We have heard a lot about the harmful effects of refined grains on our health. Interestingly, recent research seems to point in a different direction, exonerating them from the label they have held for so long. Are refined grains not so bad after all? What are the facts? In this article, we will take a closer look at why refined grains seem to have been unfairly vilified.

1. Refined grain consumption and your health

Have you been avoiding refined grains such as white bread and pasta? Do you feel bad when you do eat them? Apparently, there’s no evidence to show that refined grains are “bad” for you. Conversely, there is evidence that shows that whole grains are good for you. Somehow along the way, the message has been mixed up – putting a slice of white bread or a dish of white pasta in the same category as pie and piece of cake.

The dietary recommendation has been to make half of your grains whole grains. This does not mean “avoid all refined grains”. They too can fit into your diet.

Contrary to previous research findings, refined grain consumption is not associated with any of the adverse health effects it has been linked to, such as obesity, heart disease, and diabetes. This is according to a new study from the Healthy Lifestyles Research Center at Arizona State University (ASU) published in Advances in Nutrition. The researchers note that what counts is the number of consumed calories, not so much their source.

Analyses of existing research – including 32 publications with data from 24 distinct cohorts – showed that refined grains are not linked to increased disease risk or premature death. The study highlights that the current dietary recommendation to reduce refined grain consumption conflicts with the substantial body of published scientific evidence.

Professor Glenn Gaesser, Ph.D., Director of the Healthy Lifestyles Research Center at ASU“Simply put, refined grains are not the bad guy,” says study author, Professor Glenn Gaesser, Ph.D., Director of the Healthy Lifestyles Research Center at ASU. “Contrary to popular belief and current dietary guidance, refined grain intake is not associated with type 2 diabetes, cardiovascular disease, coronary heart disease, stroke, hypertension, cancer or death.”

Gaesser theorizes that refined grains have developed a guilt-by-association reputation. He explains that while refined grains are frequently characterized as unhealthy, this can be attributed to their inclusion in a dietary pattern that contains a range of foods that are the real culprits in the link between an unhealthy dietary pattern and an increased risk of a number of chronic diseases.

What were the results of the study?

• No association was observed between refined grain intake and cardiovascular disease or coronary heart disease.
• No association was found between refined grain intake and stroke risk. In fact, one study demonstrated a 10 percent lower reduction of stroke risk.
• No association was found between refined grain intake and risk of Type 2 diabetes.
• Cancer studies are limited. Nonetheless, one meta-analysis shows an inverse association between refined grain intake and total cancer deaths. A second meta-analysis shows that refined grain intake was not associated with the risk of rectal or colorectal cancer.
• Five out of six studies show no relationship between refined grain intake and death rate. The other study shows a statistically significant inverse association between refined grain intake and all-cause death rate.
• Three systematic reviews show no consistent relationship between refined grain intake and body mass index (BMI).

2. Is there a link between refined grains and obesity?

The demonization of refined grains has deterred people from consuming them, opting for whole grains instead. Whole grains are higher in calories but touted as more nutritionally-rich.

In reality, the association between refined grain consumption and obesity is murky, with no clear relationship. Weight gain is essentially a result of consuming more calories than you burn. It’s the number of calories that matters most, not so much the type of calories. In studies that do indicate that refined grains are associated with increased risk of weight gain, the association is “inconsequentially small.” Randomized dietary interventions of whole grains and refined grains compared head-to-head reveal no differences between the two.

Both refined grains and whole grains are important in people’s diets. Whole grains are important for health since they provide fiber and essential vitamins. Enriched/refined grains provide fiber too, and 39 percent of the dietary fiber Americans eat comes from refined grains. “As a population, US consumers still fall far short of reaching their daily goals for fiber.

It is important to note that eliminating enriched grain products will result in nutrient shortfalls. Refined grain foods that have been enriched and/or fortified help to alleviate shortfalls including B-vitamins, folic acid, thiamin, niacin, riboflavin, and iron.

A good example is that enriched grains are the largest contributor of folic acid in the American diet. This is key to preventing neural tube birth defects.

3. So, what should you eat?

To reduce disease risk and balanced nutrition, the DGA dietary recommends you eat:

• A variety of vegetables from all of the subgroups—dark green, red and orange, legumes (beans and peas), starchy, and other
• Fruits, especially whole fruits
• Grains, at least half of which are whole grains
• Fat-free or low-fat dairy, including milk, yogurt, cheese, and/or fortified soy beverages
• A variety of protein foods, including seafood, lean meats and poultry, eggs, legumes (beans and peas), and nuts, seeds, and soy products
• Oils

4. What is the future for refined grains?

Future research efforts must distinguish between staple grain foods, such as cereals, bread and pasta and indulgent grain foods, such as cakes, cookies, and donuts, according to Gaesser. Most of the studies included in the current paper did not make such distinctions, so it’s impossible to know whether the results would be different if refined grains were categorized separately as a staple or indulgent grain foods.

It is possible that the risk of chronic diseases would be different for the consumption of staple grain foods as compared to the consumption of indulgent grain foods. Randomized-comparison trials are needed to better differentiate the health effects of whole grain and refined grain foods. Most published studies have been too short and do not include enough outcome measures to draw definitive conclusions.

As currently stands, the results of randomized-comparison trials show no consistent benefits of whole-grain foods over refined grain foods. These findings are at odds with the results of large-scale observational studies, which show a clear superiority of whole grains over refined grains. This is a paradox that needs to be resolved,” Gaesser concludes.

References

1. Nutritioninsight (2019): Let us eat cake? Refined grains “falsely” linked to obesity and chronic disease risk. Retrieved from https://www.nutritioninsight.com/news/let-us-eat-cake-refined-grains-falsely-linked-to-obesity-and-chronic-disease-risk.html

2. Rust Nutrition (2019): Refined Grains Redefined. Retrieved from https://rustnutrition.com/blog/2019/07/03/refined-grains-redefined/

3. NCBI (2019): Perspective: Refined Grains and Health: Genuine Risk, or Guilt by Association? Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520038/

4. Baking Business.com (2019): Study disputes negative health claims surrounding refined grains. Retrieved from https://www.bakingbusiness.com/articles/48376-study-disputes-negative-health-claims-surrounding-refined-grains

We have been looking at metabolic inflammation and its role in the development of obesity, diabetes and other chronic diseases. Does overnutrition contribute to metabolic inflammation? How?

1. Some background on overnutrition….

It is estimated that by 2020, two-thirds of the global burden of the disease will be due to chronic non-communicable diseases, most of which are associated with diet. While hunger is a tremendous global health concern that cannot be minimized, overnutrition should similarly be given concentrated attention. Malnutrition affects up-to 1 billion people. Even though undernutrition is the main cause of malnutrition, people who are overweight could also be malnourished.

The “double burden of malnutrition” is a term coined by the World Health Organization (WHO) to describe a situation which is characterized by “the coexistence of undernutrition along with overweight and obesity, or diet-related non-communicable diseases, within individuals, households and populations, and across the life course. Globally, the problem is not the availability of food resources, but the allocation and consumption of food.

1. What is overnutrition?

Overnutrition is defined as the overconsumption of nutrients and food to the point at which health is adversely affected. Overnutrition can develop into obesity, which increases the risk of serious health conditions, including cardiovascular disease, hypertension, cancer, and type-2 diabetes.

Until recently, overnutrition had been viewed as a problem that only affected developed nations. However, this has been reviewed to affect most populations. The prevalence of obesity is increasing in developing countries with the introduction of fast food and refined sugars.

While once considered the disease of the rich, low-income groups in richer countries are also being affected by this condition.

2. What is overnutrition induced inflammation?

Inflammation is a biological response launched by the immune system against dangerous assaults that threaten the integrity and normal physiology of an organism. Chronic nutrient overload causes an increase in adipose irregularities in that, if adipose tissue expandability is low, there will be an increased presence of thickened tissue. This condition would lead to a pro-inflammatory state that can trigger insulin resistance, the release of macrophage chemoattractant proteins, and in chronic inflammation, even the death of the thickened adipose tissue itself. This creates cyclic an action that extends the insulin resistance to all adipose tissue.

An important characteristic of overnutrition-induced diseases is chronic low-grade inflammation caused by nutritional excess. Overnutrition-induced inflammation is thought to occur in the brain and thus plays an extensive and steering role in overnutrition-induced diseases.

3. Overnutrition and the metabolic syndrome

The metabolic syndrome is a constellation of metabolic risk factors including high cholesterol, elevated blood pressure, insulin resistance, and elevated serum glucose, a pro-inflammatory state, and a prothrombotic state.

Most persons with metabolic syndrome are obese and usually have abdominal obesity. Generally, obesity is a reflection of overnutrition. A current view is that when adipose tissue fails to store all excess nutrients as triglyceride, lipid begins to accumulate in various tissues (eg, muscle, liver, pancreas, and heart). The foundation of the metabolic syndrome thus appears to be overnutrition, that is, more nutrient intake than can be safely disposed of by lipid oxidation.

When obesity is present, adipose tissue becomes inflamed. This inflammation may result in a pro-inflammatory state, which could contribute to both ASCVD and diabetes.

4. What is carbohydrate overnutrition?

Most evidence supports the concept that fatty acids represent the final common pathway to tissue nutrient overload. Less attention has been given to the possible negative effects of excessive intake of carbohydrates.

Chronic overstimulation of insulin secretion induced by dietary carbohydrates could have the following adverse effects:

• The β-cell function may be impaired by chronic glucotoxicity
• Carbohydrate-induced hyperinsulinemia may suppress muscle insulin sensitivity.

Furthermore, high-carbohydrate intakes can prompt lipogenesis in the liver; fatty acids produced in this way can feed into the final common pathway of ectopic lipid accumulation. There is thus a need to look further into the role of carbohydrate overnutrition in the development of the metabolic syndrome.

5. What factors Contribute to Overnutrition?

Obesity in the United States has reached startling heights. The National Center for Health Statistics at the Centers for Disease Control and Prevention (CDC) estimated that in 2015-2016, the prevalence of obesity in the United States was 39.8% in adults and 18.5% in youth.

While obvious factors including genetics, drugs, and other medical conditions may contribute to obesity, the behavior is perhaps the most common contributor. Healthy weight on an individual level is associated with a healthy diet and regular physical activity. Restaurants serve incredibly caloric meals, with some meals containing as much as 2,000 calories. The sedentary lifestyle practiced by most adds to the epidemic.

Unfortunately, this obesogenic culture has spread to other nations, including many developing countries. China, for example, now has more than 5,000 Kentucky Fried Chicken (KFC) restaurants in 1,100 cities. Similarly, McDonald’s expects to have 4,500 restaurants in China by 2022, up from 2,500 in 2017. A growing number of Chinese households also own television sets, personal vehicles, and other technologies that reduce physical activity and facilitate weight gain.

It is of note that economic inequality in developing nations is a primary cause of both overnutrition and undernutrition. Studies conducted in India show that income inequality had the same effect on the risk of being overweight as it did on the risk of being underweight; specifically, for each standard deviation increase in income inequality, the odds of being underweight increased by 19% and the odds of being obese increased by 21%.

While some people have the resources to purchase amounts of food beyond their daily caloric requirements, others cannot meet their recommended caloric intake. However, increasing numbers of poor people are becoming overweight in more nations, as these individuals consume affordably, yet highly caloric meals, such as fast food and processed foods.

6. What then should be done to avoid overnutrition?

An approach to understanding the effects of overnutrition on the metabolic profile is through overfeeding studies. These indicate that overnutrition produces a deterioration of metabolic status. Variability in individual response is, however, is expected. Such investigations are potentially useful for identifying those who are particularly susceptible to the development of metabolic risk factors.

The host of genetic factors likely acts at tissue levels to influence the response to nutrient excess. Different people may react differently to the accumulation of fat. However, overnutrition is generally considered to trigger metabolic disorders and predispose one to chronic conditions like Type 2 Diabetes. When choosing what to eat, one should be careful to ensure they choose balanced meals rich in fiber and nutrients and avoid the modern-day fast-food craze, as there cost of bad eating is too high.

References

1. Unite for Sight (2018): Module 4: Overnutrition. Retrieved from http://www.uniteforsight.org/hunger/module4
2. NCBI (2009): From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19171470
3. NCBI(2013): Neuroinflammation in Overnutrition-induced Diseases. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389772/
4. American Federation for Medical Research (2016): Overnutrition, ectopic lipid, and metabolic syndrome. Retrieved from https://jim.bmj.com/content/jim/64/6/1082.full.pdf 
5. NCBI (2009): From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19171470

The most common endocrine dysfunction of women – affects 10-20% of women.

A life-long disease with enormous medical, emotional and financial consequences.

High risk for diabetes and metabolic syndrome & 80% are overweight/obese.

PCOS is the result of hyperinsulinemia * The effects of insulin on the ovary Theca cells results in release of testosterone * The resulting manifestations have devastating effects (obesity, facial hair, acne, and emotional disorders) on teenage girls * Many cases have been reversed with lifestyle changes that act to lower insulin * IGF plays a role but addressing hyperinsulinemia can reverse the condition and its manifestations.

Theca cells endocrine cells in the ovary made up of connective tissue surrounding the follicle. The theca cells are responsible for the production of androstenedione.

Androstenedione is a precursor of testosterone and other androgens, as well as of estrogens like estrone.
Androstenedione has weak androgenic activity.

FSH induces the granulosa cells to make aromatase that converts the androgens made by the theca internal into estradiol.

Soybean oil not only leads to obesity and diabetes but could also affect neurological conditions such as:

maternal-child bonding
autism
Alzheimer’s disease
anxiety
depression

A previous study published in 2015 suggested that soybean oil-induced obesity, diabetes, insulin resistance, and fatty liver in mice. A more recent 2020 study published in the journal Endocrinology, compared mice fed diets high in fat: soybean oil, a polyunsaturated fat vs. coconut oil, a saturated fat.

Soybean oil produced pronounced effects on the hypothalamus, which regulates body weight via metabolism, maintains body temperature, is critical for reproduction and physical growth as well as response to stress. Surprisingly, mice fed soybean oil downregulated the gene which produces oxytocin in the hypothalamus, the hormone responsible for mother-child bonding and is also known as the “love” hormone.

Nearly an additional 100 other genes were also affected by the soybean oil diet, which may have ramifications not just for energy balance, but also for brain function and diseases such as autism.

One day we will view industrial seed oils with the same disdain as cigarette smoking…

BTW: Soybean oil is polyunsaturated fat and is often touted as a healthy option over saturated fats, but the saturated fat from coconut oil, produced very few changes in the hypothalamic genes.

Dysregulation of Hypothalamic Gene Expression and the Oxytocinergic System by Soybean Oil Diets in Male Mice. Endocrinology, 2020; DOI: 10.1210/endocr/bqz044.

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

 

We have extremely limited glucose storage as glycogen, or as circulating glucose.

Glycogen:

Glycogen is a large branched polymer of glucose, stored mainly in the liver and the skeletal muscle.  Stored  glycogen can be mobilized to circulating glucose during fasting periods and to the muscle cells during muscle contraction, a process called glycogenolysis.  The total body glycogen storage capacity, in a fasted healthy 70kg human, is  100 g in the liver, and 400 g in the muscle.  The total available calorie output from glycogen reserves is approximately 2,000 calories.

Circulating glucose:

Our blood stream normally carries less than 1 1/2 teaspoons of circulating glucose at any given time (less than 5 g of glucose circulates in the blood of a 70kg human).  The total available calorie output from circulating glucose is 20 calories.

The exact circulating glucose calculation:

Average blood volume for an adult is 70ml/kg.
Assuming a 70kg male=4,900 ml=49 dl or 4.9l
1 liter is 10dl, therefore we have 50dl.
A nondiabetic glucose concentration is <100mg/dL.
Therefor 100mg/dl multiplied by 49dl equals 4900mg of circulating glucose.
4900mg equals 4.9 g of circulating glucose, where each tsp =4.2gm
Total circulating glucose=1.16tsp

As a comparison, 1 gummy bear contains 1.3g of usable sugar.  Consuming 4 gummy bears could double the available circulating glucose, but for the fact insulin rapidly shuttles the glucose out of the circulation and into fat stores.

We have nearly unlimited fat storage capacity, and the primary role of insulin is to remove circulating glucose and convert it to fat storage.  Circulating glucose rapidly oxidizes, undergoing a non-enzymatic Maillard reaction, which results in spontaneous glycation, which we measure as HgBA1C.  The Maillard reaction was initially used to describe the browning and crisping of bread.  This glycation effect changes the cell membranes to a less fluid status, interferes with protein and enzyme function, and often deforms receptor and channels.  The end result of excessive glucose is sticky and nonfunctional cells.

Other advanced glycation end-products are measured as fructosamine.  Excessive circulating glucose is also rapidly excreted through the kidney above levels of 180 mg/dl, creating excessive urination or polyuria.  Glucose metabolism is tightly regulated because it can quickly oxidize and damage cell walls, wreaking havoc on our enzymatic pathways.

What is glycemic index?

How Much Sugar Can My Body Handle? – Reversing Diabetes
The GI assigns a score to how quickly glucose from a specific food enters the bloodstream.  Foods are ranked on a scale of 0 to 100, with glucose having a value of 100. The lower a food’s glycemic index, the slower the blood sugar rises after eating that food. In general, cooking and processing foods makes the GI higher for that food. The higher the GI of a food, the greater the insulin release, and therefore the greater the conversion of circulating glucose to fat storage.

The rate of rise and peak glucose concentration after a meal is often expressed as Glycemic Index (GI).

Glycemic load (GL) measures both how quickly glucose enters the bloodstream (GI) and how much glucose per serving is present. Glycemic Load (GL) is a calculated number and gives a patient a better idea of the effect of a particular food based upon the typical serving size. Watermelon has a high glycemic index of 80,  but a serving of watermelon has so little carbohydrate, that its total glycemic load is only 5.

When glucose levels drop, insulin production also drops, resulting in a conversion of stored fat to circulating ketone bodies and circulating triglycerides.  Circulating ketone bodies are a fuel source, akin to glucose, that do not require insulin to access the cells.

The point of the discussion is that we have extremely limited circulatory capacity for glucose, about 5g glucose or about 20 calories only.  Our constant consumption of processed carbohydrate rich food is inconsistent with our human physiology; which attempts to quickly removes glucose out of circulation to prevent tissue damage.  The constant high exposure eventually overwhelms our clearance capacity, leading to metabolic inflammation, and eventual diabetes.

Wasserman D. H. (2008). Four grams of glucose. American journal of physiology. Endocrinology and metabolism, 296(1), E11-21. 10.1152/ajpendo.90563.2008

Sugar has been vilified over the years with claims of its disastrous effects on our health. Are these claims true? Does taken a soda a day guarantee one ill health? What of the effects of excess sugar on obesity? In this article, we will explore these claims and determine whether indeed excessive sugar intake leads to obesity.

1. What is obesity?

Obesity rates have skyrocketed over the past century. In 1962, 46 percent of adults in the U.S. were considered overweight or obese. By 2010,that figure had jumped to 75 percent.

So, what exactly is obesity……

Obesity is a complex disease involving an excessive amount of body fat. Obesity isn’t just a cosmetic concern. It is a medical problem that increases your risk of other diseases and health problems, such as heart disease, diabetes, high blood pressure and certain cancers.

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. Sugar and obesity

Obesity is a complex problem with multiple causes. But among the likely suspects, sugar is a top favorite. As sugar consumption has increased, so too has the size of our waistlines.

Added sugars are a controversial and hotly debated topic. Consumption of added sugars has been implicated in increased risk of a variety of chronic diseases including obesity, cardiovascular disease, diabetes and non-alcoholic fatty liver disease (NAFLD) as well as cognitive decline and even some cancers. Support for these putative associations has been challenged, however, on a variety of fronts.

The sugars in your diet can be eithernaturally occurring or added. Naturally occurring sugars are found naturally in foods such as fruit (fructose) and milk (lactose). Added sugars are sugars and syrups put in foods during preparation or processing, or added at the table.

Numerous dietary and lifestyle habits can lead to weight gain and cause you to put on excess body fat.Consuming a diet high in added sugars, such as those found in sweetened beverages, candy, baked goods, and sugary cereals, is a contributing factor in weight gain and chronic health conditions, including obesity, heart disease, and diabetes.

Many people consume more sugar than they realize. It’s important to be aware of how much sugar you consume because our bodies don’t need sugar to function properly. Added sugars contribute zero nutrients but many added calories, which can lead to extra pounds or even obesity, thereby reducing impacting our health.

The ways in which added sugar intake leads to weight gain and increased body fat are complex and involve many factors.

3. Some ways why added sugar is fattening….

1. It is high in empty calories
   Added sugars are sweeteners added to foods and beverages to improve taste. Common types of added sugar include fructose, corn syrup, cane sugar, and agave.Excess sugar may cause you to pack on weight because it’s high in calories while offering few other nutrients.Though using small amounts of added sugar is unlikely to cause weight gain, regularly indulging in foods high in added sugars may cause you to gain excess body fat quicker and more drastically.
   2. Impacts blood sugar and hormone levels

   It’s well known that eating sugary foods significantly raises your blood sugar levels.Though enjoying a sweet food infrequently isn’t likely to harm health, daily consumption of large amounts of added sugar can lead to chronically elevated blood sugar levels.

   Prolonged elevated blood sugar — known as hyperglycemia — can cause serious harm to your body, by causing insulin resistance and resulting including weight gain.

   3. May lead to overeating

   Foods high in added sugars tend to be less filling. Eating foods rich in carbs — particularly refined carbs high in added sugars — yet low in protein can negatively impact fullness and may lead to weight gain by causing you to eat more at subsequent meals throughout the day or overeat at any one particular seating.

   Animal studies indicate that fructose impacts signaling systems in your hypothalamus, increasing levels of hunger-stimulating neuropeptides — molecules that communicate with one another, influencing brain activity — while decreasing fullness signals. Additionally, your body is predisposed to crave sweetness. In fact, research shows that sugar consumption is driven by the pleasure derived from the sweet taste of sugary drinks and foods.

   4. Linked to obesity and chronic disease

   Numerous studies have linked high intake of added sugars to weight gain and chronic conditions, such as obesity, heart disease, and diabetes.This effect has been observed both in adults and in children. Recently, a review of 30 studies in more than 242,000 adults and children found a significant link between sugar-sweetened beverages and obesity.

   4. What are some of the health problems associated with obesity?

   People with obesity are more likely to develop a number of potentially serious health problems, including:

   • Heart disease and strokes. Obesity makes you more likely to have high blood pressure and abnormal cholesterol levels, which are risk factors for heart disease and strokes.
   • Type 2 diabetes. Obesity can affect the way your body uses insulin to control blood sugar levels. This raises your risk of insulin resistance and diabetes.
   • Certain cancers. Obesity may increase your risk of cancer of the uterus, cervix, endometrium, ovary, breast, colon, rectum, esophagus, liver, gallbladder, pancreas, kidney and prostate.
   • Digestive problems. Obesity increases the likelihood that you’ll develop heartburn, gallbladder disease and liver problems.
   • Gynecological and sexual problems. Obesity may cause infertility and irregular periods in women. Obesity also can cause erectile dysfunction in men.
   • Sleep apnea. People with obesity are more likely to have sleep apnea, a potentially serious disorder in which breathing repeatedly stops and starts during sleep.
   • Osteoarthritis. Obesity increases the stress placed on weight-bearing joints, in addition to promoting inflammation within the body. These factors may lead to complications such as osteoarthritis.

   5. How can obesity affect your quality of life?

   People who are obese often find themselves struggling with some issues that might diminish their overall quality of life. Some of these issues might include:

   • Depression
   • Disability
   • Sexual problems
   • Shame and guilt
   • Social isolation
   • Lower work achievement

   6. How can you keep yourself from getting obese?
   

   Whether you’re at risk of obesity, currently overweight or at a healthy weight, you can take steps to prevent unhealthy weight gain and related health problems.

   • Exercise regularly. You need to get 150 to 300 minutes of moderate-intensity activity a week to prevent weight gain. Moderately intense physical activities include fast walking and swimming.
   • Follow a healthy-eating plan. Focus on low-calorie, nutrient-dense foods, such as fruits, vegetables and whole grains. Avoid saturated fat and limit sweets and alcohol. Eat three regular meals a day with limited snacking. You can still enjoy small amounts of high-fat, high-calorie foods as an infrequent treat.
   • Know and avoid the food traps that cause you to eat. Identify situations that trigger out-of-control eating. Try keeping a journal and write down what you eat, how much you eat, when you eat, how you’re feeling and how hungry you are, stay in control of your eating behaviors.
   • Monitor your weight regularly. People who weigh themselves at least once a week are more successful in keeping off excess pounds.
   • Be consistent. Sticking to your healthy-weight plan all the time
     

     7. So, is sugar friend or foe?

     Interfering with your hormones, increasing hunger, and displacing healthy foods are just a few of the ways that added sugars can lead to weight gain.Aside from causing you to put on excess body fat, eating too much added sugar can significantly increase your risk of chronic conditions, such as obesity, heart disease, and diabetes. It is thus wise to consume added sugars with caution because a stitch in time save nine.

     References

     1. Endocrineweb(2018):Insulin Resistance Causes and Symptoms, Retrieved from

     https://www.endocrineweb.com/conditions/type-2-diabetes/insulin-resistance-causes-symptoms

     2. Healthline (2019):6 Ways Added Sugar Is Fattening. Retrieved from

     https://www.healthline.com/nutrition/does-sugar-make-you-fat#section1

     3. American Heart Association (2018): Added Sugars. Retrieved from

     https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/sugar/added-sugars

     4. NCBI (2016): Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding. Retrieved from

     https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133084/

     5. John Hopkins Medicine (2019): Obesity, Sugar and Heart Health. Retrieved from

     https://www.hopkinsmedicine.org/health/wellness-and-prevention/obesity-sugar-and-heart-health

     6. Mayo Clinic: Retrieved from

     https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742

Given that obesity and associated disorder type II diabetes mellitus have reached epidemic proportions worldwide, the development of efficient prevention and therapeutic interventions is a global public health interest. There is now a large body of evidence suggesting that the micro-organisms colonizing the human gut, known as gut microbiota, play a central role in human physiology and metabolism. Understanding how gut microbiota affects and regulates key metabolic functions such as glucose regulation and insulin resistance is an important health issue. We will highlight how prebiotic/probiotic interventions affect these bacterial processes and are now considered as promising approaches to treat obese and diabetic patients.

1. The gut microbiota of an obese person…

Obesity is a chronic, complex, and multifactorial disease representing the fifth leading cause of death in the world and accounting for almost 3.4 million deaths each year. Low-grade inflammation is the hallmark of metabolic disorders such as obesity, type 2 diabetes and nonalcoholic fatty liver disease.

Microbiota is now recognized as a real functional “organ” due to its immense impact on human health and has become the subject of intensive research over recent years. The vast majority of microbes reside in the intestinal tract, where they influence host physiology by playing fundamentally important roles in digestion, nutrition, immune regulation, and metabolism.

Gut microbiota composition and activity can fluctuate over time and depend on different factors including genetics, sex, age, health status, and drug/antibiotic consumption. Over the last decade, a large number of publications have reported a prominent role of microbiota in metabolic diseases.

Notably, accumulated evidence suggests an association between a dysregulated gut microbiome and obesity, glycemic control impairment, and therefore T2DM pathophysiology.

2. Obesity, Diabetes, and Dysbiosis

The preservation a normal and healthy gut microbiota plays a critical role in maintaining good health. Alterations of both composition and function of the microbiota, termed dysbiosis, are common features of several pathologies including metabolic diseases such as obesity and T2DM.

A number of preclinical and clinical studies have attempted to describe the differences between gut microbiota in obese, compared to lean individuals and have reported that obesity is related to lower microbial diversity and greater depletion. In early obesity, microbiota studies report that an increase of body weight is associated with a microbiota shift.

Although T2DM is generally considered as an attribute to obesity, some studies have correlated glycemic control impairment and insulin resistance to specific gut microbiota composition. Furthermore, antidiabetic drugs liraglutide and metformin have been recently shown to significantly lower body weight and improve glucose metabolism while considerably modifying the composition of gut microbiota.

Liraglutide decreased obesity-related microbial phenotypes and increased lean-related phenotypes while metformin modifies the intestinal microbiota composition by inducing the growth of several bacteria.

There is proof that gut microbiota is involved in the beneficial glucose-lowering effects of antidiabetic agents and that it is a promising therapeutic target in T2DM and the glycemic control impairment context.

3. How can Gut Microbiota be moderated?

Through several mechanisms, gut bacteria influence the chronic low grade inflammation that culminates in insulin resistance and the increase in fat deposits and body weight gain, characteristic of obese individuals.

With the acknowledgement of these obesity and inflammation induction mechanisms, several strategies to block or attenuate them are being developed and tested, in order to benefit obese and type 2 diabetic patients. We will look at these mechanisms and the effect they have:

3.1. Antibiotic Therapy

The use of broad spectrum antibiotic therapy greatly modifies the gut microbiota profile although the prevalence of surviving bacteria and the benefits for the host have not been determined, as the concept of a “healthy” gut microbiota is still under investigation.

The main mechanism suggested by antibiotic administration is a reduction in circulating LPS levels, which lessens inflammation and improves the insulin resistance induced by obesity in the liver, muscle, and adipose tissue. Improved intestinal function has also been noted as a benefit of the administration of antibiotics.

However, even with this striking metabolic improvement in antibiotic therapy experiments, it seems that translating this strategy to humans is not the best option, as there are complex issues such as antibiotic resistance in chronic administration panels and evidence that indicates a relationship between chronic low-dose antibiotic therapy and body weight gain.

3.2. Probiotics

Probiotics are live microorganisms that can be consumed through fermented foods or supplements. More and more studies show that the balance or imbalance of bacteria in your digestive system is linked to overall health and disease. Probiotics promote a healthy balance of gut bacteria and have been linked to a wide range of health benefits.

As obesity is a key cause of diabetes, probiotics can help with weight loss through a number of different mechanisms. An example is that some probiotics prevent the absorption of dietary fat in the intestine.The fat is then excreted through feces rather than stored in the body. Probiotics may also help you feel fuller for longer, burn more calories and store less fat. This is partly caused by increasing levels of certain hormones, such as GLP-1.

Probiotics may also help with weight loss directly. In one study, dieting women who took Lactobacillus rhamnosus for 3 months lost 50% more weight than women who didn’t take a probiotic. Another study of 210 people found that taking even low doses of Lactobacillus gasseri for 12 weeks resulted in an 8.5%.

It is however important to note that not all probiotics aid in weight loss. Some studies have found certain probiotics, such as Lactobacillus acidophilus, can even lead to weight gain.

3.3. Prebiotics

Prebiotics are classified as the non-digestible food ingredients that probiotics can feed off. They are used in the gut to increase populations of healthy bacteria, aid digestion and enhance the production of valuable vitamins. Galactooligosaccharides (GOS) are the most advanced form of prebiotics which belong to a group of particular nutrient fibers that feed and encourage the growth of good bacteria in the gut.

The major source of prebiotics is dietary fibre. They occur naturally in fruits and vegetables, but you can also take them in the form of nutritional supplements.

3.4. Bariatric Surgery

Bariatric surgery is an important method in the treatment of obesity. It is quite effective in achieving and protecting weight loss. This effectiveness of obesity treatment after bariatric surgery is not only related to food consumption. The altered microbiota after bariatric surgery has an impact on its effectiveness. Malabsorption status after bariatric surgery, changes in the metabolism of bile acids, changes in gastric pH, and changes in the metabolism of hormones lead to gut microbiota changes. Changes in microbiota also affect energy homeostasis. Because of these reasons, body weight loss is achieved after bariatric surgery.

4. What role will gut microbiota play in the treatment of T2DM in the future?

It is becoming increasingly clear that gut microbiota has profound impact on general health and well-being. Notably, it is now well-established that imbalanced gut microbiota is linked to host glycemic control impairment and T2DM development. Although the precise role of gut microbiota remains incompletely understood, further investigation is likely to be very helpful in the treatment and control of obesity, and resultant Type 2 Diabetes.

Current treatments of this complex chronic disease are far from being ideal since in a majority of patients, T2DM remains poorly controlled in the long run. Using pre/probiotics to control blood glucose has been considered for a long time, and the discovery of the key roles of gut bacteria in T2DM has boosted research efforts in this field.

A better understanding of how gut microbiota impacts general health will help in outlining new treatment strategies. These strategies will help in identifying probiotic strains with antidiabetic activities, or nutritional interventions that can increase helpful microbiota in the gut.

References:

1. Hindawi (2013): Influence of Gut Microbiota on Subclinical Inflammation and Insulin Resistance. Retrieved from https://www.hindawi.com/journals/mi/2013/986734/2. Frontiers in Endrocrinology (2019): Impact of Gut Microbiota on Host Glycemic Control. Retrieved from https://www.frontiersin.org/articles/10.3389/fendo.2019.00029/full

3. NCBI (2019): The effects of bariatric surgery on gut microbiota in patients with obesity: a review of the literature. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343052/

4. Bimuno(2018) : Prebiotics. Retrieved from https://www.bimuno.com/prebiotics

5. Healthline (2016): 8 Health Benefits of Probiotics. Retrieved from https://www.healthline.com/nutrition/8-health-benefits-of-probiotics

Many people living with diabetes often wonder if diabetes remission is a possibility for them.  Well, for most people, this is an achievable goal. If you are lucky enough you can go for years without taking any diabetes medication but still maintain normal sugar levels if you are willing to put in the hard work. This article will show you how.

Type 2 diabetes is a serious chronic condition that can cause debilitating effects. It can be lifelong and get worse over time for many, but only the flip side, it can also present no problems when it goes into long-term remission.

Most people embrace a triad approach to treating Type 2 diabetes; medication, diet, and exercise. Some lucky few are able to drop off their medication and still maintain normal blood sugar.  But research shows that many people can be able to achieve a similar level of success in the management of diabetes.

Is diabetes reversal the same as diabetes remission?

Remission is often confused with diabetes reversal. However, the two mean totally different things. Whereas reversal implies that one is completely cured of diabetes, remission means that a person is living symptom-free for a long duration of time without being on medication. With remission, there is always the awareness that the disease might recur. Our article on the difference between diabetes reversal and remission explains it better. You can read it here.

What is diabetes remission?

Diabetes remission occurs in people suffering from Type 2 diabetes; it means that you can maintain normal blood sugar levels without needing to take any diabetes medication. Diabetes remission is not a cure for diabetes. The term remission means that Type 2 diabetes might come back, or it might not. Also, if one resumes normal diet and lifestyle (unhealthy) then their blood sugar is likely to spike.

In 2009, the American Diabetes Association defined Type 2 Diabetes as follows:

3 Categories

Partial remission, complete remission and prolonged remission as

• Partial remission: blood sugar which does not meet the classification for Type 2 Diabetes; fasting blood glucose 5.5 – 6.9 mmol/l for at least 1 year.
• Complete remission: normal glucose values i.e. fasting blood glucose < 5.6 mmol/L for at least 1 year.
• Prolonged remission: normal glucose values i.e.
  fasting blood glucose < 5.6 mmol/L for at least 5.

For all the three categories listed above, the patient must have been off all diabetic medication for the given duration of time. According to the American Diabetes Association, when a person combines diet and exercise with blood sugar lowering medication such as Metformin they do not qualify for remission.

Remission can be achieved after bariatric surgery or by making drastic dietary and lifestyle changes.

How To Achieve Diabetes Remission

1.    Weight Loss

Losing weight around the waist can significantly increase your chances of remission.

Before embarking on a weight loss journey, it is important to first consult with your healthcare provider. This is to make sure it’s safe for you, especially if you have other health conditions. You might also need help in determining which weight loss approach works best for you.

To understand how losing weight can cause remission, we need to draw the link between being overweight and Type 2 diabetes. The fat that builds up around the midsection is dangerous because it surrounds important organs like the liver and pancreas. This makes it more difficult for those organs to work properly, leading to Type 2 diabetes.

Research has shown that almost 50% of individuals with type 2 diabetes can achieve remission to a non-diabetic state through weight loss. This has been associated with early and sustained improvement in the functioning of pancreatic beta cells.

However, not everyone who develops Type 2 diabetes is overweight. Other factors such as age, ethnicity and family history come into play as well. These factors influence how well the liver and pancreas work, and also where we store our fat. As much as we cannot change these factors, we can influence diabetes type 2 by altering the factors within our control.

Also, not everyone who loses extra weight will go into remission. However, weight loss on its own has significant health merits for a diabetic person. This may mean having to take fewer meds and having less risk for complications.

2.    Making Drastic Diet and lifestyle changes

Research has shown that a low-calorie diet could help people lose weight and go into remission. Other than promoting weight loss, switching to a non-inflammatory diet can also reduce insulin resistance. Metabolic inflammation is a key driver for insulin resistance and type 2 diabetes. Improving insulin sensitivity can trigger remission. For more on non-inflammatory diets, you can read out the article here.

Lifestyle changes such as taking up regular exercise will also help to achieve weight loss.

3.    Weight loss surgery for diabetes remission

Bariatric surgery can also help one to achieve remission. What bariatric surgery does is to actually help one to eat less and achieve healthy and sustainable weight loss. Bariatric surgery is not a quick fix for obesity and diabetes. However, in a few circumstances, your doctor may recommend this approach. Note that before approval you have to show dedication and discipline that you will be able to stick through the weight loss program.

What To Do When You Are In Remission

Diabetes remission may mean different things for different people. For others, it may last for a year before it recurs again while for others it may disappear for extended periods of time. However, it comes with reduced blood sugar, better cholesterol levels and reduced blood pressure for most people. These signs are an indication of better health outcomes in the long run.

Once you are in remission, you should strive to maintain the positive health habits that triggered the remission in the first place. Keep going to your regular check-ups and speak to your healthcare team if you’re worried about anything or have any questions. Maintain a positive and hopeful spirit as you work towards achieving prolonged remission.

References

1. Diabetes UK: What is diabetes? Retrieved from https://www.diabetes.org.uk/diabetes-the-basics/what-is-type-2-diabetes
2. Diabetes UK: Diabetes Remission. Retrieved from https://www.diabetes.org.uk/guide-to-diabetes/managing-your-diabetes/treating-your-diabetes/type2-diabetes-remission#remission%20research
3. Science Daily (2018): Why weight loss produces remission of type 2 diabetes in some patients. Retrieved from https://www.sciencedaily.com/releases/2018/08/180802141722.htm

In our previous article, I introduced the term diabesity. In case you haven’t read it, you can check it here (link to what is diabesity). In a nutshell, diabesity is the description of diabetes type 2 when it occurs in the context of obesity. Diabesity is triggered by the onset of insulin resistance which means that insulin is not able to take out glucose from the bloodstream. Insulin resistance is often accompanied by excessive insulin as the beta cells of the pancreas keep producing more insulin to get rid of excess sugar. In this article, we will discuss what role inflammation plays and why it might be the most important mechanism fuelling the diabesity epidemic.

Why are anti-inflammatory drugs not the mainstay of diabetes type 2 treatment?

Before delving into the meat of the diabesity-inflammation pendulum, I decided to throw in a teaser.  I will quote from an article published in JCI in 2006 titled “Inflammation and Insulin Resistance.”

“Clues to the involvement of inflammation in diabetes date back to more than a century ago when high doses of sodium salicylate (5.0–7.5 g/d) were first demonstrated to diminish glycosuria in diabetic patients having type 2 diabetes. In 1876 Ebstein concluded that sodium salicylate could make the symptoms of diabetes mellitus totally disappear.”

Why then are anti-inflammatory agents not the mainstay of diabetes type 2 treatment? This is indeed a controversial topic. However, it is believed that sodium salicylate was dropped because of the serious side effects it causes when given in high doses.

Now we can look at the pendulous relationship between diabesity and inflammation.

How does Inflammation Cause Diabesity?

There are several lines of evidence linking inflammation with obesity and diabetes. I will outline a few:

1. Inflammatory markers are elevated prior to the diabesity.

Elevated levels of inflammatory cytokines could indicate future weight gain and obesity. A lab study also showed that an infusion of inflammatory cytokines into healthy mice causes insulin resistance.

This idea is also supported by the fact that people with other chronic inflammatory conditions are more likely to develop diabesity and type 2 diabetes.

2. Inflammation causes insulin resistance

Inflammation of the fat tissue causes insulin resistance, which is the primary cause of diabesity. A small protein known as TNF-α which is released during inflammation has been shown to cause insulin resistance. Other inflammatory proteins such as MCP-1 and C-Reactive protein, have also been linked to insulin resistance.

3. Inflammation in the brain causes leptin resistance

Inflammatory signaling in the hypothalamus has been linked to leptin resistance in both animals and humans. Leptin is produced in fat cells but exerts its effects primarily in the hypothalamus. It is the starvation hormone, but it is also referred to as the obesity hormone. Leptin resistance means that your body is no longer responsive to the hormone leptin. When this happens, your brain is fooled into believing that you are starving and hence you need to keep eating more and more food. Eventually, this leads to diabesity.

How Does Diabesity Cause Inflammation?

For a long time, it was believed that fat is an inert tissue with no biological activity. However, it is now known that fat is a metabolically active endocrine organ that produces hormones and inflammatory molecules. The feature of fat is the key to understanding its role in diabesity and inflammation.

1. Diabesity induces inflammation as a protective mechanism.

Diabesity causes the buildup of fat around the waist. Fat storage is an anabolic process while inflammation is a catabolic process. The body may activate catabolism through inflammation so as to keep weight within acceptable limits. Experimentally induced inflammation in fat tissue has been shown to initiate weight loss and improve insulin resistance.

2. Diabesity related stresses could cause inflammation

Obesity has been associated with chronic low-level inflammation. it is hypothesized that the stresses of diabesity are similar to the stresses caused by an infection. As a result, the body responds in a similar way by triggering inflammation.

Obesity has also been linked to the release of inflammatory compounds such as TNF-α. This means that the more fat tissue you have, the more inflammation you are likely to have.

The Chicken Versus The Egg

It is clear that there is a direct relationship between diabesity and inflammation. However, it is not very clear which factor precedes the other. Inflammation is both the cause and the result of diabesity. Inflammation plays a big role in causing diabesity. On the other hand, the occurrence of diabesity can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.

We can then confidently conclude that the best approach towards the treatment or prevention of diabesity has to begin with addressing the underlying inflammation. It should also involve treating inflammation once diabesity has occurred. The modern clinical approach is focused on regulating blood sugar without addressing inflammation.  Unfortunately, such an approach is bound to produce inferior results.

References

1.   ADA: Inflammation-Sensitive Plasma Proteins Are Associated With Future Weight Gain.  Retrieved from https://diabetes.diabetesjournals.org/content/52/8/2097.full?ijkey=c30ecf67b38ac20bc59ecf06ac0a8cbb539532fc

2.   NCBI (1993): Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/7678183?dopt=Abstract

3.   NCBI (2012): Obesity is associated with hypothalamic injury in rodents and humans. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248304/

4.   JCI (2005): Inflammation, stress, and diabetes. Retrieved from https://www.jci.org/articles/view/25102/version/1