About 30 million people in the US have diabetes, of these; about one 8 million don’t know that they have it. Early diagnosis of diabetes can help in the treatment and possibly reversal of diabetes. But what is diabetes reversal?

Diabetes reversal is similar to long-term diabetes remission. As much as it is not a definite cure for diabetes, it means that a person with diabetes type 2 can have normal blood sugar levels for a number of years without having to take any diabetic medication. This can be achieved through a number of factors which we shall discuss below. Before getting there, let’s shed some light on type 2 diabetes.

Diabetes type 2 Reversal

Diabetes type two used to be a disease of the elderly. But with the adoption of a modern lifestyle, even young children are being plagued by this debilitating disease. Genetics and ethnicity play a role in the acquisition of diabetes type two, but diet and lifestyle factors are great contributors as well. And by controlling the later, a person predisposed to the disease can be able to avoid it in some cases.

Diabetes type 2 occurs due to the gradual build-up of insulin resistance. Insulin is the hormone that removes sugar from the bloodstream and stores it in cells. Over time, a person becomes less sensitive to the effects of insulin leading to a buildup of sugar in the blood. Beta cells are further stimulated to produce more and more insulin until eventually they are exhausted and depleted.

Reversal of diabetes type 2 targets the restoration of insulin sensitivity and in some cases the regeneration of beta cells. This means that a person with reversed diabetes should be able to maintain normal blood sugar levels without the use of diabetes medication. Research has shown that weight loss is one of the most effective approaches to achieving diabetes reversal.

Here are four ways to achieve healthy weight loss and diabetes reversal:

1.    Very Low-Calorie Diet

Several studies have looked at the effects of a very low-calorie diet on diabetes. In one study, two people followed a mostly liquid diet of 625-850 calories a day for 2-5 months, followed by a less restricted diet designed to help them keep off the weight they lost. Results showed that a low-calorie diet helps to reduce weight and improve insulin sensitivity. In another study, seven obese patients with type 2 diabetes were put on a very low-calorie diet of 900kcal and 115g of protein. This led to significant improvement in blood sugar control that was mainly attributed to improvements in insulin sensitivity.

Note that these types of diets are extreme. You have to work with a professional who will assess your fitness for undertaking such a drastic approach. Most people who have had success in reversing diabetes with this approach are those who have not had diabetes or a long time. This makes it important to start the weight loss journey as soon as possible after you’re diagnosed.

2.    Exercise

Regular exercise is another way of improving diabetes, but this has to be combined with diet and other measures in order to achieve diabetes reversal. Exercise needs commitment and dedication in order to bear fruits.

Regular exercise is associated with decreased demand for insulin as well as increased sensitivity to insulin. A 2015 study published showed that 67% of participants were able to achieve partial remission by taking part in a 6-months diet and exercise regimen. All the study participants were newly diagnosed with type 2 diabetes.

3.    Bariatric Surgery

Bariatric surgery helps one achieve weight loss by reducing their food intake. This, in the long run, has helped diabetes type 2 patients achieve reversal.

A 2010 study showed that bariatric surgery can help in diabetes reversal. Another 2013 study reported that 24% of participants with type 2 diabetes achieved remission six years after receiving gastric bypass surgery. The study concluded that:

“Bariatric surgery can induce a significant and sustainable remission and improvement of T2DM and other metabolic risk factors in severely obese patients. Surgical intervention within 5 years of diagnosis is associated with a high rate of long-term remission.”

Bariatric surgery is suitable only when your BMI is 35 or higher. It works best for people who’ve had diabetes for less than 5 years and they are not on insulin.

For newly diagnosed type 2 diabetics who are obese, this can be a suitable option to help them reverse diabetes.

4.    Intermittent Fasting

Intermittent means going without any food or drink with calories for a given amount of time. For example, you can restrict your eating to eight hours each day and you starve for the remaining sixteen hours. Caution: you need to consult with your doctor before embarking on a fast, even if it’s partial and for medical reasons.

A small study looked at three men between the ages of 40 and 67 who tried intermittent fasting for approximately 10 months. All were able to stop insulin treatment within a month of the study period. According to the author of the study Jason Fung, this study showed that intermittent fasting could be effective in reversing type 2 diabetes.

However, this result can only be used as anecdotal. Larger clinical trials need to be conducted to determine the clear effectiveness of this approach.

What Doesn’t Work?

There is a lot of hype when it comes to diabetes reversal. Shrewd businessmen have tried to exploit vulnerable patients by selling magic pills that they purport to cure for diabetes. They come in all forms of preparations such as:

• Over-the-counter pills
• Herbs
• Supplements
• Alternative medicines
• Homeopathic products
• Prescription drugs

If you or a loved one is living with type 2 diabetes it is important that you consult with your healthcare provider before embarking on any diabetes reversal program. As much as diabetes reversal is achievable, you need to be wary of greedy scammers eager to make a dishonest buck.

References

1. Healthline: Type 2 Diabetes Statistics and Facts. Retrieved from https://www.healthline.com/health/type-2-diabetes/statistics#1
2. NCBI (2019): Reversing Type 2 Diabetes: A Narrative Review of the Evidence. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520897/
3. NCBI (1998): Early and long-term effects of acute caloric deprivation in obese diabetic patients. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/3291612
4. Diabetes UK: Reversing Type 2 Diabetes. Retrieved from https://www.diabetes.co.uk/reversing-diabetes.html
5. NCBI (2013): Can diabetes be surgically cured? Long-term metabolic effects of bariatric surgery in obese patients with type 2 diabetes mellitus. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24018646

Flour is hard to avoid during meal times. Breakfast options mainly consist of toast, bagels, cereal, and pancakes. A convenient lunch is sandwiches, wraps, pasta or pizza. Dinner might come with its own temptations too. As a result, the average American now eats 10 servings of refined grains each day. What effect do these refined grains have on your health? Do consuming refined grains predispose you to Type 2 Diabetes? In this article, we will have a look at factors that could put you at risk.

1. What Is the Difference Between Whole Grains and Refined Grains?

While whole grains are very high in dietary fiber, refined grains are much lower in fiber and micronutrients.

Whole grains consist of three main parts:

1. Bran: The hard outer layer, containing fiber, minerals and
2. Germ: The nutrient-rich core, containing carbs, fat, protein, vitamins, minerals, antioxidants and plant compounds.
3. Endosperm: The middle layer, containing mostly carbs and small amounts of protein.

The bran and germ are the most nutritious parts of whole grains. They contain high amounts of many nutrients, such as fiber, B vitamins, iron, magnesium, phosphorus, manganese, and selenium.

During the refining process, the bran and germ are removed, along with all the nutrients they contain. Removing the nutrients from the grain has implications. On the upside, it makes things like bread doughy and spongy — textures we like and have come to crave. On the downside, the nutritional value of the food is severely compromised, and these striped grain products actually deplete our body’s reserves of important vitamins and minerals.

The nutrient content of refined flour is determined by the ‘extraction rate’ (the proportion of the grain retained after milling). Refined flour produced in Australia is milled to an extraction rate of 78-80% resulting in higher nutrient content (prior to fortification) than flour produced in countries using a lower extraction rate (e.g. 73-75% in the USA).

This leaves almost no fiber, vitamins or minerals in the refined grains. What’s left is rapidly digested starch with small amounts of protein.

2. What are the effects of consuming refined grains on our health?

• Blood sugar spikes: Because flour is easily digestible, it causes our blood sugar to spike, which could lead to a rise in insulin. The pancreas has to crank out a lot of insulin to metabolize the glucose in flour-rich foods, which can set the body up for insulin resistance, diabetes, and bodywide inflammation.Refined grains have a higher glycemic index, which is how quickly the body turns food into fuel or glucose.  A carbohydrate in wheat, called amylopectin A, is more easily converted to blood sugar than most other carbohydrates. Two slices of bread made with whole-wheat flour could raise blood sugar higher than six teaspoons of table sugar and higher than many candy bars.

• Overeating and Obesity: Obesity is the leading factor in Insulin resistance, Type 2 diabetes, and other chronic diseases. Eating too many refined carbs may be one of the main culprits. As they are low in fiber and digested quickly, eating refined carbs can cause major swings in blood sugar levels. This can contribute to overeating.
• As we have discussed above, foods high on the glycemic index promote short-term fullness, lasting about one hour. On the other hand, foods that are low on the glycemic index promote a sustained feeling of fullness, which lasts about two to three Blood sugar levels drop about an hour or two after eating a meal high in refined carbs. This promotes hunger and stimulates parts of the brain associated with reward and craving.
• These signals make you crave more food, and are known to cause overeating. This constant eating leads to obesity, a pre-diabetic state, and eventual diabetes.
• Slower Metabolism: Research shows that the body may shift nutrients into fat storage and away from muscle burning in the presence of high-glycemic-index foods. In 2004, Ludwig and his colleagues at Harvard conducted a study, published in the journal Lancet, in which they fed rats diets with identical nutrients, except for the type of starch. By the end of the study, rats in both groups weighed roughly the same, but those eating a high-glycemic diet had 71 percent more fat than the low-glycemic-index group.
• Inflammation: A diet high in grains stokes inflammation. When blood sugar spikes, glucose builds up in the blood. When glucose drifts in the blood, it could attach itself to nearby proteins. The result is a chemical reaction called glycation, a pro-inflammatory process that plays a role in a host of inflammatory diseases — everything from Type 2 diabetes to arthritis to heart disease.
• GI Disorders: Studies show that the lectins in grains inflame the lining of the gut and create fissures between cells. Also, when whole-kernel grains are refined, 80 percent of the fiber is lost, and gut health suffers. Without the fiber, you end up with rapid-release carbs in these grains, which is a bad thing for the gut. Fiber helps sweep the gut of debris and supports the body’s critically important elimination and detoxification processes, which also play a role in keeping high cholesterol and inflammation at bay.
• Food Allergies/Intolerances: Wheat, in particular, is one of the biggest dietary triggers of food allergies and intolerances. While the exact reason is unclear, many experts blame the higher gluten content of modern wheat varieties. A type of protein found in many grains, including wheat, gluten gives dough elasticity, trapping air bubbles and creating a soft texture. Because soft is considered desirable, wheat today is bred to have more gluten than ever before.
• Acid-Alkaline Imbalance: The body has an elaborate system of checks and balances to keep its pH level at a steady 7.4. A diet high in acidic foods, such as grains, forces the body to pull calcium from the bones to keep things on an even keel. When researchers looked at how the diets of more than 500 women affected their bone density, they found that a diet high in refined grains, among other nutrient-poor foods, was linked to bone loss. A highly acidic diet also chips away at our cellular vitality and immunity in ways that can make us vulnerable to chronic disease. Grains are the only plant foods that generate acidic byproducts. Wheat, in particular, is among the most potent sources of sulfuric acid, a powerful substance that quickly overcomes the neutralizing effects of alkaline bases.

3. How can we have grains in their most healthy form?

Whole grains deliver fiber, healthy fats, vitamins, minerals, plant enzymes and hundreds of phytochemicals. For those seeking a dense source of carbohydrate energy, they can be a healthy choice — but only if they are unrefined and minimally processed. Here are a few steps toward upgrading your own grain options:

• Choose whole-kernel grains when possible.
• Try sprouted grains.
• While baking, replace part of the flour with nut or seed meals.
• Stick with truly whole-grain flours.
• Don’t overdose on gluten-free foods.
• Try going flour-free.
• Consider a grain sabbatical.

4. Are refined grains a culprit in Insulin resistance and Type 2 Diabetes?

When ground into flours, most grains act like sugar in the body, triggering weight gain, inflammation, and blood-sugar imbalances. Studies show that high consumption of refined carbs is linked with insulin resistance and high blood sugar levels. These are some of the main symptoms of type 2 diabetes.

Refined carbs also increase blood triglyceride levels. This is a risk factor for both heart disease and type 2 diabetes. It is therefore advisable to keep our refined grain consumption at a minimum and if we do indulge, check that what we are having is fortified.

References

1. Grains & legumes Nutrition Council (2019): Refined grains. Retrieved from https://www.glnc.org.au/grains/grains-and-nutrition/refined-grains/

2. NCBI (2002): Effect of whole grains on insulin sensitivity in overweight hyperinsulinemic adults. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/11976158

3. Popsugar (2019): 4 Reasons to Eat Whole Grains Instead of Refined. Retrieved from https://www.popsugar.com/fitness/Why-You-Should-Eat-Whole-Grains-Instead-Refined-18361716

4. Healthline (2017): Why Refined Carbs Are Bad For You. Retrieved from https://www.healthline.com/nutrition/why-refined-carbs-are-bad

5. Experience Life (2019): The Truth about Refined Grains. Retrieved from https://experiencelife.com/article/the-truth-about-refined-grains/

Type 2 diabetes is the most prevalent metabolic disease currently known to man. Its hallmarks are pancreatic beta-cell dysfunction and insulin resistance. The Reactive Oxygen Species (ROS) is a little-understood factor as far as the progression of Type 2 diabetes is concerned. Therefore, in this article, I will shed some light on what it is and the effect it has on this chronic disease.

1. What is ROS

ROS is a type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A buildup of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death. Reactive oxygen species are free radicals, also called oxygen radicals.

2. How does ROS interact with cellular function?

Traditionally, ROS has been thought of as useless by-products of respiratory metabolism in mitochondria and believed to be generally harmful to biological systems. However, growing evidence shows that, in many instances, ROS generation is not a useless or harmful process but, rather, an essential element for certain biological responses.

Although ROS, such as H₂O₂, have been demonstrated to be critical factors in normal cellular signal transduction and have the potential to regulate glucose-stimulated insulin secretion (GSIS) in β-cells, excessive and/or sustained ROS production can directly or indirectly disturb the integrity and physiological function of cellular macromolecules, such as DNA, protein, or lipids.

3. So, when is ROS action harmful?

As discussed above, ROS action is generally beneficial. However, under diabetic conditions, chronic hyperglycemia and consequent augmentation of reactive oxygen species (ROS) deteriorate beta-cell function and escalate insulin resistance. This leads to an aggravation of type 2 diabetes. Additionally, chronic hyperglycemia and ROS are also involved in the development of atherosclerosis which is often observed under diabetic conditions.

Such disturbances contribute to the pathogenesis of various diseases, including diabetes. To counteract these insults, most cells, including β-cells, have intricate mechanisms of defense against ROS toxicity. Among these, the transcription factor NF-E2–related factor 2 (Nrf2) is a pivotal component for protecting cells from oxidative damage.

In response to oxidative stress, activation of Nrf2 dramatically increases intracellular antioxidant potential by directly increasing the transcription of many so-called antioxidant enzymes. Thus, the Nrf2-mediated induction of antioxidant enzymes is critically important for proper oxidation/reduction (redox) homeostasis to protect cells from irreversible oxidative damage.

However, a possible consequence of this augmented cellular ROS-scavenging ability is the potential to blunt normal ROS signals. Despite intensive research focused on oxidative stress and diabetes, the role of cellular adaptive responses to increased oxidative stress in β-cell dysfunction remains incompletely understood.

4.  ROS and Cardiovascular Complications in Diabetic Patients

Diabetes mellitus (DM) is an independent risk factor for heart failure. The Framingham Heart Study reported that the frequency of heart failure is 2-fold higher in male diabetics and 5-fold higher in female diabetics than in age-matched control subjects. An increase in reactive oxygen species (ROS) has been regarded as a dominant mechanism of cardiac dysfunction in patients with DM. ROS are important intracellular signaling molecules and mediate various cellular functions, including activation of transcriptional factors, protein kinases, and ion channels; however, high levels of ROS are detrimental to cardiomyocytes.

It can, therefore, be said that Reactive oxygen species (ROS) are the main facilitators of cardiovascular complications in diabetes mellitus (DM). Emerging evidence shows that mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase are dominant mechanisms of ROS production in the diabetic heart. Hyperpolarization of the mitochondrial inner membrane potentials and impaired mitochondrial function promote ROS production in the mitochondria of the diabetic heart.

In physiological conditions, ROS levels are appropriately controlled by endogenous antioxidant systems to minimize oxidative cellular damage. Oxidative stress occurs when ROS production overwhelms antioxidant capacity in pathological conditions. It is apparent that ROS production and oxidative stress are increased in the diabetic heart, and oxidative stress induces various cardiovascular complications, including cardiac dysfunction, which is facilitated by inflammation, apoptosis, and fibrosis

The rise in the ROS level in the diabetic heart is brought about by multiple mechanisms. Among these, NADPH oxidase and mitochondria play a pivotal role and mutually stimulate to enhance ROS production. UCPs regulate ROS production in mitochondria by dissipating the mitochondrial inner membrane potential. PKC, angiotensin II, AGEs/RAGE, and CaMKII facilitate ROS production in NADPH oxidase. The mechanisms of ROS increase in DM are complex because the multiple factors interact and enhance each other

5. What should we expect to see in the future?

ROS are induced under diabetic conditions, which are possibly involved in the progression of pancreatic -cell dysfunction and insulin resistance found in type 2 diabetes. Suppression of ROS in obese type 2 diabetic mice restores -cell function and insulin sensitivity, leading to amelioration of glucose intolerance. In addition, ROS is involved in the progression of atherosclerosis which is often observed as a macroangiopathy under diabetic conditions.

Taken together, it is likely that ROS is closely associated with the development of type 2 diabetes and atherosclerosis. Although at present several clinical trials with antioxidants show only a little effect, if any, on the progression of type 2 diabetes. Future therapy might look into the suppression of ROS and, infusion of stronger and more appropriate antioxidants as a way of exerting some beneficial effects against the development of type 2 diabetes and atherosclerosis.

References

1. American Diabetes Association (2007): Reactive Oxygen Species as a Signal in Glucose-Stimulated Insulin Secretion. Retrieved from https://diabetes.diabetesjournals.org/content/56/7/1783
2. Hindawi (2009): Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis. Retrieved from https://www.hindawi.com/journals/mi/2010/453892/

3. American Heart Association (2018): Reactive Oxygen Species in Metabolic and Inflammatory Signaling. Retrieved from https://www.ahajournals.org/doi/full/10.1161/circresaha.117.311401
4. NCBI (2010): Role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis. Retrieved from  https://www.ncbi.nlm.nih.gov/pubmed/20182627
5. Circulation Journal (2014): Production of Reactive Oxygen Species in the Diabetic Heart. Retrieved by https://www.jstage.jst.go.jp/article/circj/78/2/78_CJ-13-1187/_pdf

Type 2 diabetes is the most prevalent metabolic disease currently known to man. Its hallmarks are pancreatic beta-cell dysfunction and insulin resistance. The Reactive Oxygen Species (ROS) is a little-understood factor as far as the progression of Type 2 diabetes is concerned. Therefore, in this article, I will shed some light on what it is and the effect it has on this chronic disease.

1. What is ROS

ROS is a type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A buildup of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death. Reactive oxygen species are free radicals, also called oxygen radicals.

2. How does ROS interact with cellular function?

Traditionally, ROS has been thought of as useless by-products of respiratory metabolism in mitochondria and believed to be generally harmful to biological systems. However, growing evidence shows that, in many instances, ROS generation is not a useless or harmful process but, rather, an essential element for certain biological responses.

Although ROS, such as H₂O₂, have been demonstrated to be critical factors in normal cellular signal transduction and have the potential to regulate glucose-stimulated insulin secretion (GSIS) in β-cells, excessive and/or sustained ROS production can directly or indirectly disturb the integrity and physiological function of cellular macromolecules, such as DNA, protein, or lipids.

3. So, when is ROS action harmful?

As discussed above, ROS action is generally beneficial. However, under diabetic conditions, chronic hyperglycemia and consequent augmentation of reactive oxygen species (ROS) deteriorate beta-cell function and escalate insulin resistance. This leads to an aggravation of type 2 diabetes. Additionally, chronic hyperglycemia and ROS are also involved in the development of atherosclerosis which is often observed under diabetic conditions.

Such disturbances contribute to the pathogenesis of various diseases, including diabetes. To counteract these insults, most cells, including β-cells, have intricate mechanisms of defense against ROS toxicity. Among these, the transcription factor NF-E2–related factor 2 (Nrf2) is a pivotal component for protecting cells from oxidative damage.

In response to oxidative stress, activation of Nrf2 dramatically increases intracellular antioxidant potential by directly increasing the transcription of many so-called antioxidant enzymes. Thus, the Nrf2-mediated induction of antioxidant enzymes is critically important for proper oxidation/reduction (redox) homeostasis to protect cells from irreversible oxidative damage.

However, a possible consequence of this augmented cellular ROS-scavenging ability is the potential to blunt normal ROS signals. Despite intensive research focused on oxidative stress and diabetes, the role of cellular adaptive responses to increased oxidative stress in β-cell dysfunction remains incompletely understood.

4.  ROS and Cardiovascular Complications in Diabetic Patients

Diabetes mellitus (DM) is an independent risk factor for heart failure. The Framingham Heart Study reported that the frequency of heart failure is 2-fold higher in male diabetics and 5-fold higher in female diabetics than in age-matched control subjects. An increase in reactive oxygen species (ROS) has been regarded as a dominant mechanism of cardiac dysfunction in patients with DM. ROS are important intracellular signaling molecules and mediate various cellular functions, including activation of transcriptional factors, protein kinases, and ion channels; however, high levels of ROS are detrimental to cardiomyocytes.

It can, therefore, be said that Reactive oxygen species (ROS) are the main facilitators of cardiovascular complications in diabetes mellitus (DM). Emerging evidence shows that mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase are dominant mechanisms of ROS production in the diabetic heart. Hyperpolarization of the mitochondrial inner membrane potentials and impaired mitochondrial function promote ROS production in the mitochondria of the diabetic heart.

In physiological conditions, ROS levels are appropriately controlled by endogenous antioxidant systems to minimize oxidative cellular damage. Oxidative stress occurs when ROS production overwhelms antioxidant capacity in pathological conditions. It is apparent that ROS production and oxidative stress are increased in the diabetic heart, and oxidative stress induces various cardiovascular complications, including cardiac dysfunction, which is facilitated by inflammation, apoptosis, and fibrosis

The rise in the ROS level in the diabetic heart is brought about by multiple mechanisms. Among these, NADPH oxidase and mitochondria play a pivotal role and mutually stimulate to enhance ROS production. UCPs regulate ROS production in mitochondria by dissipating the mitochondrial inner membrane potential. PKC, angiotensin II, AGEs/RAGE, and CaMKII facilitate ROS production in NADPH oxidase. The mechanisms of ROS increase in DM are complex because the multiple factors interact and enhance each other

5. What should we expect to see in the future?

ROS are induced under diabetic conditions, which are possibly involved in the progression of pancreatic -cell dysfunction and insulin resistance found in type 2 diabetes. Suppression of ROS in obese type 2 diabetic mice restores -cell function and insulin sensitivity, leading to amelioration of glucose intolerance. In addition, ROS is involved in the progression of atherosclerosis which is often observed as a macroangiopathy under diabetic conditions.

Taken together, it is likely that ROS is closely associated with the development of type 2 diabetes and atherosclerosis. Although at present several clinical trials with antioxidants show only a little effect, if any, on the progression of type 2 diabetes. Future therapy might look into the suppression of ROS and, infusion of stronger and more appropriate antioxidants as a way of exerting some beneficial effects against the development of type 2 diabetes and atherosclerosis.

References

1. American Diabetes Association (2007): Reactive Oxygen Species as a Signal in Glucose-Stimulated Insulin Secretion. Retrieved from https://diabetes.diabetesjournals.org/content/56/7/1783
2. Hindawi (2009): Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis. Retrieved from https://www.hindawi.com/journals/mi/2010/453892/

3. American Heart Association (2018): Reactive Oxygen Species in Metabolic and Inflammatory Signaling. Retrieved from https://www.ahajournals.org/doi/full/10.1161/circresaha.117.311401
4. NCBI (2010): Role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis. Retrieved from  https://www.ncbi.nlm.nih.gov/pubmed/20182627
5. Circulation Journal (2014): Production of Reactive Oxygen Species in the Diabetic Heart. Retrieved by https://www.jstage.jst.go.jp/article/circj/78/2/78_CJ-13-1187/_pdf

Of all the chronic diseases currently known to mankind, diabetes is the most common. The onset of diabetes starts years before it becomes full-blown and starts affecting one’s health. How can you know if you are on the path to being a full-blown diabetic? What can you do to arrest and reverse this process? In this article, we will discuss both the signs to look out for and the remedies.

1. What Is Prediabetes?

Prediabetes is a “pre-diagnosis” of diabetes—a warning sign of sorts. It happens when your blood glucose level (blood sugar level) is higher than normal but not high enough to be considered diabetes.

Prediabetes is an indication that you could develop type 2 diabetes (T2D) if you don’t make some immediate and lasting lifestyle changes.

During the prediabetes phase, your pancreas still produces enough insulin in response to ingested carbohydrates. The insulin is less effective at removing the sugar from the bloodstream, though, so your blood sugar remains high. This condition is called insulin resistance.

2. What are the indications that you might have it?

Diabetes develops very gradually, it could take up to several years. It follows that when you’re in the prediabetes stage, you may not have any symptoms at all. You may, however, notice that:

• you’re hungrier than normal
• you’re losing weight, despite eating more
• you’re thirstier than normal
• you have to go to the bathroom more frequently
• you’re more tired than usual

All of these symptoms are typically associated with diabetes, so if you’re in the early stages of diabetes, you may notice them.

3. Understanding the risk factors that could lead to prediabetes…

It is not very clear what exactly causes the insulin process to go askew in some people. There are several risk factors, though, that make it more likely that you’ll develop pre-diabetes. These are the same risk factors related to the development of type 2 diabetes:

• Weight: Being overweight (have a body mass index—a BMI—of higher than 25), increases your risk for developing prediabetes. This is especially true if you carry a lot of extra weight in your abdomen. The extra fat cells can cause your body to become more insulin resistant.
• Being inactive: This often goes hand-in-hand with being overweight. If you aren’t physically active, you’re more likely to develop prediabetes.
• Having a close family member with type 2 diabetes: Prediabetes has a hereditary factor. If someone in your close family has (or had) it, you are more likely to develop it.
• Race/ethnicity: Certain ethnic groups are more likely to develop prediabetes, including African-Americans, Hispanic Americans, Native Americans, and Asian Americans.
• Age: The older you are, the more at risk you are for developing prediabetes. At age 45, your risk starts to rise, and after age 65, your risk increases exponentially.
• Gestational diabetes: If you developed diabetes while you were pregnant, that increases your risk of developing prediabetes later on.
• Other health problems: High blood pressure (hypertension) and high cholesterol (the “bad” LDL cholesterol) increase your risk of getting type 2 diabetes.
• Polycystic ovary syndrome (PCOS) also raises the risk of prediabetes because it’s related to insulin resistance.

• Hypothyroidism(low thyroid function; not enough circulating thyroid hormone), and you have prediabetes, then your risk of developing T2D more than doubles in comparison to individuals with normal thyroid function.

4. How then can you know for sure?

You should visit your doctor who may want to test your blood glucose levels if you’re overweight (have a body mass index—BMI—of over 25) and if you have one or more of the risk factors listed above.

If your fasting blood test indicates that you have prediabetes, your doctor may want to do an A1C blood test. On the other hand, your doctor may skip the fasting blood sugar test and go straight to the A1C blood test, which provides information about your average blood sugar levels over a 3 month period. These results are stated as a percentage:

• Normal = below 5.7%
• Prediabetes = between 5.7% and 6.4%
• Diabetes = 6.5% or higher.

It is advisable to start testing your blood glucose levels every three years beginning when you’re 45, even if you are not overweight and do not have any of the risk factors. That will ensure you catch any anomaly at an early stage as the risk of developing prediabetes (and therefore type 2 diabetes) increases with age.

5. What then if you have prediabetes?

Serious lifestyle changes are effective in preventing type 2 diabetes after you’ve been diagnosed with pre-diabetes. Your doctor will give you advice on what you need to do, but here are some additional things you can do on your own…….

• Assess Your Food Choices:  Get a healthy food plan is to assure that you are controlling your blood glucose level by keeping it in a healthy, normal range. A registered dietitian (RD) or certified diabetes educator (CDE) can assist you in creating a meal plan. It should reflect your preferred foods and be contain foods that are good-for-your-blood-glucose-level. Your meal plan should be adjusted to be comfortable and satisfying to you, taking into account your overall health, physical activity, and what you like to eat.
• Exercise regularly:  During exercise, your body burns up more glucose, thus lowering your blood glucose level. Also when you exercise, your body doesn’t need as much insulin to transport the glucose; your body becomes less insulin resistant. Since your body isn’t using insulin well when you have prediabetes, lower insulin resistance is a very good thing.
  It is recommended that you do at least 150 minutes of moderate activity a week—that’s 30 minutes five days a week. You can get that through activities such as walking, bike riding, or swimming.
• Lose weight. If you are overweight, losing just 7 percent of your starting weight can help delay or prevent diabetes. That means if you weigh 200 pounds, losing 14 pounds can make a difference. Weight loss also helps lower your blood pressure and cholesterol levels.

• Metformin: Medication might be recommended for people who are at very high risk of developing type 2 diabetes after being diagnosed with prediabetes. According to the American Diabetes Association, metformin should be the only medication used to prevent T2D. It works by keeping the liver from making more glucose when you don’t need it, thereby keeping your blood glucose level in a better range.

6. Some good news….…

If you have prediabetes, you should know you are definitely not alone. In 2015, it was estimated that 84.1 million Americans age 18 and older suffered from this condition. That is a whopping 1 in 3 Americans!

Being prediabetic doesn’t mean you will certainly develop diabetes. It is, however, a warning of what could lie ahead. People with prediabetes have a higher risk of type 2 diabetes as opposed to someone with normal blood sugar levels.

Those chances increase if you don’t make any healthy changes to your diet or activity habits.

It is not all bleak though…. “It can be reversed and you can stop the progression to diabetes. You can take control of your health by making the right choices and actively monitoring your blood sugar to ensure you do not slip into a prediabetic state or develop into a full diabetic.

References:

1. Healthline (2018): Understanding Borderline Diabetes: Signs, Symptoms, and More. Retrieved from https://www.healthline.com/health/diabetes/borderline-diabetes-know-the-signs

2. Endocrineweb (2008): Prediabetes- How to prevent prediabetes from becoming type 2 diabetes. Retrieved from https://www.endocrineweb.com/conditions/pre-diabetes/pre-diabetes
3. WebMD: Prediabetes (Borderline Diabetes). Retrieved from https://www.webmd.com/diabetes/type-2-diabetes-guide/what-is-prediabetes#1
4. org(2019): Prediabetes. Retrieved from https://familydoctor.org/condition/prediabetes/

We live in the modern-day age of convenience where everything is available to us at the touch of a button. A study published in the Journal of Translational Medicine proves that obesity and Type 2 diabetes are even more closely linked to high-calorie diets than was initially thought. According to the findings of the research, overeating can tip your body into a pre-diabetic state in less than a week. This article seeks to shed some light on some of our eating habits and how they might lead us down a path of chronic illness.

1. Diabetes Mellitus and Diet

Diabetes exists in two forms: type-1 and type-2. It is not known what the exact cause of type-1 diabetes is. Type-2 however, has been attributed to poor diet and a lack of exercise.

Approximately 95% of all cases are type 2. Both types Present with excess glucose, or blood sugar, in their blood that is not removed by the hormone called insulin. In type-2 diabetics, insulin resistance develops, and fat, liver and muscle cells no longer respond correctly to insulin. Symptoms of type-2 diabetes can include fatigue, hunger, increased thirst, blurred vision, erectile dysfunction, increased urination, and slower healing. Notably, people diagnosed with type-2 diabetes more likely to be overweight because excess fat makes it more difficult for the body to correctly utilize insulin.

Diabetes mellitus (DM) was first recognized as a disease around 3000 years ago by the ancient Egyptians and Indians, illustrating some clinical features very similar to what we now know as diabetes. DM is a combination of two words, “diabetes” Greek word derivative, means siphon – to pass through and the Latin word “Mellitus” means honeyed or sweet. In 1776, excess sugar in blood and urine was first confirmed in Great Britain.

2. What is the role of diet in T2DM?

In India, a startling observation was made. The disease was almost always confined to rich people who consumed oil, flour, and sugar in excessive amounts. This was further proved by the First and Second World Wars, where declines in the diabetes mortality rates were documented due to food shortage and famines in the countries involved such as Germany and other European countries. In Berlin, the diabetes mortality rate declined from 23.1/100,000 in 1914 to 10.9/100,000 in 1919. Adversely, there was no change in diabetes mortality rate in other countries that did not experience food shortage in the same period such as Japan and North American countries.

Though consumption of carbohydrates has been shown to increase the risk of developing T2DM, sugar is a more harmful culprit. In a study that involved more than 500 ethnically diverse schoolchildren for 19 months, it was found that for each additional serving of carbonated drinks consumed, the frequency of obesity increased. This was after adjusting for different parameters such as dietary, demographic, anthropometric, and lifestyle.

Recent evidence suggests a link between the intake of soft drinks and obesity and diabetes. This is as a result of the large amounts of high fructose corn syrup used in the manufacturing of these drinks. They have the potential to raise blood glucose levels and BMI to the dangerous levels. It was also noted that diet soft drinks contain glycated chemicals that significantly boost insulin resistance.

There has been a strong link between food and obesity. Both the composition and volume of food matter in this case. High intake of red meat, sweets, and fried foods contributes to the increased risk of insulin resistance and T2DM. Inversely, consumption of fruits and vegetables may protect against the development of T2DM, as they are rich in nutrients, fiber, and antioxidants which are considered as a protective barrier against the diseases.

A recent study of Japanese women revealed that elevated intake of white rice was associated with an elevated risk of T2DM. Dietary knowledge is a significant factor that influences dietary behaviors.

3. What then can we do to decrease our chances of getting diabetes?

• Avoid Fast Food

Several studies have shown that fast-food consumption can further the development of type-2 diabetes. A 2013 study published in the “European Journal of Nutrition” set out to clarify the role of dietary patterns in the onset of type-2 diabetes in overweight people. The study found that diets high in soft drinks and french fries, and low in fruit and vegetables, were associated with a greater risk of type-2 diabetes in overweight participants, particularly among those who are less physically active. A 2005 study published in “Lancet” concluded that fast-food consumption has a strong positive correlation with weight gain and insulin resistance, implying that fast-food intake may promote obesity and type-2 diabetes.

• Minimize Your Sugar Intake

High-sugar diets promote both weight gain and insulin resistance, which eventually leads to a susceptibility to type-2 diabetes. In addition, having type-2 diabetes significantly increases the risk of developing Alzheimer’s disease. Dietary modifications, therefore, can greatly reduce the risk of both type-2 diabetes and Alzheimer’s disease.

• Note the quality of fats you use

It may be more important to focus on the quality of the fats and carbohydrates consumed in order to prevent type-2 diabetes. High intakes of trans- fatty acids, saturated fats, refined carbohydrates, and other processed foods increase the risk for type-2 diabetes, whereas whole grains, polyunsaturated fats, fiber-rich foods, omega-3 fatty acids, and other minimally processed foods can lower your risk.

• Breakfast should not be skipped

Breakfast is an important meal that, it is even argued that it is the most important. When missed, it can result in health issues. 2012 a study published in the “American Journal of Clinical Nutrition” found that skipping breakfast increased the risk for type-2 diabetes, even after adjusting for body mass index. Snacking between meals was also found to increase type-2 diabetes risk.

• Increase Vitamin D intake

According to the National Institutes of Health, Vitamin D studies show a link between people’s ability to maintain healthy blood glucose levels and having enough vitamin D in their blood. Fish oils, trout, salmon, cheese, eggs, and mushrooms are all gold sources of Vitamin D.

• Increase Your Activity

NIDDK studies show that insulin resistance goes down when you increase how much you move throughout the day. Try increasing your time spent walking for 30 minutes, five days per week (that’s only five 6-minute walks each day at work).

• Do not Smoke

Ever. According to the CDC, smokers are 30-40 percent more likely to develop Type 2 diabetes than nonsmokers.

• Keep Your Waist in Check

According to NIH, a waist measurement of 40 inches or more for men is linked to insulin resistance and increases a person’s risk for Type 2 diabetes. This is true even if a person’s BMI falls within the normal range.

4. Everybody’s responsibility

Type 2 diabetes is largely preventable by taking several simple steps: keeping weight under control, exercising more, eating a healthy diet, and not smoking. Yet it is clear that the burden of behavior change cannot fall entirely on individuals. Families, schools, worksites, healthcare providers, communities, media, the food industry, and government must work together to make healthy choices easy choices.

References

1. NCBI (2017): Effect of diet on type 2 diabetes mellitus: A review. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5426415/
2. Livestrong.com(2017): Can a Poor Diet Cause Diabetes? Retrieved from https://www.livestrong.com/article/445709-can-a-poor-diet-cause-diabetes/
3. Men’s Journal (2019): Overeating Makes You Fat and Diabetic Faster than you Think. Retrieved from https://www.mensjournal.com/ www health-fitness/overeating-makes-you-fat-and-diabetic-faster-you-think/
4. HSPH (2019): Simple Steps to Preventing Diabetes. Retrieved from https://.hsph.harvard.edu/nutritionsource/disease-prevention/diabetes-prevention/preventing-diabetes-full-story/

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/

We are living in a diabetes pandemic.

But diabetes isn’t just about blood sugar, it’s systemic inflammation, incessant cravings-driven eating.

It’s obesity.

And it’s impacting our nation in ways most are completely unaware of.

From our children’s exposure to the U.S. dietary regulations in our public schools and the rise in ADD (Attention Deficit Disorder), to behavioral issues in the prison system where most inmates emerge severely diabetic.

We are generating a massive problem of staggering social disfunction most clearly evident in our nation’s urban areas. As a nation we are failing.

And our Forget To Eat™ Podcast guest, Dr. Gurpreet Padda is right in the middle of it. Based in St. Louis, MO, Dr. Padda and his Padda Institute is highly regarded as one of the best pain centers in St. Louis.

Watch: Rats, Food, Prisons… Reversing The Diabetes Pandemic

Interview Transcription: Rats, Food, Prisons… Reversing The Diabetes Pandemic

 

Nearly 77% of the US population is now overweight. This dramatic change in the last 50 years is correlated with the availability of highly processed foods, and with a dramatic increase in chronic pain.

In a mouse model, high-calorie foods, which induces a dopamine release, disrupted normal feeding schedules, resulting in overconsumption.

Additionally, the “knockout” mouse model which had dopamine signaling disrupted, didn’t seek the dietary “rewarding pleasure,” maintained a normal eating schedule, and did not become obese.

Practical Conclusion:

Diet-induced obesity requires dopamine (DA)-Drd1 signaling

Avoid eating outside a normal eating window, typically less than eight hours out of 24, allowing glycogen depletion in the liver and preventing insulin resistance.

How is this relevant to chronic pain:

I practice in the field of interventional pain, addiction, and obesity/ metainflammation.
1. Patients with chronic pain have a signaling mechanism, whether induced by medications or their endogenous pain, that causes them to seek out dopaminergic stimulation, to relieve their pain.

2. Some of these dopaminergic stimulation can be substituted by dietary intake.

3. Excessive non-nutritive dietary intake leads to obesity and visceral adipose tissue accumulation, which is inflammatory.

4. Excessive inflammatory mediators aggravate pain, and the cycle repeats.

Could sugar self-substitution for opioids in our patient’s be leading to insulin resistance, obesity, T2DM?

In an experiment done on mini-pigs, they found that sugar can affect the brain’s reward system in a similar “manner similar to that of drugs of abuse”

Sugar’s impact on the brain’s reward system boils down to how it affects two types of receptors in the brain.

The first set is dopamine receptors — dopamine is a central player in the brain’s reward system, released during pleasurable activities.

The second set is opioid receptors, which are also found all over the brain but are particularly found in areas involved in eating-related rewards.

The sensitivity of both receptors was dampened when pigs were allowed unrestricted access to sugar water for one hour each day for twelve days. The pigs were also fed a normal diet, so sugar consumption was unrelated to their caloric needs.

After the first day, the sugar intake lowered the “availability” of opioid and dopamine receptors, essentially dampening the ability of these receptors to bind to their natural ligands. Both Opiate and Dopamine receptor binding was attenuated 14% in the anterior cingulate cortex and the nucleus accumbent, both are areas of the hedonic reward.

At the end of the 12 days, the scientists found that the pattern held — the availability of both types of receptors continued to decrease significantly.

Could sugar self-substitution for opioids in our patient’s be leading to insulin resistance, obesity, T2DM?

Winterdahl, M., Noer, O., Orlowski, D. et al. Sucrose intake lowers μ-opioid and dopamine D2/3 receptor availability in porcine brain. Sci Rep 9, 16918 (2019) DOI:10.1038/s41598-019-53430-9.

Padda Institute