Weight loss reverses type 2 diabetes in many patients. In the clinical trial covered here, 46% of people on a strict weight-loss diet had normal blood sugar without diabetes medication after one year. Those diagnosed more recently were the likeliest to reverse.
Diabetes reversal now draws interest from many quarters. Patients, clinicians, and researchers want ways to stop this rising epidemic early. And very soon, Big Pharma may be forced to take a harder look at how it manages diabetes.
A recent study by the University of Cambridge points to weight loss as the ultimate route to diabetes reversal. But before we get to this study, let’s define the terms.
What Is Diabetes Reversal?
Diabetes reversal means a person once diagnosed with diabetes can now keep normal blood sugar without diabetes medication. It also means this person can eat a regular non-diabetic diet without spiking glucose levels.
Diabetes reversal is mostly associated with type 2 diabetes. Diet and lifestyle factors influence this type.
Earlier studies have also linked weight loss to the reversal of type 2 diabetes. This is because excess body fat affects how much insulin you make and how well your body responds to it.
Other research has shown that bariatric (weight-loss) surgery can reverse type 2 diabetes well.
Study Linking Diabetes Reversal To Weight Loss
A clinical trial by Newcastle University showed that nearly 50% of people with type 2 diabetes achieved reversal. They did it after a six-month weight-loss program.
The study involved 280 people with type 2 diabetes. Half of them went on a strict weight-loss program. Their calorie intake was restricted through a liquid diet. They took no diabetes medication for the length of the study. The other half of the group stayed on usual care with diabetes medication.
After one year, 46% of people in the diet group achieved reversal. That means normal blood sugar levels without taking medication.
One notable finding: the people who reversed had lasting improvement in pancreatic beta-cell function. This research appears to show that weight loss can revive these cells so they work well again.
The study found that the response is associated with better function of pancreatic beta cells. These are the cells in the pancreas that make insulin. If beta cells can be “re-awakened” through weight loss, many diabetes patients can regain control of their blood sugar. They can return to a non-diabetic state. These results were astonishing. It was once believed that beta-cell function is lost for good in type 2 diabetes.
The study also found that people diagnosed recently had a better chance of reversing their diabetes. Those who did not reverse had been diagnosed for a mean of 3.8 years. Those who succeeded had a mean of 2.7 years. This stresses again why early diagnosis and action matter.
Why Is Diabetes Reversal Important?
People can live with diabetes for many years. But several factors make reversal very appealing. They can be sorted into two groups: non-life-threatening and life-threatening factors.
Non-Life-Threatening Risks of Diabetes
Once you are diagnosed, you must take medication for life unless a reversal happens. This can be hard on many fronts. Diabetes drugs are costly. Taking meds every day is a hassle. If you miss your meds or do not eat the right diet, you risk hypoglycemia (low blood sugar) or hyperglycemia (high blood sugar). These two can show up with the following symptoms:
- Increased thirst
- Frequent urination
- Extreme hunger
- Unexplained weight loss
- Ketones in the urine (ketones are a byproduct of muscle and fat breakdown, which happens when there is not enough insulin available)
- Fatigue
- Irritability
- Blurred vision
- Slow-healing sores
- Frequent infections, such as gum or skin infections and vaginal infections
Life-threatening complications
Long-term complications of diabetes build up over time. When they come, they may become life-threatening. They include:
- Cardiovascular disease. Diabetes raises the risk of heart attack, stroke, and narrowed arteries (atherosclerosis).
- Nerve damage. High blood sugar can injure the walls of blood vessels that feed the nerves. This leads to a slow loss of feeling in the limbs, which are hit the most. Over time, this can lead to a complete loss of feeling.
When the nerves in the gut are affected, a person may have nausea, vomiting, diarrhea, or constipation. In men, it may lead to erectile dysfunction.
- Kidney damage. Diabetes can damage the vessels in the kidneys that filter out compounds from the urine. When these compounds build up in the kidneys, they cause toxicity and kidney damage over the long run. Kidney failure is the hallmark of end-stage kidney disease. It calls for regular dialysis or a kidney transplant, which can be costly.
- Alzheimer’s disease. Type 2 diabetes has been linked to a higher risk of Alzheimer’s disease.
Given the complications that may come with a diabetes diagnosis, reversal seems the only safe way out.
Related reading
- How to Achieve Diabetes Remission
- Type 2 Diabetes and the Carnivore Diet
- Liquid Diet to Reverse Type 2 Diabetes
References
- Mayo Clinic: Diabetes. Retrieved from https://www.mayoclinic.org/diseases-conditions/diabetes/symptoms-causes/syc-20371444
- Healthline: Is Diabetes Type 2 Reversible? https://www.healthline.com/health/type-2-diabetes-reversible
- Springer (2011): Reversal of type 2 diabetes: normalization of beta-cell function in association with decreased pancreas and liver triacylglycerol. Retrieved from https://link.springer.com/article/10.1007%2Fs00125-011-2204-7
- Newcastle University: Reversing type 2 diabetes. Retrieved from – https://www.ncl.ac.uk/magres/research/diabetes/reversal/#publicinformation
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 5, 2026
Obesity does not cause type 2 diabetes by taking up space. It causes it, in large part, by switching on an immune response. That response is a low-grade, long-running inflammatory state. It never resolves, because the thing triggering it never leaves.
That is the shortest honest summary of two decades of work on what researchers named metaflammation: metabolic inflammation. It is worth understanding. It explains why blood sugar is a late signal, not an early one. It also explains why the treatments that work are the ones that lower the inflammatory load, not the ones that chase the number.
An immune system built for a threat that ends
The innate immune system is the body’s first responder. It spots a threat within minutes. Its receptors detect the general shapes of bacteria, viruses and tissue damage. It answers with cytokines, signal proteins that raise the alarm, call in cells and start repair.
That system is built on one assumption: the threat is temporary. Inflammation costs the body a lot, so it is meant to be intense, brief and then switched off. Every part of the design depends on there being an “off.”
How does obesity cause inflammation?
Growing fat tissue acts like a constant, low-level irritant. Fat cells under metabolic stress release inflammatory signals. Immune cells pile up in the tissue. The tissue’s own signals shift from repair toward defense. The result is inflammation that never gets as intense as an infection, and never turns off either.
That difference matters more than it sounds. You do not feel this the way you feel an infection. There is no fever, no obvious swelling, nothing to point at. It shows up as slightly raised inflammatory markers on a lab report. It also shows up as tissue that slowly stops responding to insulin the way it should. How insulin resistance and inflammation drive each other.
Why this makes glucose a late indicator
Insulin resistance is the body’s tissues answering insulin more weakly. The pancreas makes up for it by making more insulin, and for years it succeeds. That is exactly why fasting glucose can look fine while the real problem is well advanced. Glucose rises when the pancreas starts to fall behind. By then, the process has been running a long time.
This is why a normal blood sugar is not a clean bill of metabolic health. The questions worth asking are about fasting insulin, triglycerides, waist size and inflammatory markers, not a single glucose value. What insulin resistance actually is.
It starts earlier than most people assume
Raised inflammatory markers linked to excess weight have been documented in children. That means young children, not teenagers. This process starts well before the age when anyone is screened for it. That is part of why adult metabolic disease keeps showing up in younger and younger patients.
How do you get rid of the chronic inflammation that obesity causes?
The useful payoff of understanding the mechanism is that it shows you the lever. If the inflammation is driven by the metabolic state of the tissue, then the treatments that matter are the ones that change that state.
- Removing the drivers. Refined carbohydrate and industrial seed oils raise the inflammatory load directly, over and over. Refined grains, insulin resistance and type 2 diabetes.
- Losing visceral fat rather than simply losing weight. Visceral fat, the fat packed around the organs, is the metabolically active part. A scale cannot tell it apart.
- Sleep and stress. Both move inflammatory markers measurably. Nearly everyone treats both as optional.
- Muscle. Skeletal muscle is the biggest glucose sink in the body. Resistance training builds it, and that lowers the insulin needed to do the same job.
None of that is a supplement or a hack. It removes a chronic trigger, so a system built to switch off finally can. More on metabolic inflammation, and how it presents as metabolic syndrome.
Why the word “inflammation” gets misused
It has become a marketing word, which makes it easy to dismiss. The version described here is specific and measurable. It is documented in tissue. It is tracked with markers such as C-reactive protein. And its mechanism is tied to how insulin signaling fails. Being oversold in a supplement ad does not make it less real in a pancreas.
Frequently asked questions
Is metabolic inflammation the same as the inflammation from an infection?
No. Infection sets off a strong response that resolves once the threat is cleared. Inflammation associated with obesity is low-grade and constant. That is why it causes no fever or obvious swelling. It shows instead as mildly raised markers and worsening insulin resistance. Learn more: metabolic inflammation explained.
Can I have normal blood sugar and still have this problem?
Yes, and it is common. The pancreas makes up for insulin resistance by making more insulin. So glucose stays acceptable while the real process moves forward. Glucose rises when that makeup effort begins to fail. Learn more: what insulin resistance actually is.
Which tests show it?
Check fasting insulin along with glucose, triglycerides and HDL, high-sensitivity C-reactive protein, and waist size. Together they give a far better picture than a single fasting glucose. No one value settles it; the pattern does. Learn more: metabolic syndrome.
Does losing weight fix it?
Losing visceral fat cuts the inflammatory signals substantially. Weight alone is a crude stand-in. The fat around the organs is the metabolically active part, and a scale cannot tell it apart. Learn more: insulin resistance and metabolic inflammation.
Do anti-inflammatory supplements help?
They do not address the trigger. This inflammation is driven by the metabolic state of the tissue. So it responds to changes in that state: what your diet is made of, visceral fat, sleep, muscle mass. It does not respond to something added on top. Learn more: refined grains and insulin resistance.
What are the warning signs of chronic inflammation from obesity?
Usually there are none you can feel. There is no fever, no obvious swelling and nothing to point at, because this inflammation never gets as intense as an infection. It shows up as slightly raised inflammatory markers, such as C-reactive protein, on a lab report. It also shows up as tissue that slowly stops responding to insulin the way it should.
What foods make this inflammation worse?
Refined carbohydrate and industrial seed oils. Both raise the inflammatory load directly, over and over. Removing them is the first lever. Pair it with losing visceral fat, sleeping well, managing stress and building muscle. None of that is a supplement or a hack. It removes the chronic trigger so the immune response can finally switch off.
Where is the practice located?
4477 Woodson Rd, Suite 209, St. Louis, MO 63134. Call (314) 481-5000.
Related reading
Sources
- Lumeng CN. “Innate immune activation in obesity.” Molecular Aspects of Medicine. 2013;34(1):12–29. PMC3888776
- Hotamisligil GS. “Inflammation and metabolic disorders.” Nature. 2006;444(7121):860–867. PMID 17167474
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Metabolic inflammation and obesity feed each other. Inflammation starts in the fat cells themselves and grows as fat mass expands. Cytokines such as TNF-α then cause insulin resistance. Inflammation in the hypothalamus causes leptin resistance, which drives more weight gain. The end point is diabesity: diabetes occurring in the context of obesity.
Obesity is a disease that has plagued modern man in recent times. Access to highly processed foods and less physical activity are key contributors to it. Researchers are hard at work on what other underlying factors lead to obesity. That matters because of its link to the onset of Type 2 Diabetes, Cardiovascular diseases, and liver disease. In this article we take an in-depth look at metabolic inflammation. We look at its role in the onset of obesity. Let’s dive in.
- What is obesity?
Obesity is marked by a low-grade chronic state of inflammation. In it, the levels of pro-inflammatory cytokines such as TNF-α, IL-6, and CRP are increased. In this state, too much subcutaneous and/or abdominal adipose tissue (fat under the skin and/or in the belly) builds up. This adipose tissue is no longer considered inert and mainly devoted to storing energy. It is emerging as an active tissue. It helps regulate physiological and pathological processes, including immunity and inflammation. Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To find your body mass index, divide your weight in pounds by your height in inches squared. Then multiply by 703. Or divide your weight in kilograms by your height in meters squared.
| BMI | Weight status |
| Below 18.5 | Underweight |
| 18.5-24.9 | Normal |
| 25.0-29.9 | Overweight |
| 30.0 and higher | Obesity |
For most people, BMI gives a reasonable estimate of body fat. However, BMI doesn’t directly measure body fat. So some people, such as muscular athletes, may have a BMI in the obesity category even though they don’t have excess body fat.
- What is Diabesity?
‘Diabesity’ is the term for diabetes occurring in the context of obesity. This form of obesity-dependent diabetes has become a major public health problem in recent times. At its base, it is explained by insulin resistance and pancreatic beta-cell dysfunction. Still, new patterns have evolved to explain these changes in the context of the modern spates of obesity and diabetes.
- Is obesity an inflammatory condition?
The link between obesity and inflammation has often been debated in the recent past. Many people do not know that the link was made decades ago. Over a century ago, doctors used high doses of a class of anti-inflammatory compounds, including aspirin, called salicylates to treat Type 2 diabetes. In some cases, the symptoms of diabetes totally went away. Unfortunately, this treatment was stopped due to the serious side effects caused by the high doses of salicylates. Now we will look in depth at the questions of our topic today. Does obesity cause inflammation? Or is inflammation caused by something secondary to obesity (like high blood sugar or triglycerides)? How about diabesity? Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body start an inflammatory response to diabesity? Let us tackle each item separately.
- How does Inflammation Cause Diabesity?
We look at some lines of evidence. They show that inflammation directly causes obesity and diabesity.
- Diabesity has been shown to develop after inflammation. Raised levels of inflammatory cytokines predict coming weight gain. In one study, infusing inflammatory cytokines into healthy, normal-weight mice caused insulin resistance. Another fact shows this too. People with other chronic inflammatory conditions are at higher risk of getting Type 2 Diabetes. For example, about one-third of chronic Hepatitis C patients develop T2DM. People with rheumatoid arthritis are also at higher risk.
- In obesity, inflammation has been noted to start in the fat cells themselves. As fat mass expands, inflammation increases. An explanation for this may be the dysfunction of the mitochondria (the “power plant” of our cells), caused by the added stress obesity puts on cell function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they make an excess of reactive oxygen species (ROS). These in turn start an inflammatory cascade within the cell.
- Further, inflammation of the fat tissue causes insulin resistance, which is the primary feature of T2DM. TNF-α is a cytokine (small protein) released during the inflammatory response. It has been repeatedly shown to cause insulin resistance. Several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein, have also been shown to cause insulin resistance.
- Also, inflammation of the brain (specifically the hypothalamus) causes leptin resistance. Leptin resistance often comes before and with insulin resistance and T2DM. Leptin is a hormone that regulates appetite and metabolism. It does this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolism are impaired. Weight gain and insulin resistance result.
- When there is inflammation of the gut, leptin and insulin resistance arise. This may occur via a rise in lipopolysaccharide (LPS). LPS is an endotoxin (a toxin from inside bacteria) made by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver and weight gain.
- 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. We now know that fat tissue is a metabolically active endocrine organ. It 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.
- Why would obesity cause inflammation?
The first theory is that obesity-induced inflammation is a protective mechanism. It keeps the body from losing mobility or fitness. Fat storage is an anabolic process, which means it builds up the organs and tissues. Inflammation, on the other hand, is a catabolic process. Catabolism breaks down organs and tissues. It’s possible that turning on catabolism via inflammation is the body’s attempt to keep weight within acceptable bounds. Evidence supports this theory. In experiments, causing local inflammation in fat tissue improves insulin resistance and causes weight loss. The second theory is that obesity-induced inflammation is simply a malfunction. Human evolution never selected against it. Obesity and its related disorders have been extremely rare throughout human history. They have only become common in the past 40 years. The surplus of modern, processed foods that comes with diabesity is also a fairly new thing. It’s possible that the stresses of obesity are similar enough to the stresses of an infection. If so, the body reacts to obesity in the same way it would to an infection: via inflammation. Evidence supports this theory. The same intracellular, inflammatory stress pathways are turned on in both obesity and infection.
- 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 set in, each can further stimulate the production of inflammatory cytokines. This forms a vicious cycle of inflammation and diabesity. Reducing inflammation is a major key in preventing and treating diabesity. Focusing only on regulating blood sugar and fat hormones, without addressing other potential causes of inflammation, is bound to produce inferior results.
Related reading
References
1. NCBI (2003): Diabesity: an inflammatory metabolic condition. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/14598860 2. NCBI (2013): Obesity, Inflammation, and Diet. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819692/ 3. NCBI (2006): Inflammation and insulin resistance. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1483173/ 4. Chris Kresser (2019): How Inflammation Makes You Fat and Diabetic (And Vice Versa). Retrieved from https://chriskresser.com/how-inflammation-makes-you-fat-and-diabetic-and-vice-versa/
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Yes. Added sugar drives weight gain and obesity. It is high in empty calories. It raises blood sugar until insulin resistance (when cells stop answering insulin) sets in. And it is less filling, so you eat more. A review of 30 studies in more than 242,000 adults and children found a significant link between sugar-sweetened drinks and obesity.
Sugar has been blamed for years for doing great harm to our health. Are these claims true? Does a soda a day guarantee ill health? What does too much sugar do to obesity? Here we look at these claims. We ask whether too much sugar really leads to obesity.
1. What is obesity?
Obesity rates have skyrocketed over the past century. In 1962, 46 percent of adults in the U.S. were considered overweight or obese. By 2010, that figure had jumped to 75 percent. So, what exactly is obesity? Obesity is a complex disease. It means having too much body fat. Obesity isn’t just about looks. It is a medical problem. It raises your risk of other diseases and health problems, such as heart disease, diabetes, high blood pressure and certain cancers. Obesity is diagnosed when your body mass index (BMI) is 30 or higher. To find your body mass index, divide your weight in pounds by your height in inches squared. Then multiply by 703. Or divide your weight in kilograms by your height in meters squared.
| BMI | Weight status |
| Below 18.5 | Underweight |
| 18.5-24.9 | Normal |
| 25.0-29.9 | Overweight |
| 30.0 and higher | Obesity |
For most people, BMI gives a fair estimate of body fat. But BMI doesn’t measure body fat directly. So some people, such as muscular athletes, may have a BMI in the obesity range even though they don’t carry extra body fat.
2. Sugar and obesity
Obesity is a complex problem with many causes. But among the likely suspects, sugar is a top favorite. As sugar intake has gone up, so has the size of our waistlines. Added sugars are a hotly debated topic. Eating added sugars has been tied to higher risk of a variety of chronic diseases. These include obesity, heart and blood vessel disease, diabetes and non-alcoholic fatty liver disease (NAFLD). They also include mental decline and even some cancers. Still, support for these possible links has been challenged on several fronts. The sugars in your diet can be either naturally occurring or added. Naturally occurring sugars are found naturally in foods such as fruit (fructose) and milk (lactose). Added sugars are sugars and syrups put in foods while they are made or processed, or added at the table. Many eating and lifestyle habits can lead to weight gain and extra body fat. Take a diet high in added sugars, such as sweetened drinks, candy, baked goods, and sugary cereals. It is a contributing factor in weight gain and chronic health problems, including obesity, heart disease, and diabetes. Many people eat more sugar than they realize. It’s important to know how much sugar you eat, because our bodies don’t need sugar to work properly. Added sugars give zero nutrients but many added calories. That can lead to extra pounds or even obesity, which hurts our health. The ways added sugar leads to weight gain and more body fat are complex and involve many factors.
3. Some ways added sugar is fattening
- It is high in empty calories Added sugars are sweeteners added to foods and drinks to improve taste. Common types of added sugar include fructose, corn syrup, cane sugar, and agave. Excess sugar may cause you to pack on weight. This is because it’s high in calories but offers few other nutrients. Small amounts of added sugar are unlikely to cause weight gain. But eating foods high in added sugars on a regular basis may cause you to gain extra body fat faster and more sharply.
- Impacts blood sugar and hormone levels
It’s well known that eating sugary foods significantly raises your blood sugar. A sweet treat now and then isn’t likely to harm your health. But eating large amounts of added sugar every day can lead to blood sugar that stays high. Blood sugar that stays high for a long time is called hyperglycemia. It can cause serious harm to your body. It does this by causing insulin resistance, which results in weight gain.
- May lead to overeating
Foods high in added sugars tend to be less filling. Some foods are rich in carbs, mostly refined carbs high in added sugars, yet low in protein. They can hurt fullness and may lead to weight gain. They do this by causing you to eat more at later meals during the day, or to overeat at any one particular sitting. Animal studies indicate that fructose affects signals in your hypothalamus (the brain’s hunger center). It raises hunger-boosting neuropeptides. These are molecules that talk to one another and shape brain activity. At the same time, it lowers fullness signals. Also, your body is built to crave sweetness. In fact, research shows that we eat sugar for the pleasure of the sweet taste of sugary drinks and foods.
- Linked to obesity and chronic disease
Many studies have linked high intake of added sugars to weight gain and chronic conditions, such as obesity, heart disease, and diabetes. This effect has been seen in both adults and children. Recently, a review of 30 studies in more than 242,000 adults and children found a significant link between sugar-sweetened drinks and obesity.
4. What are some of the health problems associated with obesity?
People with obesity are more likely to develop a number of potentially serious health problems, including:
- Heart disease and strokes. Obesity makes you more likely to have high blood pressure and abnormal cholesterol levels. These are risk factors for heart disease and strokes.
- Type 2 diabetes. Obesity can affect the way your body uses insulin to control blood sugar levels. This raises your risk of insulin resistance and diabetes.
- Certain cancers. Obesity may increase your risk of cancer of the uterus, cervix, endometrium, ovary, breast, colon, rectum, esophagus, liver, gallbladder, pancreas, kidney and prostate.
- Digestive problems. Obesity makes you more likely to get heartburn, gallbladder disease and liver problems.
- Gynecological and sexual problems. Obesity may cause infertility (trouble getting pregnant) and irregular periods in women. Obesity also can cause erectile dysfunction in men.
- Sleep apnea. People with obesity are more likely to have sleep apnea. It is a potentially serious problem in which breathing stops and starts again and again during sleep.
- Osteoarthritis. Obesity raises the stress on weight-bearing joints. It also promotes inflammation in the body. These factors may lead to problems such as osteoarthritis.
Why Is Sugar Bad For Your Health? covers how sugar also drives inflammation, heart disease, kidney disease and gout.
5. How can obesity affect your quality of life?
People who are obese often struggle with some issues that might lower their quality of life. Some of these issues might include:
- Depression
- Disability
- Sexual problems
- Shame and guilt
- Social isolation
- Lower work achievement
6. How can you keep yourself from getting obese?
Maybe you’re at risk of obesity. Maybe you are overweight now, or at a healthy weight. Either way, you can take steps to prevent unhealthy weight gain and the health problems that come with it.
- Exercise regularly. You need 150 to 300 minutes of moderate activity a week to prevent weight gain. Moderate activities include fast walking and swimming.
- Follow a healthy-eating plan. Focus on low-calorie, nutrient-dense foods, such as fruits and vegetables, along with red meat and fish. Skip refined grains, and limit sweets and alcohol. Eat three regular meals a day with limited snacking. You can still enjoy small amounts of high-fat, high-calorie foods as an infrequent treat.
- Know and avoid the food traps that cause you to eat. Find the situations that set off out-of-control eating. Try keeping a journal. Write down what you eat, how much you eat, when you eat, how you’re feeling and how hungry you are. This helps you stay in control of your eating.
- Monitor your weight regularly. People who weigh themselves at least once a week do better at keeping off extra pounds.
- Be consistent. Stick to your healthy-weight plan all the time.
7. So, is sugar friend or foe?
Added sugars mess with your hormones, raise hunger, and push out healthy foods. These are just a few of the ways they can lead to weight gain. Too much added sugar also does more than add body fat. It can significantly raise your risk of chronic conditions, such as obesity, heart disease, and diabetes. So it is wise to eat added sugars with caution, because a stitch in time saves nine.
The mechanism is covered in Understanding The Role Of Metabolic Inflammation Plays In Obesity And Diabesity.
Related reading
References
- Endocrineweb (2018): Insulin Resistance Causes and Symptoms, Retrieved from
https://www.endocrineweb.com/conditions/type-2-diabetes/insulin-resistance-causes-symptoms
- Healthline (2019): 6 Ways Added Sugar Is Fattening. Retrieved from
https://www.healthline.com/nutrition/does-sugar-make-you-fat#section1
- American Heart Association (2018): Added Sugars. Retrieved from
https://www.heart.org/en/healthy-living/healthy-eating/eat-smart/sugar/added-sugars
- NCBI (2016): Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133084/
- Johns Hopkins Medicine (2019): Obesity, Sugar and Heart Health. Retrieved from
https://www.hopkinsmedicine.org/health/wellness-and-prevention/obesity-sugar-and-heart-health
- Mayo Clinic: Retrieved from
https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 18, 2026
Metainflammation is chronic, low-grade inflammation caused by overnutrition (eating more than the body can store safely). Fat tissue can only stretch so far. When it can no longer expand to soak up a constant flood of nutrients, it becomes inflamed. Then it releases inflammatory signals such as TNF-α and IL-6. It links obesity, type 2 diabetes, heart disease and chronic pain.
This clinic began as an interventional pain practice. It quickly became clear that chronic pain was rarely a stand-alone problem. The tools here relieve symptoms well. But they do not reverse the course of a disease driven by metabolic inflammation.
What metainflammation is
Inflammation is a biological response. The immune system launches it against attacks that threaten the body’s normal workings. It is essential. It turns harmful when it fails to resolve. Too much acute inflammation damages tissue. Inflammation that never resolves makes tissue malfunction over the long term. The balance between a useful response and collateral damage is delicate.
Chronic nutrient overload throws off that balance. Say adipose tissue (body fat) has little room to expand, and the nutrients keep coming. Then the tissue becomes irregular and inflamed. That is inflammation caused by overnutrition. That is metainflammation.
Fat tissue is an endocrine organ
Obesity is marked by a low-grade chronic inflammatory state. In it, pro-inflammatory cytokines (chemical alarm signals) are high, including TNF-α, IL-6 and CRP. Too much fat piles up under the skin and in the belly. That adipose tissue stops acting as quiet storage. It begins sending signals.
Adipose tissue releases many proteins that affect inflammation. They include TNF-α, IL-6, IL-1β, leptin, adiponectin, resistin, acylation-stimulating protein, SAA3, α1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist and macrophage migration inhibitory factor. That is not a waste dump. It is an organ with an output.
Lactate is a signal, not a waste product
A study published in Nature showed that lactate is a key regulator of cell function in Warburg-associated disease. It is not just a metabolic by-product. Lactate rewires macrophages (a type of immune cell). That changes how immune cells behave. It also drives histone lactylation. That is a change that alters which genes are turned on.
Otto Warburg described the Warburg effect ninety years ago. He saw that cancer cells use glucose differently from healthy cells. They make energy in a way that supports rapid growth. The metabolic and cancer research fields are describing the same underlying machinery.
Why a pain physician cares about metabolism
People ask this question often. Why worry about a patient’s weight or metabolic function? Why not just treat the pain? Because more than 90% of the chronic pain patients seen here have metabolic dysfunction. That includes many whose waist size would not flag them.
Pain in many joints, including joints that carry no weight, tracks the inflammatory cascade. It does this apart from mechanical load. Treat the joint while the inflamed environment stays, and the relief does not hold.
Dopamine, motivation and anhedonia
Chronic inflammation directly affects the brain’s dopamine system. That system drives motivation. This offers an explanation for low motivation in metainflammation. It also offers an explanation for why many patients with diabetes get chronic pain along with anhedonia (loss of pleasure).
Nearly 77% of the US population is now overweight. That change over fifty years correlates with the spread of highly processed food. It also correlates with a marked rise in chronic pain. In mouse models, high-calorie foods that trigger dopamine release disrupt normal feeding signals.
Where the vascular disease fits
Heart disease correlates closely with the global rate of obesity and type 2 diabetes. Attention has now shifted to metainflammation as the main disease process. Early metabolic problems appear to come before the blood vessel changes, not after them. Atherosclerosis acts more like atheroscleritis (an inflamed artery, not just a clogged one).
And it is not solved by removing meat
Patients often assume the Standard American Diet is entirely to blame. They think a plant-based diet solves it. But long-term vegan diets carry their own risks. Metainflammation can persist. Sarcopenia (muscle wasting) becomes a real concern when protein intake and quality fall short. What matters is the metabolic environment, not the type of food.
Related reading
- Metabolic Inflammation: What It Is
- Does Overnutrition Cause Metabolic Inflammation?
- Sugar, Inflammation and Health
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed August 25, 2026
The secret to a healthy weight is insulin, not calorie math. The same calorie is burned or stored depending on the insulin it triggers. Eat less and move more gives poor odds of keeping weight off. Randomized trials show a higher-fat, lower-carbohydrate diet beats a low-fat diet.
Fewer than 12.2% of US adults are metabolically healthy, based on NHANES data from 2009 to 2016. That is about one adult in eight. It is the most useful number for seeing why advice to each person keeps failing.
Is overeating the root cause of obesity?
People wrongly assume that eating too many calories is the root cause of obesity. But a calorie of food energy has different metabolic fates. It depends on the hormones around it when it arrives. The same calorie may be burned or stored depending on insulin. And insulin depends on what the calorie was made of.
Weight depends on many factors. But the one most often left out is insulin’s role in fat storage. Address that, and the math changes. Ignore it, and the math does not work in real life, however sound it looks on paper.
Does eating less and moving more work for weight loss?
Dietitians and physicians usually tell you to eat less and move more. That advice does not give good odds for losing weight and keeping it off. This is what the outcomes show. It is not a criticism of anyone’s effort.
Evidence from multiple randomized controlled trials indicates that a higher-fat, lower-carbohydrate diet beats a low-fat diet. It wins for both weight loss and cutting cardiovascular risk.
Why is it harder to lose weight each time you diet?
Weight regained after a loss often exceeds what was lost. Each new attempt gets harder. The process has a name — relapse-induced hyperplasia of adipose tissue. People call it rubber-banding or the fat yo-yo. Repeated cycles raise the number of fat cells that can store fat, and the next diet does not reverse that.
Smoking or obesity: which carries the higher hazard ratio?
A hazard ratio compares hazard rates between conditions. In context, smoking and obesity are closer than most people expect. For several outcomes, obesity does not come out ahead. This is a useful correction for anyone who sees obesity as a cosmetic issue and smoking as a medical one.
A generational and national problem
Blue Cross Blue Shield studied millennial health. It found health index scores dropped fast after a certain age, with metabolic conditions prominent. Obesity is also the leading medical reason people fail to qualify for US military service. Among young people aged 17 to 24, 27% are too obese to serve.
Around the world, chronic non-communicable disease makes up most of the disease burden. Most of it is associated with diet. The dual burden is real. Hunger persists in some groups while excess kills in others, and both are malnutrition.
How does sitting in front of the TV affect your health?
On average, every hour of TV watched after age 25 cuts life expectancy by an estimated 21.8 minutes. (Br J Sports Med. 2012 Oct;46(13):927-30.) Inactivity is not just a lack of exercise. Long stretches of sitting have their own metabolic effects.
The epidemic framing
Reversing obesity, prediabetes and type 2 diabetes is the most important public health challenge right now. When every species in a setting gets the same disease, the setting is the exposure. That matters more than whether we call it an epidemic or a pandemic.
Frequently asked questions
Why am I finding it so hard to lose weight?
Because the usual plan ignores insulin. The same calorie may be burned or stored depending on insulin. And insulin depends on what the calorie was made of. Eat less and move more does not give good odds of losing weight and keeping it off. Each regain can add fat cells, so every new attempt starts from a harder place.
How can I trigger my body to burn fat?
Change what you eat, not just how much. Whether a calorie is burned or stored depends on the insulin it triggers. That depends on what the food is made of. Evidence from multiple randomized controlled trials indicates that a higher-fat, lower-carbohydrate diet beats a low-fat diet. It wins for both weight loss and cutting cardiovascular risk.
What is yo-yo dieting?
Yo-yo dieting is the cycle of losing weight and gaining it back, often ending heavier than before. The process has a name: relapse-induced hyperplasia of adipose tissue. It is also called rubber-banding or the fat yo-yo. Repeated cycles raise the number of fat cells that can store fat. The next diet does not reverse that, and each attempt gets harder.
Related reading
- Malnutrition in Obesity and Starvation
- Energy Balance Theory of Obesity
- Minority populations and obesity
- Why Counting Calories Fails
- Addiction model of obesity
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed August 25, 2026
Insulin resistance is the stage in which the pancreas has to make more and more insulin to keep blood sugar normal. That excess insulin, called hyperinsulinemia, is itself inflammatory. It shuts down fat burning and drives fat into storage, including in the liver. That fatty liver makes still more metabolic inflammation.
Most of what goes wrong in type 2 diabetes happens years before blood sugar turns abnormal. The driver is insulin itself. It stays high for years, it quietly feeds inflammation, and it is mostly invisible on the tests most people get.
What does insulin actually do?
Insulin is widely described as the hormone that pushes glucose into cells by opening a channel. That description leaves out so much that it misleads. Insulin is mainly a fat-storage hormone. It shifts the body away from burning fat for energy and toward storing it.
Without insulin, the default state is lipolysis: fat comes out of storage and turns into usable energy. When insulin is present, lipolysis stops and lipogenesis begins. Lipogenesis turns the glucose in your blood into stored fat. The more insulin present, the more fat builds up.
At the enzyme level, insulin turns on hexokinase. Hexokinase tags glucose with a phosphate and traps it inside the cell. Insulin also blocks glucose-6-phosphatase, which would otherwise let the glucose back out. It turns on phosphofructokinase and glycogen synthase too, which drives glycogen building. With plenty of glucose coming in, the liver fills its glycogen stores fast. Then it turns the extra into fat.
Insulin is the disease; glucose is the symptom
For type 2 diabetes to appear, two things must exist together. One is insulin resistance. The other is insulin output that has fallen short of what that resistance demands. Overweight people commonly have insulin resistance without diabetes, because the pancreas makes up for it by making more insulin. Diabetes only appears when that makeup effort fails.
Here is why that matters in the clinic. The makeup period, hyperinsulinemia before insulin production collapses, is not a safe waiting room. It is highly inflammatory. Significant tissue damage builds up all through it, while fasting glucose still reads normal.
Does when you eat affect insulin resistance?
Most people eat from waking until bedtime: three meals, several snacks, and often sweet drinks in between. That pattern keeps insulin output high all day and wears out the insulin receptors. Insulin is a storage hormone. So keeping it high also drives fat buildup in the liver, which makes still more metabolic inflammation.
So giving the body a stretch of time when insulin is truly low is not a fad. It is how stored energy becomes usable again.
How are insulin resistance and inflammation linked?
Hyperinsulinemia is the common link between inflamed fat tissue and metabolic syndrome. The metabolic pattern associated with obesity raises pro-inflammatory cells, M1 macrophages and NK cells. It also holds down anti-inflammatory M2 macrophages, eosinophils and regulatory T cells. Notably, lowering blood insulin partway eases the fat tissue inflammation that excess calories cause. It also improves insulin sensitivity. That points at insulin, not fat mass, as the real driver. (Mol Cell Endocrinol. 2018 Dec 5;477:15-28.)
In diabetes, blood sugar stays high for a long time. That raises reactive oxygen species, which are harmful oxygen molecules. They harm how the beta cells that make insulin work. They also make insulin resistance even worse. The same process adds to the atherosclerosis (clogged, hard arteries) so often seen with diabetes.
Insulin resistance, not LDL, is the cardiovascular signal
Total and LDL cholesterol are poor markers of heart health. High triglycerides with low HDL predict heart risk considerably better. That pattern is also a reliable marker of insulin resistance. The QRISK calculator estimates ten-year heart and blood vessel risk. It does not use LDL at all. It uses the ratio of total cholesterol to HDL.
Preventing insulin resistance in young men would prevent an estimated 42% of myocardial infarctions (heart attacks). That is a bigger drop than correcting high blood pressure, at 36%.
An unrecognized cause of chronic pain
Metabolic inflammation from obesity and hyperinsulinemia is an overlooked driver of pain. Musculoskeletal pain (pain in muscles, bones and joints) affects an estimated 13.5% to 47% of the general population. Roughly 75% of those people report two or more painful areas. Pain in many joints, and its spread, is linked on its own to the inflammatory cascade, not just to mechanical load. That includes joints that bear no weight.
That independence is the point. A joint that bears no weight does not hurt because of body mass. It hurts because it sits in an inflammatory environment. A pain physician who never addresses insulin resistance is treating half the problem.
How do you reverse insulin resistance?
Weight loss and carbohydrate restriction each help reverse diabetes on their own, and combining them works better than either alone. Weight loss helps by easing the crowding in the liver and pancreas, improving blood flow and cutting hormone signals from fat cells. Carbohydrate restriction helps by lowering the insulin signal that drives storage in the first place.
The size of the problem justifies the effort. As obesity has worsened worldwide, type 2 diabetes has followed. One in every two Americans born today is predicted to develop it.
Frequently asked questions
What are the symptoms of being insulin resistant?
Often nothing you notice. Insulin resistance does its damage quietly for years while fasting blood sugar still reads normal. That is because the pancreas keeps pouring out extra insulin to hold it there. That excess insulin is inflammatory and drives fat into storage, including in the liver. One sign worth taking seriously is pain in several joints, even ones that bear no weight. That pain tracks metabolic inflammation, not body mass.
How can I know if I am insulin resistant?
Do not rely on fasting glucose. It stays normal through the damaging years, and the tests most people get miss the problem. Look at your triglycerides and HDL instead. High triglycerides with low HDL is a reliable marker of insulin resistance. That pattern predicts heart risk considerably better than total or LDL cholesterol. Ask your physician to read the pattern, not just your sugar.
What foods increase insulin?
Carbohydrates drive the insulin signal that pushes fuel into storage. That is why cutting them is one of the two independent factors that reverse diabetes. When you eat matters as much as what you eat. Three meals, several snacks and sweet drinks from waking to bedtime keep insulin high all the time and wear out the insulin receptors. A daily stretch of truly low insulin makes stored energy usable again.
Related reading
- What Is Cotton-Mouth and Why Does It Happen?
- Reactive Oxygen Species and Type 2 Diabetes
- GGT blood test: the oracle of death
- What Is Metabolic Inflammation?
Sources
- Hotamisligil GS. Inflammation, metaflammation and immunometabolic disorders. Nature. 2017. PMID 28179656
- Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. Journal of Clinical Investigation. 2006. PMID 16823477
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed August 25, 2026
On Bethalto Today radio, Dr. Gurpreet Singh Padda, MD, MBA, MHP explains the program he built to reverse diabetes. He also explains how the diabetes industry is profiting from the African-American community.
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Related reading
Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP
Interventional pain physician, addiction medicine specialist and obesity medicine diplomate.
Licensed in Missouri and Illinois.
Last reviewed June 4, 2026