Diabetic Nerve Pain: Why Neuropathy Starts Before the Diagnosis

Diabetic nerve pain often starts before the diagnosis. That is because insulin resistance (when cells stop answering insulin) drives the nerve damage. That process runs for years before blood sugar is high enough to be called diabetes. High insulin, glycation, oxidative stress and damage to tiny blood vessels are already at work. They hit the longest nerves first, which is why symptoms begin in the feet.

Burning feet at night. Numbness that creeps up from the toes. Or a pins-and-needles feeling that will not settle. These are among the most common ways type 2 diabetes reveals the damage it has been doing quietly. Diabetic peripheral neuropathy (nerve damage in the feet and hands) is not a separate disease that just happens to show up with diabetes. It is nerve tissue reacting to years of metabolic stress. Its timeline tracks the disease that caused it.

Among people with diabetes, 50% to 66% develop diabetic peripheral neuropathy at some point.¹ The pattern over time makes the point most clearly. 10% to 20% already have it when diabetes is diagnosed. That rises to 26% after five years and 41% after ten.¹

At what stage of diabetes do you get neuropathy?

That first figure deserves a second look. Between 10% and 20% of people already have measurable nerve involvement on the day they are told they have diabetes.¹

Nerve injury does not wait for a lab value to cross a line. The metabolic process that damages nerves — high insulin over time, glycation of proteins, oxidative stress and the damage to tiny blood vessels that follows — is well underway during the years of insulin resistance before a diabetes diagnosis. By the time the diagnosis is made, that process has had a long run.

This is why insulin resistance is the more useful thing to measure and act on. It is the upstream state. It is present long before glucose is high enough to be called diabetes.

What causes diabetic nerve damage?

Nerves burn a lot of energy. They depend on a fine network of tiny blood vessels. Ongoing high blood sugar (hyperglycemia) and high insulin (hyperinsulinemia) damage both the nerve fibers and the small vessels that feed them.

Glycation — sugar binding to proteins — stiffens tissue. It also creates advanced glycation end-products, which drive inflammation. That inflammation is not limited to the nerve. That is why it shows up next to other results of the same process. The link is laid out in metabolic inflammation as a cause of insulin resistance.

The same mechanism explains why nerve pain, and chronic pain more broadly, clusters with metabolic disease. That is covered in insulin resistance and chronic pain.

Longest nerves first

Symptoms usually begin in the feet and move upward. The hands are affected later. This is not chance. The longest nerve fibers are the most vulnerable to metabolic and microvascular (tiny blood vessel) damage, because they have the most distance to supply and maintain.

That is also why symmetry matters for diagnosis. A pattern that matches on both sides and depends on nerve length points toward a metabolic cause. Pain limited to one limb or one nerve’s area suggests something else — compression, injury, or a different process. That calls for a different work-up.

What is the best treatment for diabetic neuropathy?

Treating the pain and treating the cause are different jobs, and both are valid. Medications can make symptoms bearable. They do not slow the underlying process.

What addresses the process is better insulin sensitivity and less glycemic and inflammatory load on the nerves. In practice, that means what is in the diet more than how many calories it has — the role of refined grains and of omega-6-rich vegetable oils. The foods that move the other way are described in foods that improve insulin sensitivity.

The honest framing is remission rather than cure. Type 2 diabetes can be driven into remission, and remission can be lost — it describes a state that is being maintained, not a condition that is gone for good. With nerve damage, some can recover and some cannot. The realistic goals are to halt progression, reduce pain, and protect the feet you still have feeling in.

A caution about medication during improvement

As insulin sensitivity improves, the dose of glucose-lowering medication that was right before can become too much. Then the risk of hypoglycemia (low blood sugar) rises. This is a predictable result of things going well.

It is also why metabolic change should be made with your prescriber informed and involved. Never stop, reduce or change a prescribed medication on your own — that decision belongs to the physician managing it, working from your actual numbers.

Why is numbness in the feet dangerous with diabetes?

Pain is what brings people in. Numbness is the more dangerous finding.

Once protective feeling is lost, an injury can go unnoticed long enough to become a serious problem. Poor circulation also slows healing. Checking your feet every day and treating any wound right away are not minor advice here.

Care in St. Louis

Reverse Diabetes MD is at 4477 Woodson Rd, Suite 209, St. Louis, MO 63134, with Dr. Gurpreet Singh Padda, MD, MBA, MHP as Medical Director. Call (314) 481-5000 or email info@reversediabetes.md.

Background on the practice’s approach is on the type 2 diabetes page and in why we care. You can read about the physician on the Dr. Padda page. You can browse more reading on the blog, or reach the office through the contact page.

Frequently asked questions

How common is nerve damage in type 2 diabetes?

Between 50% and 66% of people with diabetes develop diabetic peripheral neuropathy at some point. 10% to 20% already have it at diagnosis.¹ The upstream process is explained in what exactly is insulin resistance.

Can diabetic neuropathy be reversed?

Some early nerve dysfunction improves when the metabolic driver is addressed. Established damage may not. The realistic aim is to stop progression and reduce symptoms, rather than to promise reversal.

My blood sugar is only slightly high. Am I at risk?

Nerve injury tracks the insulin-resistant state that comes before a diabetes diagnosis. That is why some people already have neuropathy when they are first diagnosed.¹ Why that same insulin-resistant state also drives chronic pain is covered in insulin resistance and chronic pain.

Why does it start in the feet?

The longest nerve fibers are the most vulnerable to metabolic and microvascular (tiny blood vessel) damage. So symptoms usually appear in the feet first and move upward. The hands are affected later.

Should I change my diabetes medication if my numbers improve?

Not on your own. Better insulin sensitivity can make a dose that used to be right too high. That raises the risk of hypoglycemia (low blood sugar). So any change must be made by the physician who prescribed it.

What are the symptoms of diabetic peripheral neuropathy?

Burning feet at night, numbness that creeps up from the toes, and a pins-and-needles feeling that will not settle are among the most common signs. Symptoms usually begin in the feet and move upward. The hands are affected later. The pattern matches on both sides. Numbness deserves the most attention, because lost feeling lets injuries go unnoticed.

What foods should you avoid with diabetic neuropathy?

What is in the diet matters more than how many calories it has. The two foods this practice points to first are refined grains and omega-6-rich vegetable oils. That is because they add to the glycemic and inflammatory load on the nerves. The foods that move the other way are in foods that improve insulin sensitivity.

Where is the practice located?

4477 Woodson Rd, Suite 209, St. Louis, MO 63134. Call (314) 481-5000, or use the contact page.

Related reading

• Are You Prediabetic? How to Tell
• Does Fatty Liver Start in the Gut?
• PCOS, Fatty Liver and Insulin Resistance

Sources

1. Bodman MA, Dreyer MA, Varacallo MA. Diabetic Peripheral Neuropathy. StatPearls. NBK442009

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 10, 2026

Related reading

• Nutritional Ketosis and Time-Restricted Feeding
• What Is Metabolic Syndrome? Signs and Diagnosis
• Why treat obesity and prediabetes

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

The carnivore diet curbs obesity by cutting out sugar and carbohydrates. That drives fat loss without counting calories. Its heavy protein load also curbs appetite through satiety (fullness) hormones. And it tends to push people into time-restricted eating.

Obesity has become rampant in recent times. It is said to affect almost 50% of Americans. It has been called a leading cause of chronic illness and poor health. The carnivore diet has become very popular as the new way to lose weight, stay healthy and ward off disease. A major draw of this diet is how it melts away the fat. How well does it work against obesity? Do its effects last? Here we look at the role this diet can play in curbing obesity.

1. What is obesity?

Obesity is a complex disease that involves too much body fat. Obesity isn’t just a cosmetic concern. It is a medical problem that raises your risk of other diseases and health problems. These include heart disease, diabetes, high blood pressure and certain cancers. There are many reasons why some people have a hard time avoiding obesity. Usually, obesity comes from a mix of inherited factors, the environment, and personal diet and exercise choices.

2. What is the Carnivore diet?

The Carnivore Diet is a strict diet that only includes meat, fish, and other animal foods like eggs and certain dairy products. It cuts out all other foods, including fruits, vegetables, legumes, grains, nuts, and seeds. Its supporters also recommend cutting out dairy, or limiting it to foods low in lactose, such as butter and hard cheeses. Lactose is a sugar found in milk and dairy products.

A good number of people on the carnivore diet report faster weight loss, clearer thinking, better digestion, and even better athletic performance. Some have also reported remarkable relief from disabling chronic health problems where usual treatments did not work.

1. What does one eat on the carnivore diet?

This is what you are likely to eat if you are on the carnivore diet:

–Below is the Green List that is, food you should be eating all the time with an emphasis on fattier cuts of meat to take in enough calories:

• Meat: beef, chicken, turkey, organ meats, lamb, pork, etc.
• Fish: salmon, mackerel, sardines, crab, lobster, tilapia, herring, etc.
• Other animal products: eggs, lard, bone marrow, bone broth, etc.
• Low-lactose dairy (in small amounts): heavy cream, hard cheese, butter, etc.
• Water

Generally, salt, pepper, and seasonings with no carbs are allowed.

– Below is the RED list of what you should NOT be eating:

• Vegetables: broccoli, cauliflower, potatoes, green beans, peppers, etc.

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

Some people include some of these foods, but a true Carnivore Diet does not allow them:

• Milk
• Yogurt
• Cheese

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

The carnivore diet can be seen as a fad. Is there evidence that any traditional peoples ate this way?

3. What effect might the carnivore diet have on obesity?

On a carnivore diet, all you eat is meat, meat and more meat… Now and then you could have some eggs and cheese and maybe a cup of coffee. At a glance, what about this diet could help fight obesity?

How does the carnivore diet work?

1. Cutting out sugar and carbohydrates

With no sugar and carbohydrates, fat comes off fast and stays off, without the need to count calories. Carbohydrates are hard to store. They are actually harmful if left in your system too long. So your body always wants to use them up first.

Your body releases insulin to move blood sugar into muscles. To make sure the sugar gets used up first, insulin also tells your fat cells to store any fat you eat. It also tells them not to release stored body fat for hours afterwards. If you eat a lot of fast-absorbing carbohydrates, your body releases a ton of insulin in response. Too much insulin can then pull too much sugar out of your blood, causing hypoglycemia (low blood sugar). The fastest way to bring blood sugar back up is to eat more carbs. That puts people on the carb roller coaster to weight gain.

The carnivore diet does away with all this by cutting sugar and carbohydrates out of your diet entirely.

2. Eating a lot of protein suppresses appetite

One way protein controls appetite is through the amino acid phenylalanine. Protein you eat is broken down into amino acids so the body can absorb it. Multiple studies have shown that phenylalanine suppresses appetite. It even improves mood and helps you burn stored fat. One study found that phenylalanine increases the release of a gut hormone called cholecystokinin in humans. This hormone tells the brain you are full after eating. It also leads you to eat less at the next meal. A mouse study found that a single dose of phenylalanine raised another satiety hormone called GLP-1. It also lowered levels of the hunger hormone ghrelin.

3. Increase in dopamine

Protein foods are built from amino acids (including tyrosine), which are vital for making dopamine. So it has been suggested that eating more protein may also boost dopamine without raising appetite. Dopamine is seen as the reward hormone. Raising its levels in your brain helps make your weight loss diet less unpleasant.

4. The carnivore diet “imposes” time restricted eating

The carnivore diet tends to lead people to time-restricted eating patterns on their own. Studies show that eating at night is a common cause of obesity. Junk food actually makes you prefer late-night eating. Sugar and fat together act as a trigger that locks in the unhealthy habit of late-night eating. Worse yet, your body runs on an internal clock called circadian rhythms. These do more than set your sleep and wake times. They also set when you digest food and use energy. We’re meant to eat during the day and sleep at night. When you eat at night, your body doesn’t want to process those calories. Instead they sit there and cause metabolic dysfunction.

Protein does not seem to trigger a desire for late-night eating. So the carnivore diet also helps curb that unhealthy habit. Late-night eating also lowers the quality of your sleep, and poor sleep leads to poor eating the next day. Less sleep also raises stress and anxiety. So cutting out late-night eating does more than improve weight loss. It also helps your mood and overall sense of well-being.

5. Does the carnivore diet stave off obesity?

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

Related reading

• Carnivore Diet for Obesity and Cancer
• Why We Don’t Count Calories
• Why Does the Carnivore Diet Work?

References

1. Mayo Clinic (2019): Retrieved from https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742

2. NCBI (1994):L-phenylalanine releases cholecystokinin (CCK) and is associated with reduced food intake in humans: evidence for a physiological role of CCK in control of eating. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/8201963

3. NCBI (2012):The Carnivore Connection Hypothesis: Revisited, Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253466/

4. Lolo (2018):Carnivore Diet: Fad or the Future? Retrieved from http://unity.lolofit.com/blog/posts/carnivore-diet-fad-or-miracle-diet

5. Healthline (2019):All You Need to Know About the Carnivore (All-Meat) Diet. Retrieved from https://www.healthline.com/nutrition/carnivore-diet

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

Low gut microbiota diversity goes with higher rates of obesity, insulin resistance, fatty liver disease and low-grade inflammation, so the goal is a diverse gut. Long-term eating habits shape that diversity. Above all, a fiber-rich diet shapes it. Prebiotics and probiotics reduce low-grade inflammation in the gut. They also improve gut barrier integrity (how well the gut lining holds together).

If Hippocrates, the father of modern medicine, is to be believed, “All disease begins in the gut”. The gut and its microbiota form a complex, open, and linked ecosystem. It is widely accepted that healthy gut microbiota is essential for good health. An imbalance in the gut flora could leave one open to a wide range of diseases, both infectious and non-communicable, including diabetes and obesity. We urgently need good ways to prevent and treat metabolic disorders such as diabetes and obesity. In this article, we look at the role of gut microbiota in diabesity (diabetes plus obesity). We also review ways to reach the best metabolic health.

1. What is Gut Microbiota and Gut Microbiome?

The gut microbiota is the term for the whole community of microbes in the gut. The gut microbiome is the full set of genes those microbes carry. The gut microbiota is known to be associated with metabolic syndrome and the diseases that come with it. These associated diseases, including obesity, T2D, and fatty liver disease (NAFLD/NASH), all seem to be linked to changes in which microbes are present. However, causality has not been proven yet. For this reason, the potential causal and personal role of the human gut microbiota in obesity and T2D is a high research priority. The gut microbiome holds a huge variety of microorganisms. They range from bacteria to viruses, fungi, phages, protozoa, and archaea, and all of them live in our adult bodies. One proposed view is that our microbiota is a microbial (endocrine) organ living in partnership inside our gut. This has led to a new view. It suggests that many lines of microbes can talk to each other and shape the host’s immune system and metabolism in several ways. Some of the abilities of this “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 add to our biology in ways that help both sides. Current research data on precision (personalized) nutrition suggest that diet changes should be tailored to each person to prevent chronic diseases. That includes giving pre-, pro-, and syn-biotics, as well as antibiotic treatment. The tailoring would be based on genes, food and drink intake, and nutrient intake. It would also be based on the microbiome, metabolome, and other omic profiles (detailed lab profiles of the body).

2. The gut and diet….

Diet is essential to what lives in the gut and how it works. The microbiota changes quickly when the diet changes in big, fast ways. Short-term changes can change the human gut microbiota in function and makeup significantly in 48 hours. Examples are switching between plant- and meat-based diets, or adding more than 30 grams of fiber per day, or following a diet with a different fat/fiber mix. Fiber-rich diets have been shown to improve insulin resistance in lean and in obese subjects with diabetes. However, only long-term eating habits shape the makeup of the gut microbiota. That is because short-term diet changes 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 the gut microbiome has low diversity, there are higher rates of obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD), and low-grade inflammation. Low bacterial diversity also had pro-inflammatory traits. Two signs suggested this. There were fewer butyrate-producing bacteria. There were more mucin-degrading bacteria, which break down the gut’s mucus layer. These traits potentially weaken the gut lining. That causes low-grade inflammation through endotoxemia (bacterial toxins getting into the blood). This low-grade inflammation of visceral adipose tissue (the fat packed around your organs) may provide a link between obesity and insulin resistance. Ethnic differences between human populations may also affect which microbes are present. Karlsson et al. compared T2D-associated metagenomes (gut gene data) between Chinese and Swedish subjects with T2D. The data pointed to different gut bacterial species doing similar metabolic jobs. The authors could also tell subjects with T2D apart from healthy subjects. Their predictive power was better than 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 lipids (fats) from the diet also coordinate many metabolic, inflammatory, and innate immune processes. The role of dietary fats in nutrition is beyond doubt. Fat buildup together with low-grade inflammation is a hallmark of atherosclerosis (hardening of the arteries). There is emerging evidence that how atherosclerosis develops is related to gut microbiome differences from person to person. Atherosclerosis seems to be related to TMAO. TMAO is a new marker associated with higher risk of atherosclerosis and coronary artery disease. Bile acids are other key gut regulators of fat and cholesterol metabolism. They help the gut absorb and move nutrients, vitamins, and fats from food. Bile is made in the liver (helped by products from fat breakdown). Then 95% of all bile acids are reabsorbed in the terminal ileum (the end of the small intestine) and taken back up by the liver. This loop is called the enterohepatic circulation. The gut microbiota turns primary bile salts into secondary bile salts. It does this through bile acid de-hydroxylation. Short courses of oral antibiotics affect which gut microbes are present and how bile acids are handled in humans. Even so, researchers found differing 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 use. The brain is a key regulator that detects changes in energy balance. It triggers behavioral and metabolic responses to correct them. The hypothalamus plays an important role in controlling both food intake and energy balance. It receives hormone and (vagal) neuronal signals from the rest of the body. Changing the gut microbiome with prebiotics has also been shown to affect portal vein levels of other hormones, including GLP-1. That in turn affected food intake, followed by a drop in body weight and fat mass.

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

Dysbiosis is the disruption of the normal microbiota. It has been described as involved in a wide range of diseases, including diabetes, obesity, and insulin resistance. It does this by upsetting the energy balance. So it has been suggested that changing the microbiota may help treat these diseases. This could be done directly (by antimicrobials, diet, prebiotics and/or probiotics, stool transplant, microbial-derived signaling molecules or metabolites) or indirectly (e.g., immunotherapy).

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

Diet is one of the major lifestyle factors in the start, prevention and control of diabetes, obesity and other cardiometabolic (heart and metabolic) diseases. It is also strongly linked to changes in microbiota. Many reports have shown that a genetic risk for obesity may have interacted with an obesogenic (obesity-promoting) setting. Together they may have driven the obesity epidemic. That setting includes a major shift in how people eat, which affects the gut microbiota. It also includes a sedentary lifestyle and physical inactivity. To date, there are many popular diets, including Mediterranean, gluten-free, vegan, Western, omnivore, and vegetarian. Most of these diets have been clearly linked to different microbiome profiles. After the industrial revolution, Western countries moved from the traditional diet to a diet rich in heavily processed foods, fats, sugars, proteins, and additives. That diet stayed low in micronutrients and dietary fibers. It is also called the Western diet. These diets lacked dietary fibers. Fibers are essential for gut health because they spur the growth and/or activity of certain helpful microorganisms. In contrast, people in traditional societies with a fiber intake of almost 50–120 g/day carry a much more diverse gut microbiota, which indicates good health. SCFAs (short-chain fatty acids) are found in lower amounts in people eating a Western diet. The Western diet was correlated with a drop in total bacteria and in helpful resident bacteria. Vegan and vegetarian diets are rich in plant foods that gut bacteria can ferment. Subjects eating them were reported to have a microbiota with a lower abundance of Bacteroides sp. and Bifidobacterium sp. The Mediterranean diet (vegetables, moderate consumption of poultry, olive oil, cereals, legumes, wine, nuts, fish and a low amount of red meat, dairy products, and refined sugars) provides benefits. They come from its high content of mono-unsaturated and poly-unsaturated fatty acids. They also come from its high levels of antioxidants, fibers and vegetable protein. People on a Mediterranean diet have a gut microbiota with high levels of Lactobacillus sp., Bifidobacterium sp., and Prevotella sp., and low levels of Clostridium sp. These species are associated with weight loss, a better lipid profile and decreased inflammation. Proteins in the diet have also been reported to help shape the microbiota. People eating a diet rich in beef had high levels of Bacteroides sp. and Clostridia. They were low in Bifidobacterium adolescentis, unlike people eating a meatless diet. Several recent studies have shown that some diets are linked with microbial diversity. These include vegetarian whey/pea protein and animal protein (meats, eggs, and cheese). Eating animal-based protein was positively associated with more bile-tolerant anaerobes (bacteria that live without oxygen). These include Alistipes sp., Bilophila sp., and Bacteroides sp.

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

Growing evidence suggests that gut microbiota plays a significant role in the start and progression of metabolic syndrome (MS). The gut microbiota was proven to modulate plasma glucose, appetite, serum lipids and pro-inflammation. Prebiotics or probiotics are widely used to change the microbiota. They can reduce low-grade intestinal inflammation. They can also improve gut barrier integrity. That can reduce plasma glucose and serum lipid levels, induce weight loss and decrease insulin resistance. Based on these results so far, the gut microbiota may be a potential treatment target for MS. However, clinical trials addressing how well current or potential treatments work in metabolic syndrome are needed. Also, people who are obese are likely to have an imbalance in gut microbiota makeup. This possibility is an exciting path for more research and possible new treatment targets. However, because most studies have been done in animals, direct translation of the findings to humans is limited. Prebiotics or other newly found helpful bacterial strains are potential interventions that will be used for treatment in the near future. It will be important to test how well they work. Likewise, studies will test metabolites (by-products) of the microbiota, including SCFA butyrate supplements. They will check if this compound has similar effects on food intake, energy use, and metabolic health in humans. The human gut microbiota affects whether metabolic syndrome develops, and those effects can be changed. That makes managing it a promising treatment approach. Mapping each person’s microbes at the metagenomic (gene) level gives insight into specific treatment targets. It also supports personalized treatment.

Frequently asked questions

What is the difference between gut microbiota and the gut microbiome?

The gut microbiota is the community of microbes living in the gut: bacteria, viruses, fungi, phages, protozoa and archaea. The gut microbiome is the full set of genes those microbes carry. Together they work like an organ. They break down food we cannot digest, harvest energy and nutrients, shape the immune system and keep the gut barrier intact.

How does the gut microbiome affect insulin resistance?

Low diversity in the gut goes with more obesity, insulin resistance, fatty liver disease and low-grade inflammation. A low-diversity gut has fewer butyrate-producing bacteria and more mucin-degrading bacteria. That mix can weaken the gut barrier. It can cause low-grade inflammation through endotoxemia. Inflammation of visceral fat (the fat packed around your organs) may be the link between obesity and insulin resistance.

How quickly does diet change your gut bacteria?

Fast, but not for long. Big diet shifts can change the gut microbiota’s makeup and function within 48 hours. Examples are switching between plant- and meat-based diets or adding more than 30 grams of fiber a day. Only long-term eating habits reshape its major features, so a short diet change is not enough.

Do probiotics and prebiotics help metabolic health?

Yes. Prebiotics and probiotics are the most widely used ways to adjust the gut microbiota. They can reduce low-grade intestinal inflammation and improve gut barrier integrity. That lowers plasma glucose and serum lipids, supports weight loss and decreases insulin resistance. Prebiotics have also been shown to change GLP-1 levels, which affected food intake, body weight and fat mass.

What diet is best for gut bacteria?

A fiber-rich one. People in traditional societies eating 50 to 120 grams of fiber a day carry a far more diverse gut microbiota. The Western diet of heavily processed foods, fats and sugars lowers helpful bacteria. The Mediterranean diet brings more Lactobacillus, Bifidobacterium and Prevotella. These species are associated with weight loss, better lipids and less inflammation.

Related reading

• Gut Microbiota and Metabolic Inflammation
• What Is Metabolic Inflammation?

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/

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

Going from keto to carnivore is easier than starting keto, because you are already fat-adapted. Swap greens for meat slowly over 7 to 10 days. Rotate beef, pork, chicken, fish and organ meat. Expect loose stools, cravings or a lack of appetite while your body adjusts.

The Carnivore Diet is the new trend. It has seen people feel better, heal disease, and perform at new heights. Of all the people who try the carnivore diet, a large share come from keto dieting. Keto to Carnivore has become the natural next step. From bad diet, to Keto to Carnivore. Here is how to make this move in the most painless way.

1. How easy is it to move from keto to carnivore? While the Keto and Carnivore diets are similar in many ways, there are some critical differences one needs to be aware of when making the transition. Unlike the ketogenic diet, there are no macronutrient ratio preferences in the carnivore diet. You just eat meat. And because you’re not eating any carbs, you’ll likely reach ketosis on a carnivore diet. Going from a SAD (Standard American Diet) to a Ketogenic diet is a tough change where one needs to get “fat-adapted”. Luckily, the move from keto to carnivore does not include this phase, because it has already happened. Here are some of the things you might go through:

1. While on Keto, one gets the “Keto Flu.” When transitioning from Keto to Carnivore, there is a somewhat similar process that can either be called the “Carnivore Flu” or the “keto flu”.
2. Loose stools are common and here’s why. The major difference between keto and carnivore is vegetables. So fiber intake drops sharply. This may lead to a significant change in bowel movements. Fiber is not needed for healthy digestion (and can cause digestive issues). But it does affect how the bowel works. Fiber absorbs water, adds bulk, and keeps you regular. So it lets the colon get lazy. A major function of the colon is to reabsorb water. Since fiber does most of this work in a diet high in plant-based foods, the colon gets lazy. It quits doing its job. It’s like a muscle that hasn’t been worked out. It gets weak. Going from a Ketogenic Diet to a Carnivore Diet results in a drastic change in fiber intake. And since the colon hasn’t gotten a good workout in a while, and is now being asked to do its job, it’s lost some of its capacity. It needs to “on-ramp.”  During this “on-ramp” water gets through.
3. Your stool is also not as frequent as it used to be. This is not constipation. You are just not making all that much stool as meat gets majorly absorbed and leaves little waste behind.
4. Fiber is food for bacteria in the large intestines. Bacteria love fiber. They ferment it and create the gases that make you unpopular at parties. Removing fiber makes some of these bacteria unhappy. There is research that shows that the microbiome can signal hunger and cravings as the bacteria do everything they can to get you to feed them before they die. We know very little about the microbiome. Most of what’s written is pure speculation. Research is lacking. But this “re-balancing” of gut microflora might actually be a good thing.
5. As your body gets used to life without carbohydrates, you are likely to have intense cravings. When a craving strikes, eat more meat. Many people who come from a Ketogenic Diet are used to obsessive measuring, counting, and testing. In this state, they are told they can eat meat until satisfied, with no measuring or tracking. Then the flood gates break loose. The key is to let the appetite re-regulate and normalize. Let the body fuel up on the nutrition it needs and desires. Be in it for the long haul. After a time the appetite regulates and the cravings disappear. In fact, all you will want to do is eat a steak. Everything else seems non-satisfactory.
6. On the flip side, some people have a lack of appetite. Meat is satiating. Protein is satiating. This can lead some people who move from Keto to Carnivore to under-eat. Then come the fatigue, the low energy, and the crabby mood. The key is to eat. Early on, hunger is not the only signal to listen to for when to eat. If you are tired, dragging, and crabby – eat. 2. How can you prepare to move from Keto to Carnivore?So, you are now ready to make the transition. What do you need to do? 1. Analyze what you have been eating If you don’t already keep a food journal, then start immediately, ideally with an app like Noom. This will help you see how much nutrition you get from plants as opposed to meat. 2. Calculate how much of your calorie intake is from plants Now that you know how many calories you take in from meat and plants, you can determine how much you need to make up by replacing plants with animal products. If you’re at a healthy weight, stick to the same calories. But if you still have a way to go to reach your weight loss goals, think about cutting calories a little more. I have found that weight loss on an all meat diet is higher than on keto. And the meat seems to keep me full for longer, so I can cut my calories more easily.

3. Gradually replace greens with meats It is much easier on your body if you make the change slowly, say over 7-10 days.

4. Eat from a larger array of meats It is very hard to eat the same thing all the time. Even a delicious ribeye steak from grass-fed beef cooked in butter gets old fast. The best thing you can do is switch between beef, pork, chicken, fish, and organ meat for your meals. This has a bonus too: it gives you a wider range of vitamins and minerals.

Monitor your ketone levels As you slowly switch to more meat, you should see your ketones go up. You can buy devices and test strips that measure these levels in your urine. They are fairly accurate. It’s a good sign that you’re moving in the right direction. You should also start testing several times a day. Keep track of the numbers and write down what kind of mood you’re in. This can be a very motivating exercise, as generally speaking you’ll be in a better mood with high levels. 3. Are you now confident enough to make the transition? In the whole keto vs carnivore debate, it really shouldn’t be a question of which one is better. They definitely complement each other. In case you are completely new to it all, then start with keto and after a few weeks transition to carnivore on regular on and off cycles. The two major symptoms in switching from Keto to Carnivore are bowel changes from a lack of plant material and fiber, and appetite swings. Know these are coming. Have a game plan and the commitment to get past them. That is key to a successful move from Keto to Carnivore. If for some reason you are struggling to commit to this lifestyle, cutting your carbs is still a good health move.

Related reading

• How to Start the Carnivore Diet
• Starting Carnivore Diet: Side Effects

References

1. Kevin Stock (2018):How to go from Keto to Carnivore. Retrieved from https://www.kevinstock.io/health/how-to-go-from-keto-to-carnivore/
2. Carnivore Style (2019): Keto vs Carnivore Diet – Which One Is Actually Better? Retrieved from https://carnivorestyle.com/blog/keto-vs-carnivore-diet/
3. Perfect Keto (2019):The Carnivore Diet: Can Eating Only Meat Supercharge Your Health? Retrieved from https://perfectketo.com/carnivore-diet/

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, in many patients. The DiRECT trial used a liquid diet of shakes and soups at about 800 calories a day. It put almost half (45.6%) of participants into remission after one year. Remission tracked closely with weight loss. It is done only under strict medical supervision.

Diabetes was the leading cause of death in the US in 2015. To date, it follows closely behind cardiovascular disease and cancer.

For many people, a type 2 diabetes diagnosis can be crushing. It comes with lots of risks and unknowns. It also means facing rising health care costs to manage a long-term condition. Treating diabetes in the US costs about $7,900 per person each year.

Across the Atlantic, the UK’s National Health Service (NHS) is looking for ways to curb the type 2 diabetes epidemic. The epidemic is straining an NHS budget that is already stretched thin. Toward the end of last year, the NHS started a program to reverse the disease. It puts 5,000 patients on a liquid diet of just over 800 calories a day for 120 days. This is part of the NHS Diabetes Prevention Programme (NHS DPP), which is meant for people at risk of type 2 diabetes. The project follows a highly successful trial of the same kind. The liquid diet limits how many calories patients take in. The hope is that it helps them reach a healthy weight and a healthy lifestyle. In the end, these lifestyle changes should lead to diabetes reversal.

What is type 2 diabetes?

Diabetes is a condition that makes a person’s blood sugar too high. Type 2 diabetes happens when the body slowly stops responding to insulin. This is called insulin resistance. The pancreas then pumps out more insulin, which leads to too much insulin in the body. In time, insulin levels may fall when the cells that make it are worn out.

Type 2 diabetes is linked to obesity and cancer. The good news is that diet and lifestyle changes can prevent it.

In the US, about 100 million people live with diabetes or prediabetes. Nine out of 10 diabetes cases are type 2. The study mentioned above suggested that a liquid diet could help reverse diabetes in most patients.

What do you eat on an 800-calorie liquid diet?

A liquid diet (like the one in the study) is usually a very low-calorie diet. It usually means eating about 800 calories a day or less. To put this in perspective, that is a third of what a man usually eats. It is half of what a woman should eat.

According to the NHS, the liquid diet is made up of shakes and soups. A person should stay on it for no more than 12 weeks. They should do it only under strict medical supervision.

Side effects to expect include:

• Dry mouth
• Constipation
• Diarrhea
• Headaches
• Dizziness
• Cramps
• Hair thinning

This diet is not suitable for everyone.

Successful trial

The landmark study is called DiRECT. That stands for Diabetes Remission Clinical Trial. The study is not complete, but early findings have caused lots of excitement. So much so that NHS England has committed to piloting a type 2 diabetes remission program in 2019. It will have about 5,000 study participants.

The first-year results showed that almost half (45.6%) of those in the program were in remission after a year. By the end of the second year, 70% of them were still in remission. Overall, 30% of study participants were still in remission after two years. This is good news for people with diabetes. It kills the myth that this disease cannot be reversed.

The second-year results showed a close correlation between type 2 diabetes remission and weight loss. Most people who lost more than 10 kilos stayed in remission after two years. Weight loss was also associated with a better quality of life and better blood glucose (sugar) control. It was also associated with less need for diabetes drugs.

The researchers admitted that this approach cannot work for everyone. It is important to understand the biology behind remission before starting any treatment.

What does type 2 diabetes remission mean?

Diabetes remission means a person diagnosed with diabetes can keep normal blood glucose levels without any medication. It does not mean diabetes is gone for good. It means the person lives symptom-free and medication-free. A person in remission still needs regular check-ups and follow-up with a doctor.

What is the NHS plan for type 2 diabetes remission?

The NHS long-term plan is to help people with type 2 diabetes take charge of their own health. By cutting calories and losing weight, most patients can reverse their diabetes.

In the end, this will lower health care costs for the NHS and for patients. Speaking to the press, NHS England chief executive Simon Stevens said this:

“However this isn’t a battle that the NHS can win on its own. The NHS pound will go further if the food industry also takes action to cut junk calories and added sugar and salt from processed food, TV suppers, and fast food takeaways.”

Frequently asked questions

Can a person with type 2 diabetes go into remission?

Yes. In the DiRECT trial, people went on a liquid diet of about 800 calories a day. Almost half (45.6%) of them were in remission after one year. Remission tracked closely with weight loss. Most people who lost more than 10 kilos kept their remission after two years. The researchers were clear that the approach does not work for everyone.

How long can you stay on an 800-calorie liquid diet?

According to the NHS, no more than 12 weeks, and only under strict medical supervision. The diet gives about 800 calories a day or less. That is about a third of what a man usually eats and half of what a woman should eat. That is why it is a supervised treatment, and it is not suitable for everyone.

What are the side effects of an 800-calorie diet?

Expect some of these: dry mouth, constipation, diarrhea, headaches, dizziness, cramps and hair thinning. They come from cutting intake to about 800 calories a day of shakes and soups. That is why the diet runs for a limited time and only under strict medical supervision.

Does remission mean type 2 diabetes is cured?

No. Remission means a person diagnosed with diabetes keeps normal blood glucose levels without any medication. They live symptom-free and medication-free. But the diabetes has not gone for good. A person in remission still needs regular check-ups and follow-up with a doctor to stay there.

Related reading

• Weight Loss and Diabetes Reversal
• How to Achieve Diabetes Remission

• References

1. CDC: Death and Costs. Retrieved from https://www.cdc.gov/diabetes/data/statistics-report/deaths-cost.html
2. iNews (2019): Type 2 diabetes patients to be prescribed very low-calorie liquid diet to reverse. Retrieved from https://inews.co.uk/news/type-2-diabetes-patients-prescription-very-low-calorie-liquid-diet-reverse-condition-198716
3. BBC News (2018): Type 2 diabetes: NHS to offer 800-calorie diet treatment. Retrieved from https://www.bbc.com/news/health-46363869
4. Diabetes UK: NHS England announces Type 2 remission pilot, and plans to double the size of the NHS England Diabetes Prevention Programme. Retrieved from https://www.diabetes.org.uk/about_us/news/nhs-type2-remission-pilot

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

Addiction treatment fails when it treats only the chemistry. Drugs flood the brain’s reward center with dopamine, but loneliness and isolation are what turn exposure into addiction. Clinics that only reduce cravings, and a society that ostracizes and jails people with addiction, leave the real problem untouched, so relapse is expected.

Stephen Edward:          Good morning and welcome to today on 95.5 R&B For The Lou. I’m your host Stephen Edward and joining us back on the program, Dr. Gurpreet Padda. He joins us back on Bethalto Today. It’s great to see you, Dr. Padda. Welcome back to the show.

Gurpreet Padda:           Thank you. I appreciate being here.

Stephen Edward:          The last time you were here we talked about diabetes in women and the African American community. What a marvelous discussion we had. Dr. Padda. Got a lot of people to email me after our interview. I am so happy you had a chance to come back and discuss some other things that were on your plate. Today, our discussion is addiction and why treatment fails.

Gurpreet Padda:           Yeah, absolutely. I think that there’s a misunderstanding of what addiction is. I think it’s very important for us to understand how people get addicted so that we can treat them correctly.

Stephen Edward:          Dr. Padda, what is the relapse rate for addictive diseases and why is relapse a part of recovery?

Gurpreet Padda:           So we expect patients to have relapse. But first you have to back up and ask yourself, what is addiction? Addiction is the concept that I’d go back to a drug that I was using or go back to a substance that I was using because that substance made me feel differently. It made me feel better. It’s a central brain phenomenon. It’s part of our limbic system, and specifically it’s a section in our brain called the nucleus accumbens. When we take in a substance that goes to our nucleus accumbens and we get a dopamine release, and I know I’m using all these chemical terms, but when we get this chemical release-

Stephen Edward:          But you’re making it easy to understand that.

Gurpreet Padda:           Yeah. So you go to the nucleus accumbens, when it gets stimulated, whatever substance I took right before that, if the nucleus accumbens dumps a bunch of dopamine, my brain says, “Hey doc, this stuff is really good. Whatever it was, this was really good.” So then you back up and you ask yourself, “What are the things that caused the nucleus accumbens to dump dopamine?” Well, the primary one when you’re a little baby is oxytocin and the mom and the baby, when they are exposed to each other, they dump oxytocin and oxytocin causes the nucleus accumbens to release dopamine. So it causes bonding and it makes people feel connected to each other. As we grow certain types of food, especially in the hunter-gatherer communities that we had for two and a half, 3 million years, if we came across something that was really tasty, the brain reinforced the behavior saying, “Hey, whatever that was that you just ate, it was really good and I’m going to release some dopamine and make you want more of it.”

Gurpreet Padda:           This was all good. But then we started to refine some of these chemicals that we found in the wild. So we’ve had poppy seeds forever. We’ve grown poppy forever. It was only the last couple of hundred years that we refined poppy seed into morphine. When we refined poppy seed into morphine, then we started to get morphine addiction because we’d taken the morphine and it dumps a bunch more dopamine than we would normally expect, and all of a sudden we’re flooded with this dopamine and we go, “Hey, this stuff is really good.” So it’s a matter of perspective. We’re getting a tremendous release of dopamine. So you might think that everybody that gets morphine gets this huge amount of dopamine release and we’re all addicts.

Gurpreet Padda:           But that’s not the case. Isn’t that strange? Some people become addicted and some people don’t. So there’s more to it than just the dopamine dump. I’ll give you the example. During the Vietnam War, one of our biggest fears for people coming back from Vietnam was that they were going to be addicted to heroin.

Stephen Edward:          Sure.

Gurpreet Padda:           Because the use of heroin in the Vietnam War was between 30 to 50% of all of the armed forces. They were exposed.

Stephen Edward:          Right, right.

Gurpreet Padda:           So that would have meant that we had half of the troops coming back, zombies on the street taking heroin. That didn’t happen. It was only 4% of the population. So why-

Stephen Edward:          But they talked about it so much, doc.

Gurpreet Padda:           They talked about it, but only 4%. So that makes you wonder why is it that only 4% of the population truly was addicted, but half of it was exposed. So that brings us to an interesting study a researcher did. What he did was he took rats and he put them in a cage, and in one side of the cage he put bottles of water and next to the bottle of water he put a bottle of water with cocaine in it. He watched what would happen. The rats would taste the regular water and they go, “Well, I need water, so I’m going to drink that.” But then they would stumble upon the cocaine water and go, “Hold on. This releases dopamine. I like this.” They kept taking the cocaine water and whether it was cocaine or heroin or morphine, whatever it was, whatever he tested with, anything that we have as an addictive substance, the rats would overdose on it and die.

Gurpreet Padda:           So therefore, us as physicians concluded that if you expose a rat or a human to a substance, they’re going to overdose and die. So you would think that that would be the case. But we also know that only half of the rats, if you expose half of the rats and only 4% of them are truly addicted, what happens? So the same researcher did another study. He took the rats and he put them in a cage and he gave them water and he gave them morphine or he gave them cocaine in another set of water. But instead of just being there by themselves, he gave them things to do. He gave them other rats to have sex with. He gave them other rats to play with. He enhanced their environment. He gave them stuff to do instead of sitting in a sterile glass aquarium.

Stephen Edward:          Right.

Gurpreet Padda:           As soon as he did that, none of the rats died. The rats weren’t interested in the morphine, in the cocaine, heroin.

Stephen Edward:          They were interested in each other.

Gurpreet Padda:           They were interested in each other. The conclusion from that is the rats that are lonely become addicted. The rats that have a lot of stuff to do don’t get addicted. The same thing with humans. Fundamentally, fundamentally it’s an issue of your limbic system with the dopamine release, but it’s in the context of loneliness. When we take addicts and we isolate them because we ostracize them because they’re addicts and we make them more lonely and we imprison them, we’re only making addiction worse. Instead of ostracizing and isolating addicts, we need to treat them with love. We need to treat them with dignity. We need to bring them back. We don’t need to put them away. That’s our fundamental problem [crosstalk 00:06:44].

Stephen Edward:          So you’re saying doctor, we shouldn’t put the blame on the addicts. We’re actually putting the blame on the drug itself?

Gurpreet Padda:           I think the blame is in the context of where the person is and I don’t think that you should blame any of it because human beings and animals are hardwired to release dopamine. We’ve spent millions of years trying to get a dopamine release and we have these substances that cause dopamine release. But you don’t make an addict unless they’re lonely, unless they’re isolated.

Stephen Edward:          I never thought about that doctor. So most of these addicts out here, or doing these things because they have nothing to do.

Gurpreet Padda:           They’re bored.

Stephen Edward:          They’re bored, and some of them in some cases are lonely.

Gurpreet Padda:           They’re completely lonely and they’re completely bored. If you look at, and I’ve personally done this, so this may seem weird, but I wanted to see what it was like to be in a situation that where somebody was homeless. So I did a little experiment on myself. I became homeless for a day in San Diego and I wanted to see what the average person experienced being homeless. It is one of the most lonely experiences you’ve ever had because you are ostracized because you don’t have any money. You’re ostracized because they think that you’re homeless and you’re isolated and no one will talk to you and no one will interact. So it’s no wonder that our homeless population has the highest addiction rate. It’s no wonder that that’s the case. The more isolated we make human beings, the far worse the addiction and the harder it is to break. So the issue is you certainly have a chemical problem, but we have a societal problem. The only people that we have to blame is our own society for our own behavior and for not including and not loving these people that are desperate for attention.

Stephen Edward:          What are some of the most addictive drugs?

Gurpreet Padda:           So surprisingly, one of the hardest addictions for us to break is nicotine. It takes more quit attempts with nicotine than practically any of the other substances. That brings up something really interesting. We know that the companies that make cigarettes are really, really, really good at figuring out how to modulate and affect nicotine and affect the sales of nicotine. Those same companies are the ones that have taken over the big food corporations. That’s why since the late ’70s and the early ’80s as nicotine sales started to go down, big food sales started to go up and the food that we’re now producing is hyper addictive. You can see that because you can see that in the type of food that we have, in the glycemic index of the food that we have, in the concentration of the fructose that we have compared to what it should be.

Gurpreet Padda:           So you can see it in the way that the food is manipulated to be hyper addictive. It’s because they took the information from the cigarette industry and shifted it to the food industry. It’s just fascinating. If you watch the history of food and the history of addiction and you watch it from the standpoint of what are the things that we know are hyper addictive and cigarettes are one of the worst, and they’ve shifted those resources into big food and that’s what we’re dealing with now with this epidemic of obesity. It’s an epidemic of obesity because of addiction.

Stephen Edward:          Dr. Padda, what about the preservative that they put in the food? Is that part of it as well?

Gurpreet Padda:           Preservatives are certainly a part of it, but I’ll give you an example that’s a little bit more specific.

Stephen Edward:          Go ahead.

Gurpreet Padda:           So if I take a molecule of sucrose, table sugar, okay, and I break it in half because it’s a disaccharide. It’s two sugars bounded together. So if I break it, half of it will be glucose and half of it will be fructose. So that sounds interesting to you. Glucose and fructose comes out of one sugar molecule of sucrose. Now it’s one to one ratio. Your body knows how to handle a one to one ratio. If I did a special imaging study of your brain and I looked in your brain and I exposed you to table sugar, you would get a little tiny light up of your nucleus accumbens because that fructose activates the nucleus accumbens slightly. Now, if I give you high fructose corn syrup that’s in soda, it’s not a one to one ratio. It’s 55 to 65% fructose and 45% or less glucose, and all of a sudden I get a massive light up of your nucleus accumbens. So they’ve shifted the type of sugar in the soda so it’s more addictive.

Stephen Edward:          Our conversation this morning is with Dr. Gurpreet Padda. Our topic of discussion addiction and why current treatments fail. Dr. Padda, is it the glucose or the fructose that produces cancer cells?

Gurpreet Padda:           Any of the sugars can stimulate the cancer cell growth. Cancer is really dependent upon sugar as one of its major influences to grow and it’s called the Warburg effect. Cancer is dependent upon these necessary elements for it to grow rapidly and one of the things it really needs is glucose and fructose. It needs both. But it preferentially prefers glucose, but it doesn’t … It’s not a big deal until you get to high concentrations. Regular amounts of glucose are not a big deal. It’s the high concentrations that you see … Because we didn’t, before 1915 to 1920, we didn’t have a huge amount of cancer in the world. Dr. Warburg, who was kept alive by the Nazis, by Hitler, Warburg was a Jewish scientist. Hitler kept him alive because he was so terrified of this rapid increase in cancer in Germany and it was because we had started to get processed food.

Gurpreet Padda:           It was back then that we started to get it and it really didn’t take off until the 1960s and ’70s when we got a lot more processing of food. It became even more refined and we added vegetable oil. We added a lot of Omega-6 vegetable oils, industrial seed oils.

Stephen Edward:          Dr. Padda, you and I are in the same generation. We may be the same age, but back in the day when we were growing up, cancer was known as an old folks disease. That has changed.

Gurpreet Padda:           Yeah. It’s because of our nutrition. We haven’t changed our environment that much. We’ve changed it a little bit, but really what we’ve changed is our nutrition. We used to rarely hear of people being diabetic.

Stephen Edward:          That’s true, so true.

Gurpreet Padda:           The Joslin Institute, which is one of the preeminent institutes that studies diabetes type II, type II diabetes was rare. It was exceptionally rare and now half to two-thirds of our population is overweight or obese and half of those are going to end up with type II diabetes in the next 10 to 15 years. That’s outrageous.

Stephen Edward:          It really is.

Gurpreet Padda:           This is a trillion dollar problem. If we don’t fix this problem, we’re going to bankrupt this country with a lifestyle disease. Something that is easy to treat and easy to fix and what’s happened is our food is so addictive we can’t stop eating it. We can’t stop consuming it because we need it. Our brains are tricked into wanting it and it’s such a bad thing that it’s increasing our sugars constantly and as it increases our sugars, it increases our type II diabetes rates.

Stephen Edward:          That’s rough, doctor.

Gurpreet Padda:           It is. That’s unfortunately what addiction is. So I said, cigarettes are probably the most addictive substance and they carried that information from cigarettes into big food and here we are.

Stephen Edward:          What is the disease concept of addiction?

Gurpreet Padda:           So the disease concept of addiction is I need more of X, Y, Z substance because it makes me feel normal. It doesn’t make me feel super normal because addiction is I need that now. I got exposed to it. It made me feel better and after a while I go, “Hey, I got exposed to that and I need that just to be okay,” and without that substance-

Stephen Edward:          Dr. Padda, the opioid problem we have here in St. Louis, is it because we’re a transit community? We have a lot of people coming in and out of St. Louis. A lot of people are sharing medications. Is that the reason why St. Louis ranks so high?

Gurpreet Padda:           We’re one of two states that actually has had an increase in opioid death rates in the last year.

Stephen Edward:          Missouri?

Gurpreet Padda:           Missouri, every other state minus one other has actually had a reduction in death rate. Missouri actually has had an increase and really what it is is the synthetic analog drugs that we have. So-

Stephen Edward:          Can you give us an example?

Gurpreet Padda:           Yeah, so fentanyl and carfentanil.

Stephen Edward:          Oh, yeah, of course.

Gurpreet Padda:           Are of course the drugs we’re talking about. Fentanyl is a synthetic opiate that we use in anesthesiology because I’m an anesthesiologist. We use it in anesthesia for cardiac operations. We use it to relieve pain during anesthesia and we use it for terminal cancer patients. It’s never really been intended to be out in the wild. It’s never intended to be used for regular patients. It was always used the requirements of anesthesia or used for palliative care for people that were terminal. But once you expose it to the wild population, once you put it in the wild, it so rapidly absorbs. It gives you such a high dopamine flux. It’s nearly the perfect drug to get that dopamine release. Carfentanil is nearly a thousand times stronger than fentanyl and fentanyl is probably a thousand times stronger than morphine. So a tiny dose of this drug is just incredible. People don’t know how to regulate the dosing on it. I’ll give you an example.

Gurpreet Padda:           So there was a conflict in Russia and in Russia there were a group of terrorists that had taken over a movie theater. This group of terrorists were holding hostage several hundred people, several hundred Russians. The Russian government thought, “You know what? We’re never going to get these people out. So what we’re going to do is we’re going to gas them with fentanyl gas. We’re going to dump a fentanyl bomb into this movie theater and then we’ll run in and we know that they’re all going to stop breathing and we’ll run in and we’ll resuscitate the people that are the good people and we can then arrest the terrorist.” So they put this bomb in there, and what they ended up doing was killing almost everybody in the theater because it is so potent and worked so rapidly that they couldn’t control it. It’s the same thing with somebody who’s taking fentanyl by accident.

Stephen Edward:          But doctor, if someone is having an overdose, what should they use? Naloxone?

Gurpreet Padda:           So Naloxone turns off those receptors and it takes somebody who’s overdosing, who stopped breathing and immediately reverses that.

Stephen Edward:          So Dr. Padda, you’ve been doing this for over 20 years. 20 years ago, the need and the popularity of using opioids were nonexistent.

Gurpreet Padda:           We’ve been observing this over time. I do mostly procedures to get rid of pain and I use a very low dose medication. The medications that people are using, the medications that they’re self using are 10,000 times stronger than anything that we prescribe. The real issue, the real issue is they don’t know how to dose it. It’s the same medication that we’re using, but in anesthesia, it’s the same medication but they don’t know how to dose it. This is not like somebody smoking a cigarette. The worst thing they’re going to have is a cough and maybe develop some lung cancer. If they take a fentanyl tablet, they’re going to overdose and die and they don’t have a chance to have the remorse to figure it out. They die so quickly that they don’t have that opportunity to reverse course. That’s why the Narcan is there that perhaps we can reverse course, but this is a dose escalation phenomenon.

Gurpreet Padda:           The more rapid the rise of the drug in the bloodstream, the more the dopamine release, the more the dopamine release, the more addictive the substance, the more addictive the substance, the more adherent the person is to that substance. If they have no reason not to do it, if they’re isolated, if there’s nothing else for them to do, if they’re bored, and this is what they do, if they’re hanging out by themselves, hanging out at the corner, and this is what all their friends do, if-

Stephen Edward:          That’s what they’re going to do too.

Gurpreet Padda:           Yeah, if this is what their tribe does, then this is what they’re going to do, and all of a sudden you have three or four dead people. Yeah, it’s the reality of what we’re dealing with now.

Stephen Edward:          Dr. Padda, there’s an awful lot of clinics popping up here in the St. Louis Metro East area because now there is a problem and before, no help. Now, all the help you can get, what do you think about that?

Gurpreet Padda:           Yeah, I think that the clinics, which most of them do medicated, medication assisted treatment, MAT, most of them assist the patient in reducing their craving, but that’s not the fundamental problem. The fundamental problem is that patients’ involvement in their community. What can we do? We can reintegrate people. We can give them things to do. We can give them a better hope and a better life to live for. If we continue to isolate our addicts, they’re going to die. That’s where we’re going to end up. We can’t do that. As a society, we cannot isolate these people. We’re taking away their opportunity to get jobs.

Stephen Edward:          Right.

Gurpreet Padda:           We’re taking away their opportunity to participate because all you’re going to do is isolate them, you’re going to kill them eventually. They have nothing to live for and we’re criminalizing, and unfortunately that’s the wrong answer.

Stephen Edward:          That’s not working.

Gurpreet Padda:           It hasn’t worked.

Stephen Edward:          Dr. Gurpreet Padda. This is Bethalto Today, and we’ll be right back after this.

Steven B.:         We’re back. This is Bethalto Today on 95.5 R&B for the Lou. I’m your host Steven B. Joining us in conversation this morning, Dr. Padda and our topic of discussion addiction and why current treatments fail. Dr. Padda, before we got into our break, we were talking about sugar and its addiction. What could it lead to doctor?

Dr. Padda:        That’s why we have an epidemic of addiction and we have 60,000; 70,000 dead people. It’s a big deal. We’re probably going to have killed more people than the Vietnam War with this addiction.

Steven B.:         Opioids?

Dr. Padda:        Opioids. We’re going to have killed more people than the Vietnam War with opioids. And you remember I said food is addictive. We’re going to kill 10, 100 times that in diabetes and excess of carbohydrate consumption, which is also an addiction. It’s just you can have a little remorse and it’s not going to kill you today. The fentanyl will kill you in five minutes. That cookie will take a couple of years.

Steven B.:         Dr Padda, sugar is in everything we eat, bread, cheese.

Dr. Padda:        Well that’s part of it. So there’s three things that I always tell my patients because the food companies have engineered this stuff. They’ve got this down to a science. They know exactly how to do this. And I’ll give you a wonderful example. They came up with these Fire Doritos and I don’t know if you’ve ever seen this.

Steven B.:         Yes. I’ve eaten them.

Dr. Padda:        So Fire Doritos are very interesting. Your brain has to be constantly modulated. If I give you one substance and I just give you a steady state of it, it’s not as addictive as if I give you a substance, give you more, then give you less and give you nothing and then give you more and then give you too much.

Dr. Padda:        And so it’s the cycle of up and down. So if you look at these Doritos and you look at this food that we’ve got, what happens is the different Doritos have a different hot point. They have a different amount of spice and specifically engineered to tantalize your taste buds so you don’t know what to expect on the next Dorito. And your brain suddenly gets a burst of dopamine. And then it gets less and then it gets a burst of dopamine. It’s like kind of hitting the jackpot in the casino. Three out of a hundred times you’re going to hit the jackpot. The other 97 you’re probably not going to get anywhere. And so every once in a while you’re going to hit the jackpot and you’re going to hear all of everybody else hitting the jackpot, which makes you participate in the casino.

Steven B.:         Doctor, where is your office located?

Dr. Padda:        So we have about 10 clinic locations, 11 clinic locations. I’m mostly at the south city office on Chippewa. We have a location in Bridgeton, which is very accessible. It’s right next to DePaul Hospital. We have a location in South County and I prefer being in the city. I’m a city mouse, so I prefer hanging out in the city and dealing with the issues that are of this nature.

Steven B.:         Right, right. Of course. Dr. I mean, you’re at Laclede Town [crosstalk 00:03:02] back in the day.

Dr. Padda:        I grew up in Laclede Town.

Steven B.:         You’ve connected with the people downtown and you’re probably still connecting with friends for over years and their families.

Dr. Padda:        Yeah, we’re trying to connect as deeply as possible. There are a variety of projects that we try to connect into and try to assist in the community. My biggest thing right now is yes, we know that addiction to opiates will kill 60,000 but addiction to sugar and our fast food industry, and our processed food industry-

Steven B.:         It could happen to more.

Dr. Padda:        Well, it’ll be millions. The opioid epidemic, it’ll be 20, 30, 40, 50, 100 billion. But this epidemic of diabetes and metabolic syndrome from the food that we eat, we’re talking two or three trillion.

Dr. Padda:        And so my goal is to assist in fixing the bigger problem. And that is the consumption of the food that we shouldn’t be having. We can fix type two diabetes. We can fix it in one generation. We can fix it in three months. We can fix this entire issue. So why do we continue to ignore the biggest healthcare crisis that we have?

Steven B.:         Dr Padda cigarettes is subsidized by the government. How come we just can’t take those off the shelves?

Dr. Padda:        It’s money. These industries are heavily subsidized. They have really good lobbyists. And they continue to make money. So the people want the substance because it makes them feel better. It’s the opiate for the masses. And we give them what they want, and of course they’re going to demand more of it, but that doesn’t mean it’s necessarily healthy.

Dr. Padda:        And I understand that. I totally respect that. I own restaurants too, and I understand what it is to, to serve food and they’re trying to make money and we all get it. But at the same time, we as individuals have to make decisions that are best for our individual health.

Steven B.:         People are making money and they’re killing their own people.

Dr. Padda:        Exactly.

Steven B.:         Dr Gurpreet Padda. Thank you so very much for coming in on the show this morning.

Dr. Padda:        Thank you. I appreciate it.

Steven B.:         We got to do this again.

Dr. Padda:        Thank you, sir.

Steven B.:         Thank you. This is Bethalto Today. We’ll be right back after this.

Frequently asked questions

What is the number one cause of relapse?

Dr. Padda points to loneliness. Drugs trigger a dopamine release in the brain’s reward center, but exposure alone does not make an addict. Only about 4% of Vietnam soldiers exposed to heroin stayed addicted, and rats with company and things to do ignored the drug water. The people most likely to relapse are the ones who are isolated, bored and cut off.

Why is it so hard not to relapse?

The faster a drug hits the bloodstream, the bigger the dopamine release, and the bigger the release, the harder the brain holds on to it. If a person has nothing else to do, is alone, or spends every day with a group that uses, the drug fills that space. Without a reason not to use, the brain keeps going back.

What do you say to someone who has relapsed?

Treat them with love and dignity, and bring them back in. Dr. Padda’s point is that ostracizing, isolating and imprisoning people with addiction only makes it worse. What helps is reconnection: giving the person things to do, a place in the community, a chance at work and a better life to live for.

Why do addiction clinics fail?

Most clinics offer medication-assisted treatment, which reduces cravings. Dr. Padda says cravings are not the fundamental problem. The fundamental problem is whether the person is part of a community. Without reintegration, meaningful work and people around them, a patient who stops craving is still lonely and isolated, and that is where addiction returns.

Related reading

• Food Addiction and Hyperpalatable Food: How It Works
• Starting Carnivore Diet: Side Effects

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

The failure to develop a magic-bullet drug that safely promotes weight loss is itself evidence. It says one thing. A reductionist answer, built on a single biologic mechanism, is unlikely to explain the obesity epidemic. This is a complex system failure. Complex systems do not fail for one reason.

The numbers that frame it

In the United States, 52.3% of adults have either type 2 diabetes or prediabetes. Fewer than 12.2% were metabolically healthy in 2009–2016. On the rules used after 2021, fewer than 7% are. Six feedings a day is a recipe for insulin resistance (when cells stop answering insulin). Put those three facts together. They describe an environment. They do not describe a pile of personal failures of willpower.

Duality of interest

Drug company influence is everywhere in academic policy and among thought leaders. Say a company paid someone, and that person then recommends the company’s product. That is no longer reliably treated as a conflict of interest. It is softened into a duality of interest. The polite word is doing real work.

The link is measurable. The more money doctors get, the more brand-name drugs they tend to prescribe. Now look at the advice to reverse type 2 diabetes, hyperinsulinemia (too much insulin in the blood) and obesity. That advice points toward less medical intervention and more patient self-care. Nobody is paid to promote that.

Prescription medication as a cause of death

Prescription medications are now the third most common cause of death worldwide, after heart disease and cancer. That statistic is alarming on its face. And the groups best placed to know do not dispute it. The Academy of Medical Royal Colleges and the BMJ have published a blueprint aimed at reducing it.

How long change takes

The first published evidence linked smoking to lung cancer. It then took nearly fifty years until real rules cut tobacco use. Big tobacco’s playbook in that time is well documented, and it has been reused. Max Planck’s point applies: science moves forward one funeral at a time.

Breaking news that is not new

A study published in Obesity reported that lifestyle interventions can produce sustained weight loss. These programs change diet and physical activity through behavioral strategies. The study is presented as news. It is not new. What stands out is which findings get pushed loud and which do not. That tracks funding more closely than newness.

The clinician’s own metabolic health

Overweight or obese doctors were less likely to talk about weight with heavy patients. Only 18% of them did so, against 30% of normal-weight doctors. That is not an argument for judging clinicians. It is an argument for seeing that the same environment acts on the people giving care. In this system, most clinicians are themselves metabolically unwell. A system like that will not fix itself with pep talks.

Related reading

• The role of fructose in diabetes
• Gut Microbiota and Metabolic Inflammation

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