It’s no secret that sugar is bad for you. It spoils your teeth, packs on pounds around your belly, and provides zero nutrition. Unfortunately, these are the least of sugars crimes. The biggest reason why you should stop taking sugar is that it is one of the most pro-inflammatory foods. Current Research suggests that chronic, body-wide inflammation is associated with many modern diseases, like obesity, diabetes, and heart disease. So what role does a high-sugar diet play in chronic inflammation? In this article, we’ll delve into this and much more….

1. So, what is inflammation?

Inflammation is part of the body’s natural healing process.

Acute inflammation develops rapidly in response to an injury or infection. This type of inflammation tends to be good: It’s your body’s way of trying to fight off further damage while jump-starting healing. It usually lasts a few days to a few weeks.

Chronic inflammation is a long-term inflammation that occurs over months or years. It has several causes, including unhealthy lifestyle factors like diet. Over time, chronic inflammation can increase your risk of serious diseases.

Some foods, like sugar, can also cause inflammation in the body, which is normal. However, eating too many inflammatory foods may cause chronic low-grade inflammation. This can cause serious health problems, such as heart disease, diabetes, cancer, and

2. Sugar and inflammation

People who take diets rich in refined sugar may be increasing their risk of chronic inflammation. Research suggests that when people eat and drink less sugar, inflammatory markers in their blood decrease.

A high sugar diet can have harmful effects on health, such as increasing the risk of chronic diseases, weight gain, and tooth decay. It can also result in chronic inflammation, where the body’s immune system activates, which results in damage to healthy cells.

Inflammation resulting from lifestyle factors, such as obesity, smoking, and a sedentary existence can contribute to a range of diseases. These include heart disease, diabetes, rheumatoid arthritis, and Alzheimer’s.

3. Is too much-added sugar linked to inflammation?

A lot of research has been carried out on how sugar causes inflammation.  Diets high in added sugar are thought to signal the production of pro-inflammatory molecules in the body. Over time, that can create an environment of chronic, low-grade inflammation and lead to trouble in the future. Sugar also stimulates the production of free fatty acids in the liver. When the body digests these free fatty acids, the resulting compounds can trigger inflammatory processes.

Different kinds of sugar may contribute more or less to inflammation. For instance, some research has suggested that fructose may cause more inflammation than glucose. However, a systematic review found no difference in the inflammation from fructose and glucose, so more research is needed.

Also, the researchers saw no differences in inflammatory factors between the groups that consumed high fructose corn syrup vs. sucrose. The sample sizes were small, and the quality of the studies was low, so more research is necessary to confirm these findings.

Below are some of the common signs and symptoms of chronic inflammation:

• depression, anxiety, and other mood disorders
• body pain
• constant fatigue and insomnia
• constipation, diarrhea, acid reflux, and other digestive issues
• weight gain
• frequent infections

People with chronic inflammation may have an increased risk of diabetes, depression, and dementia.

Chronic inflammation in older adults may also have links with a higher risk of death. Doctors are working on how to reduce chronic inflammation.

4. How does added sugar affects your body?

When you consume excess added sugar and refined carbohydrates there will be a few changes in your body, which help explain why a diet high in sugar can lead to chronic, low-grade inflammation.

• Excess production of AGEs: Advanced glycation end products (AGEs) are harmful compounds that form when protein or fat combine with sugar in the bloodstream. Too many AGEs lead to oxidative stress and inflammation.
• Increased gut permeability: Bacteria, toxins and undigested food particles can more easily move out of the gut and into the bloodstream, potentially leading to inflammation.
• Higher “bad” LDL cholesterol: Excess LDL cholesterol has been associated with higher levels of C-reactive protein (CRP), a marker of inflammation.
• Weight gain: A diet rich in added sugar and refined carbohydrates can lead to weight gain. Excess body fat has been linked to inflammation, partly due to insulin resistance.

It is important to note that inflammation is unlikely to be caused by sugar alone. Other factors like stress, medication, smoking, and excess fat intake can also lead to inflammation.

5. Is natural sugar linked to inflammation?

It’s important to note that there is a difference between added sugar and natural sugar. Added sugar is removed from its original source and added to foods and drinks to serve as a sweetener or increase shelf life.

Added sugar is found mostly in processed foods and drinks, though table sugar is also considered an added sugar. Other common forms include high-fructose corn syrup (HFCS), sucrose, fructose, glucose, and corn sugar.

Among US adults, around 13% of total calories come from added sugar. This is high, considering that government guidelines advise that no more than 5% to 15% of calories should come from both solid fats and added sugar.

Natural sugar has not been linked to inflammation. In fact, many foods containing natural sugars, such as fruits and vegetables, maybe anti-inflammatory. Natural sugars include those naturally occurring in foods. Examples include fructose in fruit and lactose in milk and dairy products.

Consuming natural sugars should not be any cause for concern. That’s because they act very differently than added sugar when consumed and digested in the body.

Lifestyle Changes Can Reduce Inflammation

It is important to be aware of what we can do to minimize the inflammation in our bodies. Here are some simple tips to help reduce inflammation:

• Adopt a low glycemic diet: High sugar intake links to chronic inflammation, stroke risk, coronary heart disease risk, and type 2 diabetes risk. Soda, refined carbohydrates, and high fructose corn syrup are foods that can promote inflammation.
• Read food labels: If you are unsure about certain products, get into the habit of reading food labels. Look out for ingredients like sucrose, glucose, high-fructose corn syrup, maltose, and dextrose.
• Choose whole-grain carbs: These include oats, whole-grain pasta, brown rice, quinoa, and barley. They have lots of fiber and antioxidants, which can help control blood sugar and protect against inflammation.
• Eat more fruits and vegetables: Fruits and vegetables contain antioxidants, vitamins, and minerals, which can protect against and reduce inflammation in the body.
• Eat lots of antioxidant-rich foods: Fill your plate with foods rich in antioxidants, which naturally help counteract inflammation. These include nuts, seeds, avocados, oily fish and olive oil.
• Keep active: Regular physical activity, including both aerobic and resistance exercise, can help protect against weight gain and inflammation.
• Manage stress levels: Learning to manage stress levels through relaxation techniques and even exercise can help reduce inflammation.
• Add curcumin to food: A component in turmeric called curcumin improves several inflammatory diseases.
• Get enough fiber: Researchers have shown an association between high fiber diets and lower inflammatory factors, such as TNF-alpha and interleukin-6.
• Drink green and black teas: Scientists have associated compounds found in green and black teas with lower C-reactive protein in the blood.
• Eat more nuts: Almonds and other nuts may help to lower the risk of cardiovascular disease and diabetes. Cardiovascular diseases, such as atherosclerosis, are pro-inflammatory states. Diabetes is a chronic inflammatory disease.
• Add fish oil to the diet: Omega-3 fatty acids positively affect lower levels of inflammatory factors in the blood, such as C-reactive protein, interleukin-6, and TNF-alpha.

6. Does sugar cause inflammation?

Inflammation is a critical component of metabolic syndrome. However, chronic low-grade inflammation leads to diseases like type 2 diabetes, atherosclerosis, non- alcoholic liver diseases, and gout. Research suggests that eating lots of sugar can lead to chronic inflammation

In the United States, the amount of high fructose corn syrup people consume increased from 1978 to 1998 and then stabilized according to the  Nationwide Food Consumption Surveys. With greater awareness of the risks of added sugar, sugar intake in the U.S. has been declining. Nonetheless, people are still consuming too much sugar.

There are several things you can do to help fight inflammation, including exercising regularly and effectively managing your stress levels. Furthermore, cut down on processed foods and drinks, choose whole foods, and limit your intake of added sugar and refined carbohydrates.

References

1. Medical News Today (2017): Everything you need to know about inflammation. Retrieved from https://www.medicalnewstoday.com/articles/248423.php

2. Healthline (2017): Does Sugar Cause Inflammation in the Body? Retrieved from https://www.healthline.com/nutrition/sugar-and-inflammation

3. Medical News Today (2019): Does sugar cause inflammation in the body? Retrieved from https://www.medicalnewstoday.com/articles/326386.php

4. Mindbodygreene (2019): The Real Reason You Should Quit Sugar + How To Cut It Out Of Your Life For Good. Retrieved from https://www.mindbodygreen.com/0-24763/the-real-reason-you-should-quit-sugar-how-to-cut-it-out-of-your-life-for-good.html

5. NCBI (2014): Chronic inflammatory disorders and risk of type 2 diabetes mellitus, coronary heart disease, and stroke: a population-based cohort study. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24970784

7. NCBI (2019): Chronic Inflammation. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK493173/
8. Greatist (2019): Does Sugar Actually Cause Inflammation? Retrieved from https://greatist.com/health/sugar-and-inflammation

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

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

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

Whole grains consist of three main parts:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

1. Some background on overnutrition….

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

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

1. What is overnutrition?

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

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

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

2. What is overnutrition induced inflammation?

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

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

3. Overnutrition and the metabolic syndrome

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

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

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

4. What is carbohydrate overnutrition?

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

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

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

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

5. What factors Contribute to Overnutrition?

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

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

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

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

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

6. What then should be done to avoid overnutrition?

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

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

References

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

The 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 is an evolutionarily conserved system that senses and defends against infection and irritation. Innate immune signaling is a complex cascade that quickly recognizes infectious threats through multiple germline-encoded cell surface or cytoplasmic receptors and transmits signals for the deployment of proper countermeasures through adaptors, kinases, and transcription factors, resulting in the production of cytokines.

As the first response of the innate immune system to pathogenic signals, inflammatory responses must be rapid and specific to establish a physical barrier against the spread of infection and must subsequently be terminated once the pathogens have been cleared. Long-lasting and low-grade chronic inflammation is a distinguishing feature of type 2 diabetes and cardiovascular diseases, which are currently major public health problems.

2. How does the innate immune system work?

The ability of organisms to mount a response to infectious challenge without prior exposure is regulated by the coordinated interaction of components of the innate immune system. This preformed system is important to respond to exogenous stimuli such as bacterial, viral, and fungal infections. Beyond the initial response to a stressor, the innate immune system coordinates the resolution of inflammation, tissue repair, and the activation of the adaptive immune system to provide memory for future challenges.

While much of our understanding of innate immunity comes from models of infection, it is also clear that immune responses can be triggered by endogenous stimuli. Such mechanisms play a wide role in health and disease from the response to tissue injury, the direction of tissue remodeling, and the response to tumors.

3. The Innate Immune Response to Obesity

The increased prevalence of obesity and overweight in adults continues to rise and contributes to morbidity and mortality 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, 2006; Lee et al., 2006). Relevant to this review, increases in inflammatory biomarkers such as C-reactive Protein (CRP) and neutrophilia are seen in obese children as young as 3 years of age (Skinner et al., 2010). 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.

The long term duration of obesity-induced inflammation makes it challenging to describe this unique type of inflammatory activation based on classical models of innate immunity. Applying such models may be inaccurate and insufficient to encompass the events that are triggered by obesity in metabolic tissues such as fat. Furthermore, it is clear that the inflammation generated by obesity is not as high in amplitude as those seen in acute infectious settings (Hotamisligil, 2006). These unique challenges have led to the coining of the term “metal inflammation” 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 central to the pathogenesis of diseases such as heart disease that is modified by obesity.

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-related diseases with fundamental alterations in nutrient control derived from pro-inflammatory inputs. 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 a number of physiologic changes in hepatocyte glucose production as well as lipid oxidation and storage. Unusual hepatic lipid accumulation is connected to many obesity-associated illnesses that include non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome. The metabolic changes that occur with hepatic lipid accumulation include hepatic insulin resistance which is related to inflammatory cytokine signals.

4.2 Type 2 Diabetes (T2D)

The regulation of glucose metabolism is securely coordinated between nutrient inputs regulated by the liver and gut, nutrient utilization and storage in muscle and fat, insulin secretion by the pancreas, and central signals from the hypothalamus that coordinate these responses. 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 generation 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 comorbidities including type 2 diabetes and cardiovascular diseases. Intensive research during the last two decades has revealed that a characteristic feature of obesity linking it to insulin resistance is the presence of chronic low-grade inflammation being indicative of activation of the innate immune system.

Recent evidence suggests that activation of the innate immune system in the course of obesity is mediated by metabolic signals, such as free fatty acids (FFAs), being elevated in many obese subjects, through activation of pattern recognition receptors thereby leading to stimulation of critical inflammatory signaling cascades, like IκBα kinase/nuclear factor-κB (IKK/NF- κB), endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) and NOD-like receptor P3 (NLRP3) inflammasome pathway, that interfere with insulin signaling.

Exercise is one of the main prescribed interventions in obesity management improving insulin sensitivity and reducing 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 comorbidities.

References:

1. Journal of Biological Chemistry (2013): How Metabolism Generates Signals during Innate Immunity and Inflammation. Retrieved from http://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 from https://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

Diabetes isn’t just about bloods sugar, it’s systemic inflammation, incessant cravings-driven eating. It’s obesity.

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

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

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

And Dr. Gurpreet Padda is right in the middle of it. Based in St. Louis, MO, The Padda Institute is highly regarded as one of the best pain centers in St. Louis.

Does Meat Really Heal? Many anecdotal reports have been released claiming that the carnivore diet – which basically consists of eating a diet restricted to meat (usually red fatty meat)–has alleviated the symptoms of autoimmune disease, depression and caused weight loss and improved health. Despite these anecdotal, is there any scientific evidence to support these claims? In this article, we will examine some of the effects of this diet on some conditions.

1. What is the effect of the carnivore diet on obesity?

When you are on the carnivore diet, your intake of processed carbohydrates and sugar is completely cut off. Thesesimple sugars are the leading cause of weight gain. In the absence of these carbohydrates, your body burns fat for fuelin a process known as ketosis. This results in weight loss and the eradication of obesity. Obesity is a leading cause of chronic illnesses such as T2DM, Cardiovascular diseases and Fatty Liver disease among others.

2. What effect does the Carnivore Diet have on 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 the 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,’burns fat for energy instead of using glucose. Compared to glucose metabolism which produces large amounts of free oxygen radicals, contributing to inflammation, ketotic metabolism has been shown to produce far fewer free radicals.

In fact studies have shown that ketosis decreases inflammationand 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, short of scientific tests being carried out. With this in mind, it can be concluded that the carnivore diet can in fact guard against inflammation and ameliorate symptoms of autoimmune disease.

3. Does the Carnivore diet have any cancer fighting properties?

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 they basically act in the same way, the same can be deduced of the carnivore diet. Carcinogenesis (the development of cancer) has been related to hyperinsulinemia, hyperglycemia, and chronic inflammation. 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.

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 was disproved because normal cells too need energy, and there is no way of starving the cancer cells and feeding the normal ones.

However, there is an indirect link between cancer risk and sugar. Eating lots of 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, obesity is the single biggest preventable cause of cancer after smoking. The carnivore diet can thus reduce the risk of obesity and thereby reduce the risk of cancer.

In addition, a study published in 2019 suggested there could be something else going on. Researchers found that people who drank more sugary drinks had a slightly increased risk of cancer, regardless of body weight. The study took weight in to account, but there are still lots of answered questions. More studies will be needed to investigate this.

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.  These studies are epidemiologic. This means that causal effects cannot be implied. In other words, just because there is a correlation between meat consumption and cancer does not mean that meat consumption itself causes cancer.

4. The Carnivore Diet and cognitive functioning…

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 neuro-protective benefits.

The ketogenic diet was initially designed to manage children suffering from seizures. Studies show that as many as half of patients that are started on the ketogenic diet have 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 (a.k.a“glutamate excitotoxicity”).

Inflammation is thought to play a role in the development of other neurological diseases such as autism (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, potentially through the carnivore diet, may improve symptoms related to neurological dysfunction associated with inflammatory processes.

5. What is the effect of the Carnivore diet on depression?

From anecdotal reports, the carnivore diet has shown neurological and psychological effects beyond the treatment of seizures and chronic pain. Several people on the carnivore diet report benefits such as increased alertness, energy, mood and concentration.

Moreover, inflammation can contribute to depression, and depression itself can promote inflammation. The ketogenic diet may improve mood and ameliorate depression symptoms through its anti-inflammatory properties.

6. So, does meat heal?

It is clear that the carnivore diet has marked positive effects on the conditions we set out to explore. This is mainly due to its cutting off 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, one “take home” is 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

2. 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/

3. 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

If Hippocrates the father of modern medicine is to be believed, “All disease begins in the gut”. The gastrointestinal tract with its microbiota is a complex, open, and integrated ecosystem. It is widely accepted that healthy gut microbiota is essential for optimal health. Imbalance in the gut flora could lead to one being vulnerable to a large spectrum of infectious and non-communicable diseases, including diabetes and obesity. There is an urgent need to develop efficient strategies to prevent and treat metabolic disorders such as diabetes and obesity. In this article, we will look at the implications of gut microbiota in diabesity and review ways of achieving optimal metabolic conditions.

1. What is Gut Microbiota and Gut Microbiome?

The gut microbiota is a collective term for the microbial community in the gut, whereas the gut microbiome is defined as the full collection of genes in the gut microbiota. The intestinal microbiota is known to be associated with metabolic syndrome and related comorbidities. Associated diseases including obesity, T2D, and fatty liver disease (NAFLD/NASH) all seem to be linked to altered microbial composition; however, causality has not been proven yet. This points to the potential causal and personalized role of the human gut microbiota in obesity and T2D is highly prioritized.

The gut microbiome contains an immense diversity of microorganisms, varying from bacteria as well as viruses, fungi, phages, protozoa, and archaea all colonizing our adult bodies. There is a proposed view that our microbiota is a microbial (endocrine) organ living symbiotically inside our gut. This has led to a new perspective suggesting multiple lineages capable of communicating with each other and shaping host immune-metabolism in several ways. Some of the capabilities of these “organ” are:

• The degradation of otherwise indigestible components of our diet
• harvesting of energy and nutrients
• shaping of the host immune system
• maintaining the integrity of the gut mucosal barrier
• xenobiotic metabolism

In this way, gut microbiota complement our biology in ways that are mutually beneficial.

The current research data regarding the precision/personalized nutrition suggest that dietary interventions, including administration of pre-, pro-, and syn-biotics, as well as antibiotic treatment should be individually tailored to prevent chronic diseases based on the genetic background, food and beverage consumption, nutrient intake, microbiome, metabolome, and other omic profiles.

2. The gut and diet….

Diet is essential in the composition and the function of the gut microbiota. Microbiota alters rapidly when exposed to great and fast changes in diet. Short-term dietary changes such as switching between plant- and meat-based diets, or adding more than 30 grams of fiber per day to the diet, or following a diet with different fat/fiber content can change the human gut microbiota in function and composition significantly in 48 hours.

Fiber-enriched diets have been shown to improve insulin resistance in lean and in obese subjects with diabetes. However, only long-term dietary habits are effective in shaping the composition of the gut microbiota as short-term dietary interventions failed to change the major features and classification of the microbiota.

3. What is the impact of Gut Microbiome in Insulin Resistance and Type 2 Diabetes?

When there is low diversity in the gut microbiome, there is a higher prevalence of obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD), and low-grade inflammation. Furthermore, low bacterial diversity was characterized by pro-inflammatory properties, suggested by the reduction in butyrate-producing bacteria and the increase in mucin-degrading bacteria. These characteristics potentially impair the gut integrity causing low-grade inflammation through endotoxemia. This low-grade inflammation of visceral adipose tissue may provide a link between obesity and insulin resistance.

Ethnic differences between human populations may also affect microbiota composition. Karlsson et al. compared data of T2D-associated metagenomes between Chinese and Swedish subjects with T2D, which indicated that different intestinal bacterial species were involved in similar metabolic functions. The authors were also able to distinguish subjects with T2D from healthy subjects, with a predictive power exceeding that of body mass index (BMI).

4. What is the effect of Gut Microbiota in Lipid Metabolism?

In recent decades, it has become clear that many metabolic, inflammatory, and innate immune mechanisms are also coordinated by (dietary-derived) lipids. The nutritional importance of dietary lipids is unequivocal.

Lipid accumulation in conjunction with low-grade inflammation is a pathophysiological hallmark of atherosclerosis. There is emerging evidence that the pathophysiology of atherosclerosis is related to interpersonal gut microbiome differences. Atherosclerosis seems to be related to TMAO, which is a new marker associated with increased risk of atherosclerosis and coronary artery disease.

Other key intestinal regulators of lipid and cholesterol metabolism are bile acids, which are involved in facilitating intestinal absorption and transport of diet-derived nutrients, vitamins, and lipids. Whereas bile production takes place in the liver (and is facilitated by products derived from lipid catabolism), 95% of all bile acids will be reabsorbed in the terminal ileum and subsequently re-absorbed by the liver, constituting the so-called enterohepatic circulation.

The intestinal microbiota is responsible for converting primary bile salt to secondary bile salts via bile acid de-hydroxylation. Although short courses of oral antibiotics affect intestinal microbiota composition and bile acid metabolism in humans, we found differential effects on glucose metabolism.

5. What effect does the Gut Microbiome have on Appetite?

Obesity is defined as an imbalance between energy intake (usually food intake) and energy expenditure. The brain is a key regulator in detecting alterations in energy balance and induces behavioral and metabolic responses to correct these alterations. The hypothalamus plays an important role in regulation of both food intake as well as energy homeostasis, receiving hormonal and (vagal) neuronal information from the periphery.

Changing the gut microbiome composition with prebiotics has also been shown to affect portal vein levels of other hormones including GLP-1, which in turn affected food intake, followed by a decrease in body weight and fat mass.

6. What are the Microbial Signatures in T2DM and Obesity?

Dysbiosis, which is the disruption of normal microbiota, has been described to be involved in a large spectrum of diseases, including diabetes, obesity, and insulin resistance, through disturbing the energy balance. It has therefore been suggested that the modulation of microbiota, either directly (by antimicrobials, diet, prebiotics and/or probiotics, stool transplant, microbial-derived signaling molecules or metabolites) or indirectly (e.g., immunotherapy) may contribute to the therapeutic management of these pathologies.

7. What is the Influence of Diet on Gut Microbiota in Diabetes and Obesity?

Diet is one of the major lifestyle factors involved in the genesis, prevention and control of diabetes, obesity and other cardiometabolic diseases, being also strongly linked to changes in microbiota. Many reports have shown that the genetic susceptibility to obesity may have interacted with an obesogenic environment (e.g., a major shift in dietary patterns influencing the gut microbiota, a sedentary lifestyle and physical inactivity) in determining the obesity epidemic. To date, there are many popular diets including Mediterranean, gluten-free, vegan, Western, omnivore, vegetarian. To date, most of these diets have been clearly linked to different microbiome profiles.

Following the industrial revolution, countries in the West underwent a nutritional transition from the traditional diet to a diet rich in heavily processed foods, fats, sugars, proteins, plus different additives, while remaining low in micronutrients and dietary fibers (also referred to as Western diet). These diets were deficient of dietary fibers, which are essential for gut health due to their role in stimulation of the growth and/or activity of certain beneficial microorganisms.

Conversely, people in traditional societies, with a fiber intake of almost 50–120 g/day harbor a much more diverse gut microbiota, which indicates good health. SCFAs are found in lower amounts in individuals consuming a Western diet. Western diet was correlated with a decrease in the total bacterial load and in beneficial commensals. On the other hand, subjects consuming vegan and vegetarian diets which are rich in fermentable plant-based foods were reported to have a microbiota characterized by a lower abundance of Bacteroides sp. and Bifidobacterium sp.

The Mediterranean diet (vegetables, moderate consumption of poultry, olive oil, cereals, legumes, winenuts, fish and a low amount of red meat, dairy products, and refined sugars) provides beneficial effects through the elevated content in mono-unsaturated and poly-unsaturated fatty acids, as well as high levels of antioxidants, fibers and vegetable protein content. The gut microbiota in individuals receiving Mediterranean diet is characterized by a high colonization by Lactobacillus sp., Bifidobacterium sp., and Prevotella sp., and low levels of Clostridium sp, species which are associated with weight loss, improvement of the lipid profile and decreased inflammation.

Dietary proteins have also been reported to be involved in shaping the microbiota. Individuals consuming a diet rich in beef had high levels of Bacteroides sp. and Clostridia and were low in Bifidobacterium adolescentis unlike individuals eating a meatless diet. Several studies have recently shown that diets including vegetarian whey/pea protein, and animal protein (meats, eggs, and cheese) are linked with microbial diversity. Consumption of animal-based protein was positively associated to a richness in bile-tolerant anaerobes, including Alistipes sp., Bilophila sp., and Bacteroides sp.

8. What are the Future Perspective on the Gut Microbiome?

Accumulating evidence suggests that gut microbiota plays a significant role in the initiation and progression of MS. The gut microbiota was proven to modulate plasma glucose, appetite, serum lipids and pro-inflammation. In addition, prebiotics or probiotics, which are widely used to manipulate the microbiota, can reduce low-grade intestinal inflammation and improve gut barrier integrity to reduce plasma glucose and serum lipid levels, induce weight loss and decrease insulin resistance. Based on these current achievements, the gut microbiota may be a potential therapeutic target for MS. However, clinical trials addressing the efficacy and efficiency of current or potential treatments on therapeutic applications in metabolic syndrome are needed.

Also, Individuals who are obese are likely to have an imbalance in gut microbiota composition. This possibility is a thrilling avenue for further research and possible novel treatment targets. However, because most studies have been undertaken in animals, direct translation of the findings to human is limited.

Prebiotics or other newly identified beneficial bacterial strains are potential interventions that will be used for treatment in the near future, and it will be important to evaluate their efficacy. Similarly, interventional studies with metabolites of microbiota will be performed (including SCFA butyrate supplementation) to evaluate if this compound has similar effects on food intake, energy expenditure, and improved metabolic features in humans.

The modifiable effects of the human gut microbiota on the development of metabolic syndrome make its handling a promising therapeutic approach. Analyzing and mapping individual microbial composition on a metagenomic level provides insight into specific targets for treatment and contributes to personalized therapeutic interventions.

References

1. Frontiers in Nutrition: Gut Microbiota, Host Organism, and Diet Trialogue in Diabetes and Obesity. Retrieved from https://www.frontiersin.org/articles/10.3389/fnut.2019.00021/full

2. NCBI (2018): The Gut Microbiome as a Target for the Treatment of Type 2 Diabetes. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6013535/

3. NCBI (2017): Gut microbiota as a potential target of metabolic syndrome: the role of probiotics and prebiotics https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5655955/

Can certain foods really help you fight heart disease, arthritis, and dementia?

In health, as with so many things, our greatest strength can be our greatest weakness. Take our astonishingly sophisticated response to injury and infection. Our bodies unleash armies of cellular troops to slaughter invaders and clear out traitors. Their movements are marshaled by signaling chemicals, such as the interleukins, which tell cells where and when to fight and when to stand down. We experience this as the swelling, redness, and soreness of inflammation—an essential part of healing.

But when the wars fail to wind down, when inflammation becomes chronic or systemic, there’s hell to pay. I’m looking at you, arthritis, colitis and bursitis, and at you, diabetes, colon cancer, Alzheimer’s and cardiovascular disease.

Cardiovascular disease is the world’s biggest killer, and we’ve known for 20 years that inflammation (along with too much cholesterol) ignites the buildup of plaque in our arteries. Still, no one knew if runaway inflammation could actually pull the trigger on heart attacks and strokes—until this summer. Results from a large, well-designed trial showed that certain high-risk patients suffered fewer of these “events” (as doctors so mildly call them) when given a drug that precisely targets inflammation (aiming at interleukin 1). It was sweet vindication for the cardiologist and principal investigator Paul Ridker of Harvard University, director of the Center for Cardiovascular Disease Prevention at Brigham and Women’s Hospital, who had long contended that inflammation was as vital a target as cholesterol.

The patients in Ridker’s study had already suffered a heart attack and had persistent inflammation (as measured by blood levels of C-reactive protein). But it is tempting to extrapolate lessons for all of us. Given that chronic inflammation plays a nefarious role in heart disease and many other disorders, shouldn’t we all do what we can to keep it in check? And I’m not talking about taking drugs like ibuprofen, which ease short-term inflammation. I mean something we can do every day of our lives: eat right.

Hop on the Internet or visit a bookstore, and you will see “anti-inflammatory” diets galore, dishing out recipes and hope. Many aims at specific ailments—arthritis, breast cancer, heart disease, various autoimmune disorders. Health guru Andrew Weil goes so far as to offer an “Anti-Inflammatory Food Pyramid.”

The underlying science, however, is somewhat shaky. Sure, plenty of foods have been found to reduce inflammation—many of them in laboratory experiments as opposed to in people: turmeric, blueberries, ginger, tea, various vegetables, dark chocolate, fish. University of South Carolina epidemiologists James Hébert and Nitin Shivappa valiantly surveyed 1,943 such studies and published in 2014 a Dietary Inflammatory Index, with 45 food elements. They created it as a research tool for evaluating diets but concede it’s built from studies that varied widely in methodology.

When I asked Ridker his views on anti-inflammatory diets, he grew uneasy. “This has caught on like wildfire,” he says, “but I have seen extremely little data that say this piece of food is ‘anti-inflammatory’ and this piece is ‘pro-inflammatory.’” He advises his own patients to eat a Mediterranean-type diet, heavy on vegetables, whole grains and fish and light on red meat and processed foods.

That diet, long endorsed by cardiologists, has been shown in well-designed studies to reduce key markers of inflammation and the risk of heart disease. Would it be even more effective if it incorporated more blueberries and turmeric? No one knows for sure.

may work anti-inflammatory wonders for mice, but “that’s in the context of rodent chow with a whole different set of macro and micronutrients,” explains Martha Clare Morris, a nutritional epidemiologist at Chicago’s Rush University. And context matters. The typical Mediterranean diet calls for loads of seafood a week, and yet studies of people taking fish oils as a supplement has not found many benefits. The virtues of fish may lie elsewhere or have more to do with displacing meat.

That’s why researchers such as Morris prefer to study overall dietary patterns rather than particular ingredients. Her current project examines whether cognitive decline can be slowed with a regimen called the MIND diet, which combines elements of the Mediterranean diet with another well-studied diet called DASH. It will look at inflammation, but results won’t be out before 2021.

Until then, there is no harm in adding more so-called anti-inflammatory ingredients to your diet. Hébert suggests a spicy chai (loaded with ginger, turmeric, and pepper). But remember the context! So don’t drink it with cookies and chips.

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 adipose irregularities in that, if adipose tissue expandability is low, there will be an increased presence of thickened tissue. This condition would lead to a 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 a 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.

Despite it being an essential response to infection and tissue injury, inflammation has also been associated with several pathological processes. Excessive acute inflammation causes tissue damage and non-resolving inflammation leads to chronic tissue malfunction, suggesting a delicate balance between the rapid and effective response to distresses in tissue homeostasis and the collateral damage on tissue function.

As a cluster, obesity, raised fasting plasma glucose, high cholesterol and hypertension comprise the metabolic syndrome.