Obesity is a disease that has plagued the modern-day man in recent times. Access to highly processed foods and a decrease in physical activity are key contributors to this ailment. Researchers are hard at work looking into what other underlying factors lead to obesity, especially given its relationship with the onset of Type 2 Diabetes, Cardiovascular diseases, and liver disease. We will take an in-depth look at metabolic inflammation and its role in the onset of obesity in this article. Let’s dive in.

1. What is obesity?

Obesity is characterized by a low-grade chronic state of inflammation in which the level of pro-inflammatory cytokines such as TNF-α, IL-6, and CRP are increased. It is a state in which there is an over-accumulation of subcutaneous and/or abdominal adipose tissue. This adipose tissue is no longer considered inert and mainly devoted to storing energy; it is emerging as an active tissue in the regulation of physiological and pathological processes, including immunity and inflammation.

Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To determine your body mass index, divide your weight in pounds by your height in inches squared and multiply by 703. Or divide your weight in kilograms by your height in meters squared.

BMI	Weight status
Below 18.5	Underweight
18.5-24.9	Normal
25.0-29.9	Overweight
30.0 and higher	Obesity

For most people, BMI provides a reasonable estimate of body fat. However, BMI doesn’t directly measure body fat, so some people, such as muscular athletes, may have a BMI in the obesity category even though they don’t have excess body fat.

2. What is Diabesity?

‘Diabesity’ is the term for diabetes occurring in the context of obesity. This form of obesity-dependent diabetes has emerged as a major public health problem in recent times. Though it is basically explained by insulin resistance and pancreatic beta-cell dysfunction, new patterns have evolved to explain these modifications in the context of the modern spates of obesity and diabetes.

3. Is obesity an inflammatory condition?

The connection between obesity and inflammation has been often come up in debate in the recent past. Unbeknownst to many, the link between these conditions was made decades ago. Over a century ago, high doses of a class of anti-inflammatory compounds including aspirin called salicylates were used to treat Type 2 diabetes. In some cases, the symptoms of diabetes totally disappeared. Unfortunately, this treatment was discontinued due to the serious side effects caused by the high doses of salicylates.

We will now look at the questions of our topic today in-depth; Does obesity cause inflammation, or is inflammation caused by something secondary to obesity (like high blood sugar or triglycerides)? How about diabesity? Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body initiate an inflammatory response to diabesity? Let us tackle each item separately.

4. How does Inflammation Cause Diabesity?

We look at some lines of evidence that show that inflammation directly causes obesity and diabesity.

• The development of diabesity has been shown to follow inflammation. Raised levels of inflammatory cytokines predict impending weight gain. In a study carried out, the infusion of inflammatory cytokines into healthy, normal-weight mice caused insulin resistance. This concept is also illustrated by the fact that people with other chronic inflammatory conditions are at higher risk of developing Type2 Diabetes, for example, about one-third of chronic Hepatitis C patients develop T2DM, and those with rheumatoid arthritis are also at higher risk.
• In obesity, inflammation has been noted to start in the fat cells themselves. As fat mass expands, inflammation increases. An explanation for this may be the dysfunction of the mitochondria (the “power plant” of our cells) caused by the increased stress obesity puts on cellular function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they produce an excess of reactive oxygen species (ROS) which in turn starts an inflammatory cascade within the cell.
• Further, inflammation of the fat tissue causes insulin resistance, which is the primary feature of T2DM. TNF-α, a cytokine (small protein) released during the inflammatory response, has been repeatedly shown to cause insulin resistance. Several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein, have also been shown to cause insulin resistance.
• Also, inflammation of the brain (specifically the hypothalamus) causes leptin resistance, which often precedes and accompanies insulin resistance and T2DM. Leptin is a hormone that regulates appetite and metabolism. It does this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolism are impaired and weight gain and insulin resistance result.
• When there is inflammation of the gut, there arises leptin and insulin resistance. This may occur via an increase in lipopolysaccharide (LPS), an endotoxin produced by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver and weight gain.

5. How does Diabesity Cause Inflammation?

In the past, fat was considered an inactive tissue with no biological action. It wasn’t considered for much other than storing energy. It has now emerged that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. This metabolic activity of fat is the key to understanding its role in diabesity.

6. Why would obesity cause inflammation?

The first theory is that obesity-induced inflammation a protective mechanism that prevents the body from losing mobility or fitness. Fat storage is an anabolic process, which means it builds up the organs and tissues. Inflammation, on the other hand, is a catabolic process. Catabolism breaks down organs and tissues. It’s possible that the activation of catabolism via inflammation is the body’s attempt to keep weight within acceptable bounds. Evidence that experimentally induced local inflammation in fat tissue improves insulin resistance and causes weight loss supports this theory.

The second theory is that obesity-induced inflammation is simply a malfunction that was never selected against human evolution. Obesity and its related disorders have been extremely rare throughout human history, and have only become common in the past 40 years. The surplus of modern, processed foods that accompanies diabesity is also a relatively new phenomenon. It’s possible that the stresses of obesity are similar enough to the stresses of an infection that the body reacts to obesity in the same way it would to an infection: via inflammation. Supporting this theory is evidence that the same intracellular, inflammatory stress pathways are activated in both obesity and infection.

7. Tackling Inflammation in the control of diabesity

We can, therefore, conclude that inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.
Reduction of inflammation is a major key in preventing and treating diabesity. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.

References

1.    NCBI (2003): Diabesity: an inflammatory metabolic condition. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/14598860

2.    NCBI (2013): Obesity, Inflammation, and Diet. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819692/

3.    NCBI(2006): Inflammation and insulin resistance. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1483173/

4.    Chris Kessler (2019): How Inflammation Makes You Fat and Diabetic (And Vice Versa). Retrieved from https://chriskresser.com/how-inflammation-makes-you-fat-and-diabetic-and-vice-versa/

In previous articles, I have discussed the role of metabolic Inflammation in obesity and diabetes. Today, we will narrow down to the specifics of what insulin resistance is, its effects and how metabolic inflammation increases the chances of one developing it.

1. What is Insulin resistance?

Approximately 30% of Americans, and up to 50% in the 60 years and over the bracket, have a silent blood sugar problem known as insulin resistance. Insulin resistance increases the risk for prediabetes, Type 2 diabetes and a host of other serious health problems, including heart attacks, strokes, and cancer.

What therefore is Insulin Resistance? It is when cells in your muscles, body fat and liver start repelling or ignoring the signal being sent out by the hormone, insulin—which is to take glucose from the bloodstream into our cells for breakdown or storage. Glucose, commonly called blood sugar, is the body’s main source of fuel.

1. How does Insulin Resistance Develop?

Some factors that determine insulin resistance are aging and ethnicity but the driving forces seem to be excess body weight, too much belly fat, a lack of exercise, smoking, and even sleep depravity.

With time, and as the insulin resistance develops, more insulin is produced by your body as it tries to fight back. After an accumulated period of time, several years even, the beta cells in your pancreas get worn out because of all the extra work and can no longer keep pace with the increased demand for insulin. Then – years after insulin resistance stealthily started – your blood sugar may spike and you may manifest prediabetes or type 2 diabetes. You are also at risk of developing the non-alcoholic fatty liver disease (NAFLD), a condition that increases your risk for liver damage and heart disease.

2. What are the Signs and Symptoms of Insulin Resistance?

Insulin resistance does not always manifest to the naked eye but here are some signs to look out for:

• A large waist. Experts say the best way to tell whether you’re at risk for insulin resistance involves a tape measure and moment of truth in front of the bathroom mirror. A waist that measures 35 inches or more for women, 40 or more for men (31.5 inches for women and 35.5 inches for men if you’re of Southeast Asian, Chinese or Japanese descent)6 increases the odds of insulin resistance and metabolic syndrome, which is also linked to insulin resistance.
• You have additional signs of metabolic syndrome. According to the National Institutes of Health, in addition to a large waist, if you have three or more of the following, you likely have metabolic syndrome, which creates insulin resistance.
• High triglycerides. Levels of 150 or higher or taking medication to treat high levels of these blood fats.
• Low HDLs. Low-density lipoprotein levels below 50 for women and 40 for men – or taking medication to raise low high-density lipoprotein (HDL) levels.
• High blood pressure. Readings of 130/85 mmHg or higher, or taking medication to control high blood pressure
• High blood sugar. Levels of 100-125 mg/dl (the prediabetes range) or over 125 (diabetes).
• High fasting blood sugar (or you’re on medicine to treat high blood sugar). Mildly high blood sugar may be an early sign of diabetes.
• You develop dark skin patches. If insulin resistance is severe, you may have visible skin changes. These include patches of darkened skin on the back of your neck or on your elbows, knees, knuckles or armpits. This discoloration is called acanthosis nigricans.8

3. Chronic low-grade inflammation and the development of insulin resistance

As early as the 1950’s, there was epidemiological evidence suggesting a correlation between inflammation and insulin-resistant states such as obesity, but the mechanistic links were unknown. In the last decade, however, it has become increasingly evident that obesity and the concomitant development of inflammation are major components of insulin resistance. Studies in human obesity and insulin resistance have revealed a clear association between the chronic activation of pro-inflammatory signaling pathways and decreased insulin sensitivity. For example, elevated levels of tumor necrosis factor-α (TNF), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin-resistant states. In addition, the inflammatory marker C-reactive protein (CRP), a non-specific acute phase reactant, is commonly elevated in human insulin-resistant states. Also, experiments in naturally occurring rodent models of obesity, knockout and transgenic mice, as well as detailed studies of insulin signaling at the molecular level have begun to elucidate the mechanistic links between obesity-induced inflammation and insulin-resistant states.

4. What Health Conditions are Related to Insulin Resistance?

An estimated 87 million American adults have prediabetes; 30-50% will go on to develop full-blown type 2 diabetes. In addition, up to 80% of people with type 2 diabetes have NAFLD. But those aren’t the only threats posed by insulin resistance.

Thanks to years of high insulin levels followed by an onslaught of cell-damaging high blood sugar, people with insulin resistance, prediabetes, and type 2 diabetes are at high risk for cardiovascular disease. Insulin resistance doubles your risk for heart attack and stroke – and triples the odds that your heart attack or ‘brain attack’ will be deadly, according to the International Diabetes Federation.

Meanwhile, insulin resistance and metabolic syndrome are also linked with higher risk for cancers of the bladder, breast, colon, cervix, pancreas, prostate and uterus.11, 12  The connection: High insulin levels early in insulin resistance seem to fuel the growth of tumors and to suppress the body’s ability to protect itself by killing off malignant cells. 13

Research has also found a strong association between insulin resistance and memory function decline, increasing the risk of Alzheimer’s disease.

5. Can understand the causes of Insulin Resistance aid in future preventive approaches?

As obesity-associated chronic low-grade inflammation is responsible for the decrease of insulin sensitivity, obesity is a major risk factor for insulin resistance and related diseases such as type 2 diabetes mellitus and metabolic syndromes. The state of low-grade inflammation is caused by over-nutrition which leads to lipid accumulation in adipocytes.

Obesity might increase the expression of some inflammatory cytokines and activate several signaling pathways, both of which are involved in the pathogenesis of insulin resistance by interfering with insulin signaling and action. It has been suggested that specific factors and signaling pathways are often correlated with each other; therefore, both of the fluctuations of cytokines and the status of relevant signaling pathways should be considered during studies analyzing inflammation-related insulin resistance.

References

1. NCBI (2007): Inflammation and Insulin Resistance. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2246086/
2. Scientific American(2009): Does Inflammation Trigger Insulin Resistance and Diabetes? Retrieved from https://www.scientificamerican.com/article/inflammatory-clues/

3. NCBI (2006): Inflammation and Insulin Resistance. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1483173/
4. org (2008): Skeletal muscle insulin resistance: role of inflammatory cytokines and reactive oxygen species. Retrieved from https://www.physiology.org/doi/full/10.1152/ajpregu.00561.2007
5. Hindawi (2015): Mechanisms Linking Inflammation to Insulin Resistance. Retrieved from https://www.hindawi.com/journals/ije/2015/508409/

6. Endocrineweb(2019): Insulin Resistance Causes and Symptoms. Retrieved from https://www.endocrineweb.com/conditions/type-2-diabetes/insulin-resistance-causes-symptoms

A growing body of data shows that type 2 diabetes is at least in part rooted in inflammation. The higher a person’s body mass index, the more pro-inflammatory macrophages they have in their adipose tissue, and the higher their chances of developing T2D. In this article, we will highlight the emerging role of inflammation in the pathophysiology of diabetes. We will also analyze the implicated inflammatory pathways and biomarkers of inflammation in diabetes and metabolic diseases.

1. The metabolic syndrome and metabolic Inflammation

Metabolic syndrome often precedes type 2 diabetes and cardiovascular disease. It is characterized by high blood pressure, a large waist circumference, elevated fasting glucose and triglycerides, and low HDL cholesterol.

Metabolic inflammation is currently a hot research topic, wherein peculiarities in metabolic and inflammatory pathways are looked into for their possible contribution to atherosclerosis, Type 2 diabetes and insulin resistance (IR). In MI, insulin signaling is impeded by inflammation caused by obesity. Metabolically activated macrophages are key cells in the process. They are believed to spike both pro- and anti-inflammatory pathways in reaction to lipid spillover from adipocytes.

Diabetes is a complex metabolic disorder affecting the glucose status of the human body. The main clinical diagnostic features are impaired glucose tolerance and hyperglycemia. These occur as the result of an absolute or relative insulin deficiency or resistance to its action. Chronic hyperglycemia associated with diabetes can result in end-organ dysfunction and failure which can involve the retina, kidneys, nerves, heart and blood vessels. There is a  clinical relationship between diabetes and atherosclerotic cardiovascular disease, with the risk for cardiovascular disease (CVD) being significantly elevated in patients with diabetes.

Typically, CVD occurs one to two decades earlier in people with diabetes, with the more aggressive, severe and diffuse distribution. The first WHO Global report on diabetes published in 2016 demonstrates that the number of adults living with diabetes has almost quadrupled since 1980 to 422 million adults and this is expected to rise to 552 million by 2030. There is, therefore, a need for effective novel therapeutic approaches for the treatment and/or prevention of diabetes and atherosclerotic disease.

Various proposals and hypotheses have been developed to describe the mechanisms involved in the propagation of diabetes, mainly focusing on T2D. The increase in the prevalence of the condition has been related to well-recognized risk factors, such as the adoption of a western lifestyle, sedentary lives, lack of physical activity and an energy-dense diet.

Genetic predisposition, ethnicity, and aging are not modifiable risk factors for T2D. Other factors such as being overweight or obese, an unhealthy diet, insufficient physical activity and smoking are modifiable through behavioral and environmental changes. However, increasing evidence has shown that inflammatory pathways are common in both modifiable and non-modifiable factors.

2. When was inflammation first thought to cause diabetes?

Observational studies provided the first evidence for the possible association between inflammation and diabetes. Over a century ago, the administration of high doses of sodium salicylate led to decreased glycosuria in people with a suspected or definite diagnosis of diabetes.  Later studies on the role of inflammation in diabetes revealed that this hypoglycaemic action was related to the inhibition of the serine kinase IkappaB kinase-beta (IKKbeta), which correlates with the post-receptor action of insulin.

A landmark study to correlate inflammation with diabetes was conducted in animal models by Hotamisiligil et al., in 1993 and it revealed that the role of tumor necrosis factor-alpha (TNF-alpha) in obesity and particularly in insulin resistance and diabetes. Epidemiologic associations of inflammation with obesity and T2D were made when circulating concentrations of markers and mediators of inflammation and acute-phase reactants including fibrinogen, C-reactive protein, interleukin (IL)-6, plasminogen activator inhibitor-1, sialic acid, and white cells, have been shown to be elevated in these conditions.

Over the next decades, numerous studies on human and animal models provided further supporting evidence for the role of inflammation in the initiation and progression of diabetes. Accumulative evidence suggests that chronic activation of pro-inflammatory pathways in target cells of insulin action may contribute to obesity, insulin resistance and related metabolic disorders including T2D. The identification of potential pathways connecting inflammation to diabetes has produced growing interest in targeting inflammation to help prevent and control diabetes and related conditions, as well as improving risk stratification for diabetes by using inflammatory biomarkers as potential indexes.

3. What is the relationship between Metabolic Disorders and Inflammation in Type 2 Diabetes?

In several pathophysiological studies carried out, our understanding of insulin resistance and secretion in the course of disease onset and progression has been expanded. Subjects at risk of T2D display an initial state of insulin resistance compensated by hypersecretion of insulin in the beta cells. In the clinical course of the disease this pancreatic functional reserve is eventually unable to cope with the required insulin secretion and by the time diabetes is diagnosed, beta cells are no longer able to secrete enough insulin.

Although the relative contribution of beta-cell dysfunction and insulin resistance can vary in people with T2D, it is generally accepted that abnormal insulin sensitivity precedes the clinical diagnosis of diabetes by up to 15 years. Therefore, along with mechanistic studies investigating mechanisms forming the basis of insulin resistance, more recent research has also focused on the pathways leading to beta-cell failure.

4. Is there evidence of Inflammation in Other Organs in People with Type 2 Diabetes?

There is inconclusive evidence that the inflammatory state in T2D can spread to other organs such as the liver, the neural system and possibly skeletal muscle. More research is needed to support this evidence.

5. What are the Future Perspectives for the Treatment of Diabetes?

Below are some of the approaches currently being investigated.

1. Innovative approaches on T2D to gauge anti-inflammatory diets and moderate an individual’s microbiome are under study.
2. Clinical trials examining the effects of vitamin D supplementation on serum levels of inflammatory markers have provided inconsistent results, with no evidence of effects in most trials, or effects on selected markers in others.
3. There are also studies investigating whether antagonists of leukotriene production enzymes – 5-lipoxygenase (5-LO), 5-LO-activating protein and LTA4 hydrolase – or receptor binding BLT1 have cardiometabolic outcome benefits, however, these results have not yet been reported.
4. The potential for targeting cholinergic pathways, immune modulation or other mediators of inflammation such as JNK and toll-like receptors (TLRs) are also being researched.
    

6. What is the future of understanding metabolic inflammation as a cause of diabetes?

Given the increasing prevalence of diabetes, it is crucial that research focuses on its prevention as well as its treatment. Heart disease, metabolic syndrome and type 2 diabetes (T2D) all have in common the increased concentration of circulatory cytokines as a result of inflammation. Inflammatory cytokines are produced by different cell types and secreted into the circulation, where they regulate different tissues through their local, central and peripheral action.

An improved understanding of the mechanisms linking inflammation to diabetes and related complications has stimulated interest in targeting inflammatory pathways as part of the strategy to prevent or control diabetes and its complications.

T1D is considered to be more of an immunological response rather than a metabolic disorder and the preliminary results of trials using anti-inflammatory and immunomodulatory medication are promising. These treatments in combination with the possible use of stem cells to regenerate pancreatic beta cells could potentially be the key to the permanent treatment of T1D. Therefore, after a holistic review of the possible mechanisms that lead to T1D and T2D and the numerous already described inflammation pathways that are involved, it becomes more and more clear that future research should focus on simultaneous suppression of various inflammatory response pathways rather than focusing on one pathway at a time.

References

1. NCBI (2017): Nutritional modulation of metabolic inflammation. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28710289

2. EM-Consulte (2012): Inflammation and type 2 diabetes. Retrieved from https://www.em-consulte.com/en/article/735580

3. ECR (2019): The Role Of Inflammation In Diabetes: Current Concepts And Future Perspectives. Retrieved from https://www.ecrjournal.com/articles/role-inflammation-diabetes-concepts-future

The modern diet contains a large number of simple sugars. From bread to donuts, to carbonated drinks to chocolate, cookies, and candy, everywhere you look, temptation abounds. The potential impact on the health of diets rich in free sugars, and particularly fructose, is of major concern. Does the sugar we take have an impact on insulin resistance and obesity? In this article, we look at this risk and the effects of insulin resistance.

1. Sugar and Insulin resistance….

Sugar has a bittersweet reputation when it comes to health. It occurs naturally in all foods that contain carbohydrates, such as fruits and vegetables, grains, and dairy. Consuming whole foods that contain natural sugar is safe. Plant foods also have high amounts of fiber, essential minerals, and antioxidants, and dairy foods contain protein and calcium.

Where does the problem with sugar come about? Added sugar, which is usually extracted or synthesized ……

There is plenty of evidence to suggest that consuming too much sugar can have a negative effect on our metabolic health. Regular sugar consumption produces a constant release of the hormone insulin. Over a period of time, it can lead to serious problems, such as the synthesis of triglycerides, insulin resistance, fatty liver disease, type II diabetes, an increase in very-low-density lipoprotein (the bad kind of cholesterol), and the accumulation of fat on all tissues.

Added sugar intake may contribute to and certainly does exacerbate insulin resistance. For example, added sugar intake is associated with higher blood pressure, inflammation, weight gain, fatty liver disease, health issues that can lead to insulin resistance, and further exacerbation of these issues. Added sugars cater to particularly energy-hungry but metabolically inefficient cells, including senescent cells, cancerous cells, and even quickly proliferating pathogenic bacteria in the gut.

Several genetic and lifestyle factors can contribute to how likely you are to develop insulin resistance. But even if you have a genetic risk, you can help yourself with regular exercise, a balanced diet, avoidance of added dietary sugars, healthy sleep patterns, and stress reduction activities.

Risk factors for insulin resistance and prediabetes include:

• Obesity
• Aging
• physical inactivity
• high cholesterol
• blood pressure
• sleep disorders or circadian rhythm disruption

It is said that one in three Americans—including half of those age 60 and older— have insulin resistance.

2. What exactly is Insulin Resistance?

Insulin resistance is when cells in your muscles, body fat, and liver start resisting or ignoring the signal that the hormone insulin is trying to send out—which is to grab glucose out of the bloodstream and put it into our cells. Glucose, also known as blood sugar, is the body’s main source of fuel. We get glucose from grains, fruit, vegetables, dairy products, and drinks that bring break down into carbohydrates.

3. How does Insulin Resistance develop?

While genetics, aging, and ethnicity play roles in developing insulin sensitivity, the driving forces behind insulin resistance include excess body weight, too much belly fat, a lack of exercise, smoking, and even not getting enough sleep.

As insulin resistance develops, your body fights back by producing more insulin. Over months and years, the beta cells in your pancreas have been working so hard to make insulin get worn out and can no longer keep pace with the demand for more and more insulin. Then – years after insulin resistance silently began – your blood sugar may begin to rise, and you may develop prediabetes or type 2 diabetes. You may also develop non-alcoholic fatty liver disease (NAFLD), a growing problem associated with insulin resistance that boosts your risk for liver damage and heart disease.

4. What are the Signs and Symptoms of Insulin Resistance?

Insulin resistance can be triggered by a combination of factors linked to weight, age, genetics, being sedentary, and smoking.

– Polycystic ovary syndrome (PCOS): Insulin resistance can worsen the symptoms of PCOS, which can include irregular menstrual cycles, infertility, and periods that cause pain.

– A large waist. Experts say the best way to tell whether you’re at risk for insulin resistance involves a tape measure and a moment of truth in front of the bathroom mirror. A waist that measures 35 inches or more for women and 40 or more for men (31.5 inches for women and 35.5 inches for men if you’re of Southeast Asian, Chinese, or Japanese descent) increases the odds of insulin resistance and metabolic syndrome, which is also linked to insulin resistance.

– You have additional signs of metabolic syndrome. According to the National Institutes of Health, in addition to a large waist, if you have three or more of the following, you likely have metabolic syndrome, which creates insulin resistance.

• High triglycerides. Levels of 150 or higher, or taking medication to treat high levels of these blood fats.
• Low HDLs. Low-density lipoprotein levels below 50 for women and 40 for men – or taking medication to raise low high-density lipoprotein (HDL) levels.
• High blood pressure. Readings of 130/85 mmHg or higher or taking medication to control high blood pressure
• High blood sugar. Levels of 100-125 mg/dl (the prediabetes range) or over 125 (diabetes).
• High fasting blood sugar (or you’re on medicine to treat high blood sugar). Mildly high blood sugar may be an early sign of diabetes.

– Acanthosis nigricans: This skin condition can develop in people with insulin resistance. It involves dark patches forming on the groin, armpits, and the back of the neck.

5. What health conditions are related to Insulin Resistance?

The most common health condition related to Insulin Resistance is prediabetes and the resultant Type 2 Diabetes. Insulin resistance also doubles your risk for heart attack and stroke – and triples the odds that your heart attack or ‘brain attack’ will be deadly.
Insulin resistance and metabolic syndrome are also linked with a higher risk for cancers of the bladder, breast, colon, cervix, pancreas, prostate, and uterus. This is because the high insulin levels early in insulin resistance seem to fuel the growth of tumors and suppress the body’s ability to protect itself by killing off malignant cells.

Furthermore, research has found a strong association between insulin resistance and memory function decline, increasing the risk of Alzheimer’s disease.

6. Can you prevent or reverse insulin resistance?

The good news is that, yes, insulin resistance can be prevented and also reversed in some cases. Here is what you can do:

• Get recommended amounts of physical activity and structured exercise
• Get adequate sleep
• eat when the sun is up(we are more insulin resistant at night and after a night of poor sleep, due to disrupted circadian rhythms that help regulate our metabolic state)
• Reducing stress and, therefore stress-related inflammation
• Maintaining a healthy weight
• Increasing your plant fiber intake.

All of the above can help improve your insulin sensitivity. It has been shown that combining both diet and exercise have the most impact on insulin sensitivity.

In a fascinating University of New Mexico School of Medicine, study published in the International Journal of Obesity, overweight people who lost 10% of their weight through diet plus exercise saw insulin sensitivity improve by an impressive 80%. Those who lost the same amount of weight through diet alone got a 38% increase. And those who simply got more exercise, but didn’t lose much weight, saw almost no shift in their level of insulin resistance.

Intermittent fasting is also another way in which you can reverse your insulin resistance. This is because it gives your body a break from insulin and glucose signaling pathways that promote cell proliferation and inflammation and may help increase insulin sensitivity.

7. What, therefore, is the relationship between sugar and Insulin Resistance?

There is an association between diets high in sugars (predominantly sucrose) and the risk of disease, and experimental studies have shown that high intakes of fructose (over 100 g/d) can reduce insulin sensitivity. However, somewhat lower intakes may affect serum TG. The mechanisms for such associations or effects have not been convincingly demonstrated.

References:

1. NCBI (2016): A review of recent evidence relating to sugars, insulin resistance, and diabetes. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5174139/

2. Endocrineweb (2019): Insulin resistance causes and symptoms. Retrieved from https://www.endocrineweb.com/conditions/type-2-diabetes/insulin-resistance-causes-symptoms

3. Medical News Today (2019): What to know about insulin resistance. Retrieved from https://www.medicalnewstoday.com/articles/305567.php

4. The Sugar Movement (2016): Sugar vs Fat. Retrieved from https://thatsugarmovement.com/sugar-vs-fat/

5. Harvard Health Publishing (2017): The sweet danger of sugar. Retrieved from https://www.health.harvard.edu/heart-health/the-sweet-danger-of-sugar

6. NCBI (2014): Weight Loss, Exercise, or Both and Cardiometabolic Risk Factors in Obese Older Adults: Results of a Randomized Controlled Trial https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835728/