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What is Diabesity, and how to reverse it

Important Points:

  • Diabesity
  • Type 2 diabetes
  • Insulin resistance
  • Obesity
  • Sedentary lifestyle

What is Diabesity, and how to reverse it

If you are like most people you are probably thinking that I have confused diabetes for diabesity, or you are probably wondering whether I intended to say obesity. You are not so far away from the truth as diabesity is a modern disease that links obesity with type 2 diabetes. Diabesity should be a concern for people with normal blood sugars who may be accustomed to unhealthy eating and lifestyle patterns. It is unfortunate that much is not mentioned about diabesity which can predispose you to severe obesity, diabetes, and other fatal chronic conditions.

What Is Diabesity?

Diabesity is a sequence of events that starts with optimal blood sugar balance, to progressive insulin resistance, to being overweight, then becoming obese, and finally to full-blown Type-2 Diabetes. It comes in a spectrum that includes elevated blood sugar, elevated blood pressure, high cholesterol, and other health complications. These problems stem from diet, lifestyle, and environmental toxins interacting with our unique genetic susceptibilities. A study published in NCBI in 2013 concluded that “(diabesity) makes a strong call for utilizing indigenous, low-cost means of enhancing healthy dietary and physical activity habits.” Diabesity can also be described as the coexistence of obesity and type 2 diabetes.

What Are The Triggers For Diabesity?

Diabesity occurs following the development of insulin resistance and obesity. When your diet is full of empty calories: quickly absorbed sugars, liquid calories (soda, juice, sports drinks), and refined carbohydrates, you are likely to develop a resistance to insulin. Insulin (produced by beta cells in the pancreas) is the hormone that is responsible for grabbing glucose out of the bloodstream and storing it in cells. This ensures that blood sugar levels remain stable in the blood. When the body starts ignoring the signal sent out by insulin we call this insulin resistance. Beta cells will keep releasing more and more insulin to try to remedy the situation, so a high insulin level is one of the first signs. Unfortunately, the higher your insulin levels are, the worse your insulin resistance becomes. High insulin levels will also cause a spike in appetite which leads to overeating. Very soon you develop weight gain around the belly, more inflammation, oxidative stress, and other effects such as high blood pressure, high cholesterol, low HDL, atherosclerosis, and increased risk of cancer, Alzheimer’s, and depression.

It is important to note here that the root cause of the problem is insulin resistance and not elevated blood sugar. Fortunately, insulin resistance can be reversed since it is strongly linked to poor diet and an unhealthy lifestyle.

Most people can save themselves from diabesity by eliminating the factors that are upending the balance of their biology and replacing them with what’s needed to help the body re-balance itself.

Diabesity and Genetics

Many people believe that insulin resistance and diabesity are genetic conditions that cannot be extraneously controlled. True enough, our genetic predisposition plays a role in the way we choose what to eat and how to live. It also plays a role in the development of insulin resistance. However, insulin resistance and diabesity are greatly influenced by diet and lifestyle, so controlling these factors can greatly minimize your chances of developing the conditions.

How To Reverse Diabesity

Before reversing diabesity, there are a few things you can do to keep safe. They include:

1.   Know the signs of insulin resistance.

One of the first tell-tale signs of insulin resistance is uncontrollable weight gain. You might also experience increased blood pressure and skin discoloration (acanthosis nigricans) on rare occasions. Unfortunately, insulin resistance may go unnoticed for years. Hence, you may be better off having some tests done.

2.  Get the right tests done

You should get tested if you have a positive family history of type 2 diabetes and are affected by a poor diet as well as a sedentary lifestyle. An insulin response test is the best test to tease out the condition.

If you have already been diagnosed with diabesity, here are three things you can do to start your reversal journey.

Make healthy diet choices

This may involve the input of your physician, nutritionist/ dietician, and yourself to come up with the right meal plan. A healthy diet will start with the elimination of sugary and processed foods. Opt for wholesome grains, fresh vegetables and fruits, nuts, white meat, and unsaturated fats instead. You can read more about this type of diet here. (hyperlink to foods that improve insulin sensitivity).

Get adequate rest

Stress is a major contributor to insulin resistance and blood sugar imbalance. Stress also contributes to making unhealthy food choices and overeating. You need to make a conscious effort to de-stress frequently by:

  • Sleeping for at least 7 hours daily
  • Practicing relaxation techniques such as yoga
  • Taking breaks in between work like every two hours
  • Taking sabbaticals and vacationing periodically

Quit a sedentary lifestyle

Modern jobs involve sitting at an office desk and hitting the keypad hours on end. In a world where work is compensated by the hour, it can be difficult to make time for exercise. However, when you consider the negative long-term effects of a sedentary lifestyle you will be forced to reconsider the value of the extra money. What is the point if it’s going to cost your health in the long run? Quitting a sedentary lifestyle involves making deliberate choices about exercise and fitness. This may mean walking at least 30 minutes every day or engaging in more vigorous aerobic exercise 4-6 times a week.

References

1.   Science Daily (2012): Genetic variant is linked to obesity and insulin resistance. Retrieved from https://www.sciencedaily.com/releases/2012/06/120626151107.htm

2.   NCBI (2011): Is fast food addictive? Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21999689

3.   NCBI (2013): Diabesity. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23905459

 

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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.

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Does chronic overnutrition play a role in metabolic inflammation?

Important Points:

  • Inflammation
  • overnutrition
  • obesity
  • carbohydrates
  • fatty acids

Does chronic overnutrition play a role in metabolic inflammation?

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?

Background on Overnutrition

It is estimated that by 2020[b1] , two-thirds of the global burden of disease will be due to chronic non-communicable diseases, most of which are associated with an unhealthy 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 and doesn’t just affect those who are thin due to food shortages; 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 which threaten the integrity and normal physiology of an organism. Chronic nutrient overload causes an increase in fat tissue (adipose) irregularities in that, if adipose tissue expandability is low, there will be an increased presence of thickened tissue. This would lead to a proinflammatory state that can trigger insulin resistance, release of macrophage chemoattractant proteins, and in chronic inflammation, even the death of the thickened adipose tissue itself. This creates cyclic 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 triglycerides, lipids (fats) begin to accumulate in various tissues (e.g., muscle, liver, pancreas, and heart). The foundation of the metabolic syndrome thus appears to be overnutrition – more nutrient intake than can be safely disposed 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 cardiovascular disease 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:

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

Furthermore, high-carbohydrate intakes can prompt the formation of fatty acids in the liver by way of lipogenesis; fatty acids produced in this way can feed into the final common pathway of ectopic lipid accumulation. There is thus 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, 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 obesity trend 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 affordable, yet highly caloric meals, such as fast food and processed foods.

6. What 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 to be 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 act at tissue levels to influence the response to nutrient excess. Different people may react differently to accumulation of fat, but 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 the 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 the 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

 

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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.

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Metabolic signals and innate immune activation in obesity

Important Points:

  • Obesity
  • Inflammation
  • Innate immune activation
  • Non-alcoholic fatty liver disease
  • Infection

Metabolic signals and innate immune activation in obesity

The interplay between immunity, inflammation, and metabolic changes is a growing field of research. Exciting new evidence is emerging with regard to their role in the regulation of metabolism and the activation of inflammatory pathways during the progression of metabolic disorders such as Type 2 Diabetes and Atherosclerosis.

 1. The innate immune system

The innate immune system was made to sense and defend against infection and irritation. It sends signals creating a cascade of action from recognizing a threat of infection or irritation to the right cells which respond with the proper countermeasures. As the front line of defense, the innate immune system must be swift in recognizing these threats in order to establish a barrier that will keep the rest of the body healthy and disease free, and then it must provide a way to release that barrier once the threat has dissipated. When it sends many signals to set up barriers and not enough signals to remove the barriers, chronic inflammation is established. Long-lasting and low-grade chronic inflammation can often lead to Type 2 Diabetes and cardiovascular diseases.

2. How does the innate immune system work?

The innate immune system guards against all threats of infection and irritation even ones it hasn’t seen before including bacterial, viral, and fungal infections or a break in the protective barrier of any organ, especially skin, which causes irritation. Its response is swift, within about four hours, and coordinates the following components:

  • T-cells and B-cells bind antibodies to antigens that have invaded the body
  • Phagocytes essentially “eat” infectious organisms to get rid of them
  • Cytokines kick in with the inflammatory response which may include pain, tenderness, redness and warmth due to increased blood flow, or fever

Once the infection or irritation is contained, the innate immune system will work on its resolution including tissue repair and activation of the process by which antibodies are made; these antibodies will prevent an infection by the same organism later. While much of our understanding of this system comes from what we know about our responses to infection, it is thought that immune responses can also be triggered by internal problems such as inflammation.

3. The Innate Immune Response to Obesity

The increased prevalence of obesity and overweight in adults continues to rise and contributes to disease and death that is estimated to cost $147 billion dollars a year in the U.S. (Finkelstein et al., 2009) and up to 0.6% of the gross domestic product of European countries (Muller-Riemenschneider et al., 2008). More ominous is the high rates of childhood obesity which is a strong predictor of adult obesity (Lee et al., 2009). This has also shifted the prevalence of adult diseases such as type 2 diabetes and pre-diabetes into childhood and has generated new treatment and prevention challenges (Lee, 2006Lee et al., 2006). One study (Skinner et al., 2010) showed an increase in inflammatory bio-markers in obese children as young as 3 years of age. This indicates that many of the origins of obesity-induced inflammation may actually be initiated during childhood. Therefore, many people will face a lifetime threat to health from obesity.

Because the innate immune system is supposed to be relatively short acting, the response to obesity-induced inflammation is hard to compare. Applying the same models may be inaccurate and insufficient to fully explain how the body is affected. Furthermore, it is clear that the inflammation generated by obesity does not require as swift and dedicated a response as those seen in acute infectious settings (Hotamisligil, 2006). These unique challenges have led to the coining of the term “metainflammation” to describe the chronic low-grade inflammatory events that occur in obesity and its associated diseases.

A frequently asked question is why would obesity trigger an immune response? For the most part, this question remains unanswered, but one answer to this may lie in the fact that many of the key regulators of metabolism also play critical roles in regulating inflammatory responses.

4. Inflammation as a link between obesity and disease

The interest in obesity-induced inflammation relates to the understanding that inflammatory mechanisms are aid in the development of diseases found more often in those who are obese such as heart disease.

It is impossible to cover the scope of all of these diseases so we will focus our attention on the inflammatory mechanisms of fatty liver disease and Type 2 Diabetes. This will set the stage for future discussion of the innate immune components activated in obesity. I will highlight both clinical and pre-clinical studies in animal models of obesity that have built our understanding of the mechanisms that drive obesity-associated diseases.

4.1 Non-alcoholic Fatty Liver Disease (NAFLD)

The liver plays a critical role in the regulation of glucose and lipids levels in the blood. Obesity generates changes in the function of the body; glucose production and the breakdown (oxidation) and storage of fats specifically in the liver. Unusual fat accumulation in the liver is connected to many obesity-associated illnesses that include non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome. The metabolic changes that occur with this fat accumulation include insulin resistance propagated by the liver which is related to inflammatory cytokine signals.

4.2 Type 2 Diabetes (T2D)

The regulation of glucose metabolism is securely coordinated from the hypothalamus between nutrients regulated by the liver and gut, the use of these nutrients and storage in muscle and fat, and insulin secreted by the pancreas. The dysregulation of almost all of these processes with obesity is now known to be associated with the activation of innate pro-inflammatory pathways. The net result of this is the rise of systemic insulin resistance and hyperglycemia.

5. Why obesity affects the innate immune system

The blend of a sedentary lifestyle and surplus energy intake has led to an increased occurrence of obesity which constitutes a major risk factor for several diseases including type 2 diabetes and cardiovascular diseases. Intensive research during the last two decades has revealed that one main feature of obesity linking it to insulin resistance is the presence of chronic low-grade inflammation, a result of the innate immune system being activated.

Recent evidence suggests that activation of the innate immune system in the course of obesity starts with an elevation in metabolic signals which sets up a pattern of recognition receptors and leads to stimulation of critical inflammatory signaling cascades which interfere with insulin signaling.

Exercise is one of the main prescribed interventions in obesity management because it helps improve insulin sensitivity and reduce obesity-induced chronic inflammation. A deeper understanding of the effects of exercise on inflammatory signaling pathways in obesity is useful to optimize preventive and therapeutic strategies to combat the increasing incidence of obesity and its related diseases.

References:

  1. Journal of Biological Chemistry (2013): How Metabolism Generates Signals during Innate Immunity and Inflammation. Retrieved fromhttp://www.jbc.org/content/288/32/22893.full.html
  2. Physiological reviews (2018): Innate Immune Signaling and Its Role in Metabolic and Cardiovascular Diseases. Retrieved fromhttps://www.physiology.org/doi/abs/10.1152/physrev.00065.2017
  3. NCBI (2012): Innate Immune Activation in Obesity. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3888776/
  4. NCBI (2015): Metabolic signals and innate immune activation in obesity and exercise. Retrieved from

https://www.ncbi.nlm.nih.gov/pubmed/25825956

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Understanding the role metabolic inflammation plays in obesity and diabesity

Important Points:

  • Inflammation
  • Obesity
  • Diabesity
  • Insulin resistance
  • Adipose tissue

Understanding the role metabolic inflammation plays in obesity and diabesity

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

1. What is Obesity?

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

  Weight (Pounds) x 703       OR         Weight (Kilograms) 

 
Height (Inches) x Height (Inches)      Height (Meters) x Height (Meters)  

Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To determine your body mass index, use one of these formulas:

BMI =  

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. Because BMI doesn’t directly measure body fat, some people such as muscular athletes may have a BMI in the obesity category even though they don’t have excess body fat.

2. What is Diabesity?

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

3. Is Obesity an Inflammatory Condition?

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

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

4. How Does Inflammation Cause Diabesity?

Listed are some lines of evidence that show inflammation directly causes obesity and diabesity.

  • The development of diabesity has been shown to follow inflammation. Raised levels of inflammatory cytokines predict impending weight gain. In a study, infusion of inflammatory cytokines into healthy, normal weight mice caused insulin resistance. This concept is also illustrated by the fact that people with other chronic inflammatory conditions are at higher risk of developing Type2 Diabetes; for example, about one-third of chronic Hepatitis C patients develop Type 2 diabetes, and those with rheumatoid arthritis are also at higher risk.
  • In obesity, inflammation has been noted to start in the fat cells themselves. As fat mass expands, inflammation increases. One explanation may be that dysfunction of the mitochondria (the “power plant” of our cells) caused by obesity puts increased stress on cellular function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they produce an excess of reactive oxygen species (ROS) which in turn starts an inflammatory cascade within the cell.
  • Inflammation of the fat tissue causes insulin resistance, which is the primary feature of Type 2 diabetes. TNF-α, a cytokine (small protein) released during the inflammatory response and several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein have been repeatedly shown to cause insulin resistance.
  • Inflammation of the brain (specifically the hypothalamus) causes leptin resistance, which often precedes and accompanies insulin resistance and Type 2 diabetes. Leptin is a hormone that regulates appetite and metabolism this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolisms are impaired and weight gain and insulin resistance result.
  • When there is inflammation of the gut, there arises leptin and insulin resistance. This may occur via an increase in lipopolysaccharide (LPS), an endotoxin produced by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver, and weight gain.

5. How  does Diabesity Cause Inflammation?

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

6. Why would obesity cause inflammation?

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

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

7. Tackling Inflammation in the control of diabesity

We can therefore conclude that inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.  

Reduction of inflammation is a major key in preventing and treating diabesity. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.

 

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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.

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Meat Heals: What is the effect of the carnivore diet on obesity and cancer?

Important Points:

  • Carnivore Diet
  • Meat
  • Ketosis
  • Obesity
  • Cancer

Meat Heals:
What is the effect of the carnivore diet on obesity and cancer?

Does meat really heal? Many anecdotal reports have been released claiming that the carnivore diet, consisting of eating a diet restricted to meat, has alleviated the symptoms of autoimmune disease and depression while causing weight loss and improved health. Despite the anecdotal evidence, is there any scientific data to support these claims? Let’s consider the effect of the carnivore diet on several health conditions.

1. The Carnivore Diet and Obesity

When you are on the carnivore diet, your intake of processed carbohydrates and sugar is completely eliminated. These simple sugars are the leading cause of weight gain. In the absence of these carbohydrates, your body burns fat for fuel in a process known as ketosis resulting in weight loss and the eradication of obesity. Obesity is a leading cause of chronic illnesses such as type 2 diabetes, cardiovascular diseases, and fatty liver disease.

2. The Carnivore Diet and Autoimmune Diseases

Studies have shown that excess intake of sugary foods and processed carbohydrates increases systemic levels of inflammation in the body which can increase the risk for cancer and autoimmune diseases. Eliminating sugar intake through this meat diet can therefore theoretically decrease levels of inflammation in the body.

But does the meat diet directly decrease levels of inflammation in the body? The carnivore diet sends the body into a metabolic state called ketosis where it burns fat for energy instead of using glucose. Compared to glucose metabolization which produces large amounts of free oxygen radicals contributing to inflammation, ketone metabolization has been shown to produce far fewer free radicals.

In fact, studies have shown that ketosis decreases inflammation and reactive radicals in animal models of multiple sclerosis, an autoimmune condition that affects the brain. It also decreases markers of liver inflammation in people with non-alcoholic fatty liver disease. Since the ketogenic diet has also been shown to produce anti-inflammatory effects by directly inhibiting pro-inflammatory immune pathways in the body, it is assumed that the carnivore diet does the same though scientific data isn’t readily available. With this in mind, it can be concluded that the carnivore diet can in fact guard against inflammation and ameliorate symptoms of autoimmune diseases.

3. The Carnivore Diet and Cancer

The development of cancer, known as carcinogenesis, has been linked to hyperinsulinemia, hyperglycemia, and chronic inflammation. Not enough studies have been done on the carnivore diet, but emerging evidence suggests that the ketogenic diet may decrease the risk of cancer through its anti-inflammatory properties. Because the carnivore diet works in basically the same way as the keto diet, the same can be deduced of the carnivore diet. Along those same lines, the ketogenic diet is hypothesized to decrease risk of cancer by decreasing levels of insulin and glucose in the body and also by decreasing systemic levels of inflammation, and the carnivore diet would achieve the same thing.

Initially, it was thought that cancer cells use a lot of glucose for energy, thus starving them of glucose would stop their growth. Unfortunately, this theory has not produced new treatment or a cure because normal cells need energy too, and there is no way of starving the cancer cells and feeding the normal ones.

There is also an indirect link between cancer risk and sugar. Eating excess sugar over time can cause you to gain weight, and scientific evidence shows that being overweight or obese increases the risk of 13 different types of cancer. In fact, keeping obesity at bay is the single biggest preventable cause of cancer after quitting smoking. The carnivore diet can thus reduce the risk of obesity and the risk of cancer.

One other study published in 2019 showed evidence that people who drank more sugary drinks had a slightly increased risk of cancer regardless of body weight. Because the carnivore diet eliminates sugary drinks, this is one more benefit of this diet. 

But what of the studies that show a correlation between red meat and cancer? There is one major flaw in the way these studies are interpreted: they seem to suggest a causal link between meat consumption and cancer that isn’t really there.

4. The Carnivore Diet and Cognitive Function

Although there is limited evidence on the neuroprotective effects of the carnivore diet specifically, there is much evidence on the neuroprotective of the ketogenic diet, which the carnivore diet closely resembles. Data suggests that the ketogenic diet has anti-inflammatory effects on the brain and holds neuroprotective benefits.

The ketogenic diet was initially designed to manage children suffering from seizures. Studies show that as many as half of patients that used the ketogenic diet had fewer seizures after starting the diet. In children with specific genetic epilepsies or epilepsy syndromes, studies have shown up to 90% of patients achieve seizure freedom on the ketogenic diet.

Because inflammation is thought to play an important role in epilepsy and seizures, the ketogenic diet, and therefore the carnivore diet, may decrease seizure occurrence through its anti-inflammatory effects. The anti-inflammatory mechanisms of the ketogenic diet involve reduced mitochondrial production of pro-inflammatory molecules and reduced production of excess excitatory neurotransmitter glutamate, which can cause neuronal damage.

Inflammation is thought to play a role in the development of other neurological diseases such as autism which is increasingly associated with maternal inflammation, Alzheimer’s Disease, and Parkinson’s Disease, as well as cognitive dysfunction in people with diabetes and obesity. Thus, decreasing inflammation through the carnivore diet may improve symptoms related to neurological dysfunction associated with inflammatory processes.

5. The Carnivore Diet and Depression

From anecdotal reports, the carnivore diet has shown neurological and psychological effects beyond the treatment of seizures and chronic pain. It’s also known that inflammation can contribute to depression, and depression itself can promote inflammation. Many people on the carnivore diet report benefits such as increased alertness, energy, mood, and concentration.

6. So, Does Meat Heal?

It is clear that the carnivore diet has marked positive effects on the conditions we set out to explore, mainly due to its elimination of sugars and carbohydrates. It can be said that getting on a carnivore diet is likely to bring about improved health outcomes.

It is important to note that there is not a ‘one-size-fit all’ when it comes to diet. Every individual has a different body, genetics, digestive system, and immune system, which all of play a role in the body’s reaction to food. However, even if the carnivore diet is not for you, please note that everyone should cut down on sugar and processed carbohydrates because these are known to cause weight gain, pro-inflammatory states, and health problems.

References:

  1. Neurogal (2018): Does Meat Really Heal? Show me the Evidence for the Carnivore Diet. Retrieved from

https://neurogal.com/neuro-blog/2018/12/7/does-meat-really-heal-show-me-the-evidence-for-the-carnivore-diet

  • Cancer Research UK (2017): Sugar and cancer – what you need to know. Retrieved from
https://scienceblog.cancerresearchuk.org/2017/05/15/sugar-and-cancer-what-you-need-to-know/
  • The BMJ (2019):Sugary drink consumption and risk of cancer: results from NutriNet-Santé prospective cohort. Retrieved from

https://www.bmj.com/content/366/bmj.l2408

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Malnutrition is Both Obesity and Starvation

Important Points:

  • Obesity
  • Malnourished
  • Nutrient intake
  • Vitamin deficiency
  • Starvation

Malnutrition is Both Obesity and Starvation

Malnutrition is a word we usually associate with the tragically thin figures from TV news reports of third world famines. In fact, it’s a shockingly common problem the world over. Though not at starvation level, there are millions of patients who aren’t getting sufficient calories, protein, vitamins, and minerals.

Doctors say our growing reliance on fast food coupled with mounting rates of binge-drinking means many people lack the vitamins and minerals essential for health. The result, in the most extreme cases, is pot-bellies, wasted limbs and emaciated bodies – all conditions more often associated with famine victims in the developing world. While malnutrition can be fatal, in more mild forms it can cause a host of symptoms that impact our everyday life, from hair loss and muscle wastage to food cravings and lethargy.  It is possible to be obese and still be malnourished.

1.  What is Malnutrition?

Malnutrition is a serious condition that occurs when a person’s diet doesn’t contain the right amount of nutrients. Malnutrition means “poor nutrition” and can refer to:

  • undernutrition – when you don’t get enough nutrients
  • overnutrition – when you get more nutrients than you need

2.  Who is Affected by Malnutrition?

Malnutrition is a common health problem. There are an estimated 3 million malnourished people in the UK at any time, with many more at risk of becoming malnourished. Around one in three people admitted to hospital or care homes in the UK are found to be malnourished or at risk of malnourishment.

Malnutrition is caused by having an inadequate diet or a problem absorbing nutrients from food which can be caused by having reduced mobility, a long-term health condition, or a low income.

3.  What are the Signs of Malnutrition?

The most common symptom of undernutrition is unintentional weight loss (losing 5-10% or more of your body weight over three to six months), and other signs include weak muscles, fatigue, low mood, and an increase in illnesses or infections. 

The main sign of overnutrition is being overweight or obese, however, people with undernutrition can also be overweight if they eat a diet high in energy (calories) but low in other nutrients.

4. Malnutrition of Excess: Obesity

The number of people who are malnourished despite being obese is shocking, a leading weight loss surgeon has said today. A recent study showed despite high levels of obesity in the U.S., many people are undernourished. 

A diet of pizza, fries, crisps, pasta, rice, biscuits, cakes leaves many people consuming a lot of calories but few nutrients, says Dr Sally Norton, an NHS consultant specializing in weight loss and upper gastrointestinal surgery. 

Drug companies push the sales of expensive drugs which treat the symptoms of the disease but not the cause. The multi-million-dollar drug industry encourages doctors to treat type 2 diabetes, high cholesterol, heart disease and other conditions related to poor nutrition with expensive drugs rather than healthier food.

Hippocrates, the father of medicine, was so right when he said, over 2,000 years ago: ‘let food be thy medicine’. And yet, fast-forward to the 21st century and a recent study of Americans shows that many Americans, despite their access to plenty of food, are undernourished. 

5. Can obese people really be malnourished? 

Picture a malnourished hospital patient…..

The person you’re imagining probably doesn’t weigh 300 pounds, does she? Yet obese patients can develop malnutrition, before or during hospitalization and have worse outcomes as a result.

In fact, according to a recent study, malnutrition counteracts the “obesity paradox,” which holds that, among the critically ill, heavier patients do better than normal- or underweight patients. Researchers who looked specifically at malnourished obese patients showed that they had a higher risk of mortality than well-nourished patients of similar body mass index, according to results published in the January issue of Critical Care Medicine.

Yet these patients’ nutritional deficiencies often pass under hospital clinicians’ radar, according to experts. “We as physicians don’t necessarily have a great handle on who is malnourished,” said Kenneth B. Christopher, MD, co-author of the study. “You can always tell if someone’s profoundly malnourished, because they start appearing to be cachectic, but it’s less severe degrees of malnutrition that are actually harder to see.”

In addition to judgments based on appearance, a number of other factors can make it difficult to diagnose or prevent malnutrition in obese inpatients, including shortcomings in history taking, limitations of lab testing, and challenges in nutrition delivery. According to experts, hospitalists can help correct these deficits by raising their own index of suspicion and working with the health care team to focus on patients’ nutritional status.

While malnutrition can be fatal, in more mild forms it can cause a host of symptoms that impact our everyday life. How many nutrients do you get in biscuits, pieces of cake, crisps, fries, pizza, white rice, pasta and bread? Not a whole lot. So, if you are eating these ‘nutrient deficient’ foods regularly, you should make sure to get nutrients from real, fresh, whole foods, too.

6. Diagnosing Malnutrition

Accurate screening for malnutrition begins with the recognition that you can’t see it with your eyes or even a scale. “Nutritional status is not body mass index,” summarized Dr. Christopher, who is a nephrologist and critical care specialist at Brigham and Women’s Hospital in Boston. For one thing, excess weight may not represent body fat.

Obesity could also distract from recent weight loss, an important marker of malnutrition. “Somebody could be obese but have a gastrointestinal problem and have been losing weight. Even though they’ve lost a considerable amount of weight, they started off so obese that they’re still technically obese,” said Dr. Mechanick.

Because our society has so much stigma around overweight and obesity, when many obese people lose weight, however they lose it, they get more positive feedback,” said Charlene W. Compher, PhD, a professor of nutrition science at the University of Pennsylvania in Philadelphia. If a patient lost weight due to bariatric surgery, he is particularly at risk for malnutrition. “The odds of having vitamin deficiencies are very high with patients with gastric bypass, especially if they do not take all of the vitamin and mineral supplements that they are instructed to,” said Dr. Compher. And obese individual could be getting enough calories, but not enough protein or other nutrients due to an unhealthy diet.

7. How Can You Tell if You’re Malnourished?

“There’s no lab test for malnutrition,” said Dr. Kirkland. “People rely on albumin. It’s not helpful for malnutrition. Albumin just reflects the acuity of illness or the duration of malnutrition, but not the severity of it or the presence of it.”

Whatever your weight, ensure to always have well balanced healthy meals, with regular supplementation where necessary, as malnutrition could potentially lead to other chronic illnesses such as type 2 diabetes, heart issues and others.

References:

  • International Journal of Obesity (2019): Overfed but undernourished: recognizing nutritional inadequacies/deficiencies in patients with overweight or obesity. Retrieved from

https://www.nature.com/articles/s41366-018-0143-9

  • NCBI (2012): The Malnutrition of Obesity: Micronutrient Deficiencies That Promote Diabetes. Retrieved from

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3313629/

  • ACP Hospitalist (2015): Obesity and malnutrition are not mutually exclusive. Retrieved from

https://acphospitalist.org/archives/2015/02/nutrition.htm

  • Critical Care Medicine (2015):  The True Obesity Paradox

Obese and Malnourished? Retrieved from

https://journals.lww.com/ccmjournal/Citation/2015/01000/The_True_Obesity_Paradox__Obese_and_Malnourished__.33.aspx

  • NHS Inform (2019): Malnutrition. Retrieved from

https://www.nhsinform.scot/illnesses-and-conditions/nutritional/malnutrition

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How effective is the Carnivore diet in curbing chronic obesity?

Important Points:

  • Carnivore Diet
  • Meat
  • Obesity
  • Weight loss

How effective is the Carnivore diet in curbing chronic obesity?

Obesity has become rampant in recent times. It is said to affect almost 50% of the American population, and it has been credited with being a leading cause of chronic illness and ill health. The carnivore diet has become very popular as the new way to lose weight, maintain a healthy lifestyle, and ward off these diseases. A major proponent of this diet is its ability to melt away the fat, but just how effective is it in the management of obesity? Do its effects last? Let’s consider these questions here.

  • What 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. There are many reasons why some people have difficulty avoiding obesity including inherited factors, environmental factors, and personal diet and exercise choices.

  • What is the Carnivore diet?

The Carnivore Diet is a restrictive diet that only includes meat, fish, and other animal foods like eggs and certain dairy products. It excludes all other foods including fruits, vegetables, legumes, grains, nuts, and seeds. Its proponents also recommend limiting dairy intake to foods that are low in lactose — a sugar found in milk and dairy products — such as butter and hard cheeses.

Many people who have adopted the carnivore diet report faster weight loss, improved mental clarity, healthier digestion, and even improved athletic performance. Some have also reported remarkable relief from debilitating chronic health problems where conventional methods failed.

What does one eat on the carnivore diet?

Promoted (Green List) Foods, with emphasis on the fattier cuts of meat to take in enough calories:

  • Meat: beef, chicken, turkey, organ meats, lamb, pork, etc.
  • Fish: salmon, mackerel, sardines, crab, lobster, tilapia, herring, etc.
  • Other animal products: eggs, lard, bone marrow, bone broth, etc.
  • Low-lactose dairy (in small amounts): heavy cream, hard cheese, butter, etc.
  • Seasonings: salt, pepper, and seasonings with no carbs
  • Water

Forbidden Foods:

  • All Carbs
  • Vegetables: broccoli, cauliflower, potatoes, green beans, peppers, etc.
  • Fruits: apples, berries, bananas, kiwi, oranges, etc.
  • High-lactose dairy: milk, yogurt, soft cheese, etc.
  • Legumes: beans, lentils, etc.
  • Nuts and seeds: almonds, pumpkin seeds, sunflower seeds, pistachios, etc.
  • Grains: rice, wheat, bread, quinoa, pasta, etc.
  • Alcohol: beer, wine, liquor, etc.
  • Sugars: table sugar, maple syrup, brown sugar, etc.
  • Beverages other than water:  fruit juice, soda

Discretionary Foods

  • Milk, Butter, Yogurt
  • Eggs
  • Coffee and tea: These may be plant-based, but some people keep these in the diet.

What effect might the carnivore diet have on obesity?

When on a carnivore diet, you consume primarily meat… Occasionally you could have some eggs and cheese and maybe a cup of coffee. At a glance, what about this diet could help in combating obesity?

How does the carnivore diet work?

  • Cutting out sugar and carbohydrates

The absence of sugar and carbohydrates cause rapid and sustained fat loss without the need to count calories. Carbohydrates are hard to store and actually harmful if left to circulate in your system too long, so your body always wants to use them up first. Your body releases insulin to shuttle blood sugar into muscles. To make sure the sugar gets used up first, insulin also tells your fat cells to store any fat you consume and to not release stored body fat for hours afterwards. If you eat a lot of easily-absorbed carbohydrates, your body releases a ton of insulin in response. Excess insulin can remove too much sugar from your blood stream, resulting in hypoglycemia, and the quickest way to restore blood sugar levels is to eat more carbs. The fat stored never gets used up, and people live on the carb roller coaster resulting in weight gain.

The carnivore diet does away with all this by totally eliminating sugar and carbohydrates from your diet.

  • Eating a lot of protein suppresses appetite

One way that protein controls appetite is through the amino acid phenylalanine. Consumed protein is broken down into amino acids so it can be absorbed by the body. Multiple studies have shown how phenylalanine suppresses appetite and even improves mood while helping you burn stored fat. One study found that phenylalanine increases the release of an intestinal hormone called cholecystokinin which signals the brain to feel satiated after eating and causes a reduction in subsequent food intake. A mouse study found that a single dose of phenylalanine caused an increase in another satiety hormone called GLP-1 and reduced levels of the hunger-hormone ghrelin.

  • Increase in dopamine

Protein foods are made from the building blocks of amino acids (including tyrosine) which are essential to the production of dopamine. It has therefore been suggested that upping protein intake may also boost dopamine production without increasing appetite. Dopamine is considered the reward hormone, and increasing its levels in your brain is helpful for making your weight loss diet less unpleasant.

  • The carnivore diet “imposes” time restricted eating

The carnivore diet tends to make people naturally adopt time-restricted eating patterns. Studies show that eating at night is a common cause of obesity. Junk food actually causes you to prefer late-night eating. Sugar and fat together act as a trigger that cements the unhealthy habit of late-night eating. Worse yet, your body’s internal clock (circadian rhythm) determines your digestion and energy usage times along with your sleep and wake times. We’re meant to eat during the day and sleep at night. When you eat at night, your body doesn’t want to process those calories leaving them to sit and cause metabolic dysfunction.

Protein does not seem to trigger a desire for late-night eating, so the carnivore diet also helps curb that unhealthy practice. With late-night eating eliminated, the quality of your sleep will improve producing a better mood the next day and making you less apt to make poor food choices out of hunger or being cranky. Better sleep will decrease stress and anxiety too.

  • Does the carnivore diet stave off obesity?

There is a link between the Carnivore diet and sustained weight loss. In the absence of carbohydrates, fat can be kept off for long periods of time. The question becomes how safe it is to do the carnivore diet long term. More studies on this need to be carried out, but in the meantime, this diet is one of the best in keeping obesity and its associated diseases at bay.