Categories
Uncategorized

Refined Grains: The Good, the Bad, the Ugly

Important Points:

  • whole grains
  • refined grains
  • Western dietary pattern
  • diabetes
  • obesity

Refined Grains: The Good, the Bad, the Ugly

Flour is all around us and a temptation at every meal. Breakfast toast, bagels, cereal, and pancakes fill our tables. Lunch revolves around sandwiches, wraps, pasta and pizza. Refined grains have been vilified as one of the leadings causes of ill health. Is there any truth to this? Should we toss all refined grain products off our tables? We will have an in-depth look at the good, the bad, and the ugly of refined flour to give you a better understanding of the goodies on your plate.

What are Refined Grains?

Refined grain is the term used to refer to grains that are not whole, because they are missing one or more of their three key parts (bran, germ, or endosperm). White flour and white rice are refined grains, for instance, because both have had their bran and germ removed, leaving only the endosperm. Refining a grain removes about a quarter of the protein in a grain and half to two thirds or more of a score of nutrients, leaving the grain a mere shadow of its original self.

Further refining includes mixing, bleaching, and brominating; additionally, thiamin, riboflavinniacin, and iron are often added back in to nutritionally enrich the product. Because the added nutrients represent a fraction of the nutrients removed, refined grains are considered nutritionally inferior to whole grains. However, for some grains the removal of fiber coupled with fine grinding results in a slightly higher availability of grain energy for use by the body.

Grain refining led to disastrous and widespread nutritional problems, like the deficiency diseases pelagra and beri-beri. In response, many governments recommended or required that refined grains be “enriched.”

The Good

The federal government’s 2010 Dietary Guidelines for Americans recommend that half your daily grain intake be from high-fiber whole-grain sources, foods like brown rice, oatmeal and whole-wheat bread. Nutritionists often exhort people to choose whole grains over refined ones whenever they can.

But according to one leading nutrition researcher, Julie Miller Jones, a professor emeritus at St. Catherine University, we shouldn’t be so eager to throw out refined grains altogether. Refined grains do have some benefits — namely, nutrients added to refined flours.

Since folic acid was added to bread, cereal and other grains in 1999, the rate of newborns with neural tube defects — a known consequence of folic acid deficiency — has decreased 46%. Additionally, important nutrients like copper and iron are more easily absorbed when eaten with refined grains. Whole grains are healthy because they’re so high in fiber, which Americans don’t get enough of, but that fiber also fast-tracks food through the digestive system, absorbing nutrients along the way.

The Bad

As our national appetite for flour has inched up, so has the incidence of diet-related ills, such as obesity, heart disease and diabetes. Coincidence? Many nutrition experts don’t think so. When they weigh the evidence linking food choices and disease, they see the white, dusty fingerprints of flour everywhere.

Flour started out as an ingenious fix to a vexing problem. Grass seeds were plentiful, but the tough outer shell (the husk) made the seeds difficult to chew and digest. Early humans outsmarted the seeds by grinding them between stones, crushing the outer layers to get at the goodness inside. The result — a coarse powder — was the first whole-grain flour.

The downside was spoilage. Crushing the germ released its oils, which quickly turned rancid when exposed to air. With the advent of industrial milling in the late 1800s, machines began filtering out the germ and pulverized the remaining endosperm into a fine, white powder that lasted on the shelf for months. And so all-purpose white flour was born — along with a host of health problems.

Beneath their rigid architecture, whole-kernel grains conceal an array of vitamins, minerals, phytonutrients and fiber. But when machines pulverize kernels into flour, even whole-grain flour, what’s left behind is a starchy powder capable of wreaking havoc on the body.

The Ugly

Overconsuming flour can lead to a number of problems in the body, including:

  • Food Allergies/Intolerances. Gluten intolerance is a term that has become synonymous with the current generation. Wheat 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
  • Blood-Sugar Spikes. The difference between a whole-kernel grain and a processed grain all boils down to the glycemic index, which is how quickly the body turns food into fuel, or glucose. Foods made with wheat flour are particularly damaging. A carbohydrate in wheat, called amylopectin A, is more easily converted to blood sugar than just about any other carbohydrate. Two slices of bread made with whole-wheat flour raise blood sugar higher than six teaspoons of table sugar and higher than many candy bars.
  • Food Cravings.  One of the biggest changes in modern wheat is that it contains a modified form of gliadin, a protein found in wheat gluten. Gliadin releases a feel-good effect in the brain by morphing into a substance that crosses the blood-brain barrier and binds onto the brain’s opiate receptors and makes you want to eat more.
  • Caloric Overload. A refined grain packs more calories than a whole-kernel grain because it is more concentrated, and foods that are high in grains also tend to be high in sugar and industrialized fats. These foods contribute largely to obesity and the diabetes epidemic.
  • Metabolic Slowdown. 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 significantly. When glucose drifts in the blood, it attaches itself to nearby proteins resulting in a chemical reaction called glycation, a pro-inflammatory process that plays a role in a host of inflammatory diseases.
  • 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. Additionally, 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.
  • 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.

The Bottom Line….

Grains are not essential, and there is no nutrient in there that you can’t get from other foods.

Categories
Uncategorized

What’s on your plate? Does overeating cause diabetes?

Important Points:

  • Diabetes
  • Diet
  • Sugar
  • Physical activity
  • Obesity

What’s on your plate? Does overeating cause diabetes?

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, and approximately 95% of all cases are type-2. It is not known what the exact cause of type-1 diabetes is, but type-2 has been attributed to poor diet and a lack of exercise.

Both types present with excess glucose, or blood sugar, in their blood that is not removed by the hormone called insulin as it should be. In type-2 diabetics, fat, liver, and muscle cells no longer respond correctly to insulin creating an insulin resistance. 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 are 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. The Role of Diet in Type 2 Diabetes

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 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 at the same period such as Japan and North American countries.

Though consumption of carbohydrates has been shown to increase the risk of developing Type 2 Diabetes, sugar is a more harmful culprit. In a 19-month study that involved more than 500 ethnically diverse schoolchildren, 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, principally as a result of 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 some foods and obesity; both the composition and volume of food matter in this case. High intake of red meat, sweets, and fried foods contribute to the increased risk of insulin resistance and Type 2 Diabetes. Inversely, consumption of vegetables may protect against the development of Type 2 Diabetes, as they are rich in nutrients, fiber and antioxidants which are considered 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 Type 2 Diabetes. Dietary knowledge is a significant factor that influences dietary behaviors.

3. How 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 lead 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 just as 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 and sometimes thought to be the most important. When missed, it can result in health issues. A 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 good 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.

Categories
Uncategorized

What is the relationship between metabolic Inflammation and type 2 diabetes?

Important Points:

  • Inflammation
  • Diabetes
  • Obesity
  • Metabolic syndrome
  • Beta cells

What is the relationship between metabolic Inflammation and type 2 diabetes?

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

1. The Metabolic Syndrome and Metabolic Inflammation

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

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

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

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

Various proposals and hypotheses have been developed to describe the mechanisms involved in the propagation of diabetes, mainly focusing on Type 2. The increase in prevalence of the condition has been related to well-recognized risk factors, such as the adoption of a western lifestyle, lack of physical activity, and high sugar diet. 

Genetic predisposition, ethnicity, and aging are not modifiable risk factors for Type 2 diabetes, but other factors such as being overweight or obese, an unhealthy diet, insufficient physical activity, and smoking are modifiable through behavioral and environmental changes. However, increasing evidence has shown that inflammatory pathways are common in both the modifiable and non-modifiable factors.

 2. When was inflammation first thought to cause diabetes?

Observational studies provided the first evidence for the possible association between inflammation and diabetes. Over a century ago, the administration of high doses of salt led to decreased blood sugar in people with a suspected or definite diagnosis of diabetes.Later studies on the role of inflammation in diabetes revealed that this hypoglycaemic action was related to the inhibition of an enzyme which is one component in the insulin response pathway.

A landmark study to correlate inflammation with diabetes, conducted in animal models by Hotamisiligil et al. in 1993, revealed that tumor necrosis factor-alpha (TNF-alpha) played a role in obesity and particularly in insulin resistance and diabetes.Causal connections between inflammation and obesity or Type 2 diabetes were made because of these findings. 

Over the next decades, many studies provided more supporting evidence for the role of inflammation in the initiation and progression of diabetes.Accumulative evidence suggests that chronic inflammation in target cells of insulin action may contribute to obesity, insulin resistance, and related metabolic disorders including Type 2 diabetes. 

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

In several studies, our understanding of insulin resistance and insulin secretion in the onset of Type 2 diabetes and its progression has been expanded.Subjects at risk of T2D display an initial state of insulin resistance compensated by hypersecretion of insulin in the beta cells. As it progresses, this shift in pancreatic function is eventually unable to cope with the required insulin secretion, and by the time diabetes is diagnosed, beta cells are no longer able to secrete enough insulin. 

Although the relative contribution of beta cell dysfunction and insulin resistance can vary in people with Type 2 diabetes, it is generally accepted that abnormal insulin sensitivity precedes the clinical diagnosis of diabetes by up to 15 years.Therefore, along with looking into the mechanism of insulin resistance, studies have investigated the pathways leading to beta cell failure.

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

The evidence is inconclusive whether the inflammatory state in Type 2 diabetes can spread to other organs such as the liver, the neural system, and possibly skeletal muscle. More research is needed to determine this.

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

Below are some of the approaches currently being investigated.

  1. Gauging anti-inflammatory diets in streamlining an individual’s microbiome through innovative approaches for Type 2 diabetes
  2. Examining the effects of vitamin D supplementation on serum levels of inflammatory markers through clinical trials; results so far are inconsistent
  3. investigating whether antagonists of leukotriene production enzymes or receptor binding BLT1 have benefits for metabolic and cardiovascular health; results have not been reported yet

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

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

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

Type 1 diabetes is considered to be more of an immunological response rather than a metabolic disorder and the preliminary results of trials using anti-inflammatory and immunomodulatory medication are promising. These treatments in combination with possible use of stem cells to regenerate pancreatic beta cells could potentially be the key to permanent treatment of Type 1 diabetes. Therefore, after a holistic review of the possible mechanisms that lead to Type 1 and Type 2 diabetes and the numerous already described inflammation pathways that are involved, it becomes more and more clear that future research should focus on simultaneous suppression of various inflammatory response pathways rather than focusing on one pathway at a time.

Categories
Uncategorized

Is there a solution to rising insulin prices?

Important Points:

  • Insulin price
  • Diabetes
  • Ration

Is there a solution to rising insulin prices?

The subject of the rising cost of insulin has been a contentious topic of debates about policies in the eyes of the public; however, the human struggle of patients trying to cope has been given less exposure. Patient struggles include hospitalization and even the death of those who tried rationing their insulin supply to make it last longer.

Aside from rationing, some patients resulted to decreasing their carbohydrate intake just to reduce their insulin dose, while others cut cost by reusing insulin needles and blood glucose test strips, all the risk of inaccurate measurements and infection.

Despite this alarming news, the exact number of people who died or were harmed because of these rationing practices is not known most likely because patients and family members are embarrassed about reporting.

Because of these difficulties, grassroots advocacies were formed including the campaign hashtag #Insulin4all under the support of UK nonprofits T1 and Pendsey Trust.  Most of the supporters within #Insulin4all are very critical of those involved in making policies especially politicians. They go as far as accusing the pharmaceutical industry of making diabetics an underclass.

The alleged reason for the skyrocketing prices of insulin has been attributed to the monopoly of three companies with a choke hold on setting the price for insulin.

The theory behind preventing deaths from rationing is that having a more open communication between the patients and the clinician is the key. Many times, this conversation is limited due to patient’s feelings of failure, of not being seen as independent, of embarrassment about not being able to afford their own medication.

One foreseen consequence of the rising prices is the desire to go back to using older generation human insulins called NPH and Regular. This is inconvenient for the patient since it requires a syringe and a needle, and unlike modern prefilled doses that comes in pens, could result in the patient not getting the right dose or figuring out the right dosing schedule.

Given the problem stated above, the solution may lie in making laws. Some experts are a fan of transparent pricing in which drug companies are required to reveal detailed information on how prices for insulin are determined.  Associations like the American Medical Association have strongly urged the US Federal Trade Commission and the Department of Justice to strictly monitor insulin pricing and to enforce actions when possible.

It is important to note that the brands Novo Nordisk, Sanofi, and Eli Lilly promised means and ways to remain affordable to the patients, but relying on corporate promises may not be the best solution to this serious problem either.

Diabetes Patients Beg, Ration Insulin in Deepening Crisis

https://www.medscape.com/viewarticle/901660?src=WNL_infoc_180926_MSCPEDIT_diab&uac=214448FJ&impID=1745588&faf=1

Categories
Uncategorized

How much inactivity can trigger diabetes symptoms?

Important Points:

  • Diabetes
  • Active
  • Inactivity
  • Health benefits

How much inactivity can trigger diabetes symptoms?

One of the core risk factors for diabetes and general unhealthiness is sticking to a sedentary lifestyle. Not moving around or having no physical activity not only promotes muscular decline and weakness of the heart, it can also lead to the development of type 2 diabetes.

According to a study published in The Journals of Gerontology, two weeks of inactivity in pre-diabetic individuals was enough to trigger symptoms of diabetes. Researchers asked the study participants to limit their daily steps to no more 1000 steps per day using a pedometer, and after two weeks’ worth of inactivity, the symptoms of diabetes became apparent, including an increase blood sugar levels, an increase in the onset of insulin resistance, reduction in skeletal muscle mass, and hastening of the onset of diabetes itself.  Researchers expected these results but what shocked them the most was how much harder reversing the symptoms was. Even more alarming is the fact that it takes two weeks of normal activity to restore the body into its prediabetic symptoms state.

The silver lining we can get from this study is knowing the importance of staying active. If you want a more serious incentive to keep moving, keep in mind that activity directly prevents diabetes as well as producing overall health benefits.  The National Institute of Diabetes and Digestive and Kidney Diseases recommends losing just 5 to 7 percent of your body weight as it helps delay the onset of type 2 diabetes, and keeping active will aid in losing that body weight, thus furthering the relationship between activity and diabetes prevention. Keeping yourself active – even just 40 minutes of moderate intensity exercise 3 to 4 times a week – will reduce your blood pressure and help regulate your cholesterol level.

Sedentary lifestyle and risk of obesity and type 2 diabetes

https://www.ncbi.nlm.nih.gov/pubmed/12733740

Failed Recovery of Glycemic Control and Myofibrillar Protein Synthesis With 2 wk of Physical Inactivity in Overweight, Prediabetic Older Adults

https://academic.oup.com/biomedgerontology/article-abstract/73/8/1070/4583629?redirectedFrom=fulltext

Health Risks of Being Overweight

https://www.niddk.nih.gov/health-information/weight-management/health-risks-overweight

American Heart Association Recommendations for Physical Activity in Adults

https://www.heart.org/en/healthy-living/fitness/fitness-basics/aha-recs-for-physical-activity-in-adults

Categories
Uncategorized

How can intermittent fasting help with your health?

Important Points:

  • Intermittent Fasting
  • Benefits
  • Diabetes

How can intermittent fasting help with your health?

Intermittent fasting may be a new concept for some, but it’s gaining a lot of popularity especially because of its touted health benefits. Intermittent fasting is not a diet in a classical sense since it does not limit the amount of food or restrict the type of foods eaten. Instead, it changes the time in which a person eats, most often practiced by fasting the whole day and only eating at a specified time once a day. 

A research article published on Annual Review of Nutrition states that the benefits of intermittent fasting include prevention of obesity and its related conditions including diabetes and cancer. Another study in mice found that mice who fasted lived healthier and longer compared to mice that had free access to food.  One study published in the journal Science Translational Medicine found that people who fasted showed marked improvements on disease indicators. Their fasting blood sugar, which is an indicator of diabetes risk, and their cholesterol and triglyceride levels all improved.  It’s notable that participant’s lost abdominal fat without losing muscle mass.

How exactly does fasting help our body stay healthy such that we can reap these benefits? The current theory is when a person fasts, the body uses stored fat as a primary source of energy instead of using glucose. This is why those who fast showed a marked reduction in body fat compared to those who didn’t.

It is important to understand that despite having these benefits, not everyone should practice intermittent fasting. Those already in top health would not see as much benefit from fasting, and those who already have diabetes will struggle to achieve these benefits. 

If you want to try out intermittent fasting, be safe and get help with your diet.

Metabolic Effects of Intermittent Fasting

https://www.annualreviews.org/doi/pdf/10.1146/annurev-nutr-071816-064634

Daily Fasting Improves Health and Survival in Male Mice Independent of Diet Composition and Calories

https://www.sciencedirect.com/science/article/pii/S1550413118305126?dgcid=rss_sd_all

Fasting-mimicking diet and markers/risk factors for aging, diabetes, cancer, and cardiovascular disease

http://stm.sciencemag.org/content/9/377/eaai8700

Categories
Uncategorized

Gut Bacteria’s Effect on Brain Health

Important Points:

  • Diabetes
  • Chronic Fatigue Syndrome
  • Fatigue
  • Multiple Sclerosis

Gut Bacteria’s Effect on Brain Health

Our brain is one of the most complex living structures know to man. Until recently, we have viewed the brain as sole and central to our bodies function, but today there is new information telling us that the brain might not be working on its own. We would never typically associate the brain’s complicated functions with the system responsible for processing our food, but there is a strong connection. Our brain function is heavily influenced by our gut, specifically by our gut bacteria.

Through science, we have determined that there is good and bad microbiota within our digestive system. Its careful balance is important in our nutrition and ultimately our survival. According to the study done by the European Academy of Neurology, the function of those bacteria may not be limited to nutrition alone. They have determined that this microbiota is capable of eliciting bravery and even triggering the disease process for multiple sclerosis.  The research points out those mice that have a germ-free intestinal environment experience a state of relaxation, relatively free from anxiety, producing an effect of increased bravery. It was also shown that when the gut is maintained germ-free, there is an associated increased in the formation of the brain’s protective structure in the form of myelination.  Lack of myelination or damage to the myelin sheath is one of the pathologic processes behind Multiple Sclerosis.

The strong link between the gut and the brain does not end there. A research finding published by the University of Illinois shows that gut microbiota can alter the body’s endocrine function. In the study, it was found out that black males with Type 2 Diabetes have significantly lower number of good bacteria and more of the bad ones.

Another recent study confirms the importance of a healthy microbiota to healthy rest and was published by Cornell University. Chronic Fatigue Syndrome, a condition in which normal activity causes extreme weakness which is not alleviated by rest, has stumped doctors for decades. The findings revealed that those with the condition have a distinct inflammation found in the gut. Upon further analysis, it was found out that people with chronic fatigue syndrome have intestinal bacteria that can trigger the immune response causing the debilitating condition.

Recent studies all point out the significance of the gastrointestinal system in neurologic, endocrine, and inflammatory diseases. Perhaps a better approach is to start exploring the gut for the culprits first instead on focusing on the affected organ. It also opens up the playing field to new classes of drugs that can alter the microbiota instead of targeting the brain itself.

European Academy of Neurology. (2016, May 29). Connections between gut microbiota and the brain. ScienceDaily. Retrieved July 5, 2016 from www.sciencedaily.com/releases/2016/05/160529174445.htm

University of Illinois at Chicago. (2015, March 6). Gut bacteria may contribute to diabetes in black males. ScienceDaily. Retrieved July 5, 2016 from www.sciencedaily.com/releases/2015/03/150306102752.htm

Cornell University. (2016, June 27). Chronic fatigue syndrome is in your gut, not your head. ScienceDaily. Retrieved July 5, 2016 from www.sciencedaily.com/releases/2016/06/160627160939.htm

Categories
Uncategorized

Does gut microbiota fuel metabolic inflammation and dysregulation?

Important Points:

  • Probiotics
  • Microbiota
  • Diabetes
  • Antibiotics
  • Prebiotics

Does gut microbiota fuel metabolic inflammation and dysregulation?

Given that obesity and the 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. Obesity, Diabetes, and Dysbiosis

Obesity is a chronic, complex, and multifactorial disease representing the fifth leading cause of death in the world 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 is affected by 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 Type 2 Diabetes pathophysiology.

The preservation of 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 Type 2 Diabetes.

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

Although Type 2 Diabetes is generally attributed 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 Type 2 Diabetes and any glycemic control impairment context.

2. How can Gut Microbiota be moderated?

Through several mechanisms, gut bacteria influenced 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. Here are a few of these mechanisms and their effects:

2.1. 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.

2.2. 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 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% loss.

It is 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.

2.3. 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 fiber occurring naturally in fruits and vegetables, but you can also take them in the form of nutritional supplements.

2.4. 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 too. Malabsorption status after bariatric surgery, changes in the metabolism of bile acids, changes in gastric pH, and changes in the metabolism of hormones all lead to gut microbiota changes. Changes in microbiota also affect energy homeostasis. Because of these reasons, body weight loss is achieved after bariatric surgery.

  • What role will gut microbiota play in the treatment of Type 2 Diabetes in the future?

It is becoming increasingly clear that gut microbiota has profound impact on general health and well-being. It is now well-established that imbalanced gut microbiota is linked to host glycemic control impairment and Type 2 Diabetes 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, Type 2 Diabetes 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 Type 2 Diabetes 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

Categories
Uncategorized

Diabesity and Inflammation: A Case of Chicken and Egg

Important Points:

  • Diabesity
  • Diabetes
  • Obesity
  • Inflammation
  • Anti-inflammatory

Diabesity and Inflammation:
A Case of Chicken and Egg

In a previous article, I introduced the term “diabesity”, the description of Type 2 diabetes when it occurs in the context of obesity. Insulin resistance is defined by an inability of the body to respond to insulin and use up glucose in the blood. When insulin resistance sets in and glucose builds up in the blood, pancreatic beta cells produce excess insulin in an effort to bring down that glucose level. Diabesity is triggered by the onset of insulin resistance.

Because diabesity is diabetes in the context of obesity, we have to recognize that inflammation caused by obesity also plays a role in the onset of diabetes. Here, we will discuss what role inflammation plays and why it might be the most important mechanism fueling the diabesity epidemic.

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

Before delving into the connection of the diabesity-inflammation pendulum, I decided to throw in a teaser.  This quote is taken 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. It is believed that sodium salicylate was dropped because of the serious side effects it causes when given in high doses.

Let’s move on to the pendulous relationship between diabesity and inflammation.

How does Inflammation Cause Diabesity?

There are several lines of evidence linking inflammation with obesity and diabetes; here are 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, the primary cause of diabesity. A small protein known as TNF-α which is released during inflammation has been shown to cause insulin resistance, and 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 a hormone produced in fat cells that sends signals to the hypothalamus in order to regulate hunger and energy. It is sometimes called the starvation hormone and sometimes the obesity hormone. Leptin resistance happens when your body is no longer responsive to leptin, causing your brain to be fooled into believing that you are starving 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 builds up in anabolic processes while inflammation breaks down in catabolic processes. 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, setting up a proportional connection between the amount of fat tissue you have and the amount of inflammation your body experiences.

The Chicken Versus the Egg

It is clear that there is a direct relationship between diabesity and inflammation, but it is very difficult to determine which comes first. Inflammation is both a major cause of diabesity and occurs as a result of 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 believe the best approach towards the treatment or prevention of diabesity has to begin with addressing the underlying inflammation, and it should also involve treating inflammation once diabesity has occurred. Current 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