin resistance worse. Hyperinsulinemia is also associated with the following conditions:

Metabolic syndrome: 

Insulin resistance is also the main feature of metabolic syndrome, which is a set of features that link excess fat around the waist and insulin resistance to increased risk of cardiovascular disease, stroke, and Type 2 diabetes. Features of metabolic syndrome include:

  • Elevated blood glucose levels.
  • An elevated triglyceride level.
  • Low levels of high-density lipoprotein (HDL) cholesterol.
  • High blood pressure.

You don’t have to have all four of these features to have metabolic syndrome