Why Counting Calories Fails

Counting calories fails because the body does not treat every calorie the same. Insulin decides whether a calorie is burned for body heat or stored as body fat. Even careful tracking is off by as much as 20 to 50 percent. And the standard calorie-reduction approach gives an obese person a 1 in 167 chance of reaching a normal weight.

Counting calories often fails. Instead, focus on eating real food.
What is a calorie?

In physics, a calorie is the energy needed to raise the temperature of 1 gram of water by 1 °C. The calorie you see on a food package, however, is actually a kilocalorie, or 1,000 calories. That is the energy needed to raise the temperature of 1 kilogram of water 1 degree Celsius. The original method for finding the calories in a food directly measured the energy it produced. The food was placed in a bomb calorimeter, a sealed container surrounded by water. The food was burned completely, and the rise in water temperature was measured.

What is a nutritional calorie?

Calories in food and calories measured in physics are not the same. Nutritional calories leave out the parts we cannot digest (non-digestible components), such as dietary fiber and artificial sweeteners. Both of these could be burned in a bomb calorimeter to make heat. Many of the components humans can’t digest, such as cellulose, are the main energy source for other species. Human calories depend on the body’s ability to catabolize (break down) them. That usually involves enzymatic action rather than a high-temperature oxidation reaction.

Food labeling

Food labels are based on estimating the calories in each food component. The label adds up the calories from the energy-containing nutrients: protein, carbohydrate, fat, and alcohol. Carbohydrates contain some fiber that the body does not digest and use. Because of this, the fiber is usually subtracted from the total carbohydrate before the calories are calculated. The Atwater system uses the average values of 4 Kcal/g for protein, 4 Kcal/g for carbohydrates, 9 Kcal/g for fat, and 7 Kcal/g for alcohol.

http://www.nal.usda.gov/fnic/foodcomp/

http://www.nat.uiuc.edu

These nutritional calories are the energy available in food. Our body can use that energy for chemical reactions or store it in reserve as fat or glycogen. We count the calories the body can extract from the food we eat. But we ignore the interaction of that food as a signaling molecule. We also ignore the non-digestible components and the thermic energy used in breaking the food down.

Nutritional science has a paradox. A high-calorie intake of one food substrate causes weight gain. Yet the same calorie value of another substrate seems to cause weight loss. This leads some to suggest that calories don’t count.

The laws of physics are not broken, however. Calories do matter for energy balance. Whether fat, protein, or carbohydrate, a surplus of calories will lead to weight gain. What matters is the quality of the calorie. It is also the body’s response to those specific nutrients as signaling molecules, beyond their direct calorie value. The body turns food into usable energy through a highly complex process. It starts with the mechanical breakdown of food. Chemical and enzymatic processes follow throughout the gut, and these are significantly affected by the individual microbiome. The body is not static. How it uses a nutrient changes all the time. So does the extraction of energy associated with that nutrient. The real issue in managing obesity and type 2 diabetes is how the body uses the nutrients it is given. It is also whether that specific approach works for that specific person, at that specific time.

Food as a nutrient and as programming:

Food should be viewed as a source of nutrient energy (globally translated as calories). But it is also a set of instructions to the body, a program directing the body to a specific action. Food is not completely broken down to its basic parts during digestion. It keeps components intact, which then program the cells. A corrupted program can lead to outcomes such as obesity or diabetes or even an autoimmune state. These instructions are read not just by the body, but also by the gut microbiome. The microbiome can translate the instructions on its own. It creates its own programming subroutine, which then affects the body. Conventional nutrition advice ignores the program code carried in the food we eat. But these instructions cannot be ignored.

Focusing on what you can’t have only makes you want it more.

It’s easier to track not eating sugars and artificial sugars than to count their calories. Tracking and reliving the calories of carbohydrates you didn’t eat stimulates ghrelin, the hunger hormone.

Instead of calories, focus on real food.

It’s easier to track pounds of steak, fish, shrimp, or chicken than calories. It’s not what you didn’t eat. It’s what you did eat and who you are that matters. You are a person that doesn’t eat sugars (artificial or natural). You don’t fall prey to the big processed food manufacturers. And you know the truth about vegetable oil.

Focus on feeding windows and time-restricted feeding.

It’s easier to track the hours of healthy eating than calories. Say you know that you will only eat in a limited time window of 6 to 8 hours per day. Then the rest of your time becomes available for real activity.

A calorie is a calorie only if it is burned in a bomb calorimeter and the heat given off is measured. Biologically derived calories from different foods have entirely different metabolic effects on the human body. Equal calorie portions of sugar, alcohol, meat or olive oil have widely differing effects on hormonal systems such as insulin. They also differ in their effects on satiety (fullness) signals such as cholecystokinin or peptide YY. It does not matter how many calories a portion of food on a plate contains. What matters is how our body responds to eating and absorbing those calories, and how they are metabolized. It also matters how full we feel as a result, which is called satiety.

The current calorie-reduction strategies promoted for weight loss do not work. The standard calorie-reduction approach gives a 1 in 167 chance of reaching a normal weight. That is a greater than 99% failure rate.

Fildes A et al. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015;105: e54–e59

It is wrongly assumed that eating too many calories is the root cause of obesity. A calorie of food energy has different metabolic fates depending on the hormonal stimulation. That same calorie may be used to make body heat or be stored as body fat. Obesity is a disease of failed energy partitioning (how energy is divided up), not one of total energy intake. The main driver of this partitioning is the hormone insulin, which is specifically a fat storage growth hormone.

Focusing on calories in and calories out creates a built-in bias against high-fat food. Yet high-fat food may actually protect against obesity and related diseases. The simple calorie focus results in dietary guidelines that support replacing fat with starch and sugar. That swap promotes insulin resistance.

We hope to shift focus away from calories and toward a dietary pattern built on food quality rather than quantity. It is our hope that this shift will reduce obesity, related diseases and cardiovascular risk.

Malhotra A, DiNicolantonio JJ, Capewell S. It is time to stop counting calories, and time instead to promote dietary changes that substantially and rapidly reduce cardiovascular morbidity and mortality. Open Heart 2015;2(1) DOI: 10.1136/openhrt-2015-000273.

Snacking will make you fat because of the chronic high insulin from the constant feeding.

There have been two major changes in our eating habits since the 1970s, before the obesity epidemic began. The change to a high-carbohydrate, low-fat diet has been well documented. It has played an important role in causing obesity. However, the increase in meal frequency plays an equal, if not larger, role. That change has been largely ignored. In the 1970s, the average number of eating opportunities was three: breakfast, lunch and dinner. By 2005, that number had almost doubled. Now we eat breakfast, snack, lunch, snack, dinner, and snack. Each of these contains refined carbohydrates more often than not.

Cameron JD. 6 meals per day do not result in greater weight loss. Br J Nutr. 2010 Apr;103(8):1098-101

Popkin BM. Does hunger and satiety drive eating anymore? Am J Clin Nutr 2010;91:1342–7

Tracking calories to make sure you are eating less is self-deception. Even if you did track calories carefully, you would be off by as much as 20-50 percent. Even if you were perfect at tracking the actual calories, your math wouldn’t account for the bio-availability of nutrients (how much your body can absorb). It also wouldn’t account for the effect of anti-nutrients from vegetables, or the thermic effect of food. Your resting metabolic calorie needs change from day to day, hour to hour, and season to season. Your gut microbiome determines nutrient absorption. It changes all the time and interacts with your enteric nervous system (the nerves of the gut) and central nervous system.

Some people assume that the “calories burned” number on their workout equipment is accurate, but it’s not. Many people also reward themselves with a snack for exercising. That is a bad idea.

Instead of calorie counting:

Practice Hara Hachi bu, a Confucian teaching that instructs people to eat until they are 80 percent full. “Eat until you are eight parts (out of ten) full” or “belly 80 percent full.”

Simple changes to your eating patterns or the environment will dramatically increase the joy of food.

First, eat more slowly. Eating faster results in eating more. Slow down so your body can respond to the cues that tell us we are no longer hungry. You have a hormone called leptin that lets you know you are full. But if you wolf down your food, it doesn’t have enough time to work. So focus on food. Turn off the TV and the computer. If you’re going to eat, just eat.
Second, use small plates and tall, narrow glasses.
Third, cut out all the snacks. People eat from boredom or they eat from chemical signaling. Most of this chemical signaling can be eliminated when you remove artificial flavors, refined sugars, and industrial seed oils.

You probably have the mantra “breakfast is the most important meal of the day” stuck in your head. This was a baseless marketing phrase created in 1944 by General Foods to sell more cereal. John Harvey Kellogg of the Kellogg’s cereal company was a deeply religious Seventh-day Adventist. He believed that cereal would improve Americans’ health and keep them from masturbating and desiring sex. Before the invention of cereal (to reduce masturbation), breakfast was not as standard or routine. Kellogg might actually have been half right. Breakfast didn’t improve health. But eating more often, with processed cereal foods, results in more insulin resistance and worse male impotence.

Cut out breakfast, unless it is one of your two meals of the day and it falls inside your eating window. Regular breakfast consumption increases weight and insulin resistance by adding unnecessary calories to diets. https://doi.org/10.1136/bmj.l42

Eliminate vegetable oil.

One of the easiest swaps you can make is cutting out vegetable oil and replacing it with real fat. Real fat tastes better and makes your food more flavorful. It also carries fat-soluble vitamins.

Bottom line:

If you are eating real food, your willpower is better spent somewhere other than calorie counting and calorie restriction. Remember, you are retraining your body to know when it’s actually full and what real hunger is. Your goal is to eat only when truly hungry.

Cutting out breakfast and eating only in a 6 to 8 hour period each day makes this simple. Get rid of artificial flavorings, artificial and refined sugars, and refined foods. Healthy fat keeps you satiated (full) for a long time. Satiety and the nutrient density of food are the ultimate test.

It’s not what you didn’t eat; it’s what you did eat and who you are that matters. It’s more about how your body responded to the food you did eat.

Reframe who you are:

You are a person that doesn’t eat sugars (artificial or natural). You don’t fall prey to the big processed food manufacturers. And you know the truth about vegetable oil.

Frequently asked questions

Can I lose weight by just counting calories?

Rarely. The standard calorie-reduction approach gives an obese person a 1 in 167 chance of reaching a normal weight. That is a failure rate above 99 percent. Calories do count. But insulin decides whether a calorie is burned for body heat or stored as body fat. And even careful tracking is off by as much as 20 to 50 percent.

Should I count calories or just eat healthy?

Eat real food and stop counting. It is easier to track pounds of steak, fish, shrimp or chicken than calories. It is easier still to track hours. Eat only within a 6- to 8-hour window, cut out snacks, and drop sugars, artificial flavorings, refined foods and vegetable oil. Healthy fat keeps you full for a long time, so you eat only when truly hungry.

Why am I not losing weight eating 1500 calories a day?

Because the number on your tracker is not what your body does with the food. Counts run 20 to 50 percent off. They ignore how food signals your hormones. And your resting calorie needs change from day to day. Snacking keeps insulin high, and high insulin sends calories into fat storage. Workout machines overstate calories burned, and a reward snack after exercise undoes the effort.

Related reading

• Nutritional Ketosis and Time-Restricted Feeding
• The Calorie Paradox: Why Counting Calories Fails
• The Secret to a Healthy Weight: Insulin, Not Calories

Sources

1. Fildes A, Charlton J, Rudisill C, et al. Probability of an obese person attaining normal body weight: cohort study using electronic health records. American Journal of Public Health. 2015. PMID 26180980
2. Ludwig DS, Ebbeling CB. The carbohydrate-insulin model of obesity: beyond “calories in, calories out.” JAMA Internal Medicine. 2018. PMID 29971406
3. Ebbeling CB, Feldman HA, Klein GL, et al. Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial. BMJ. 2018. PMID 30429127

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 31, 2026

Eat real food: meat, fish, whole eggs, green leafy vegetables, seeds and tree nuts, with water, coffee or unsweetened tea to drink. Don’t eat vegetable oils, sugars, artificial sweeteners, grains, bread, potatoes or other refined carbohydrates, and don’t snack.

There are some misconceptions about food and what to eat and not eat. The truth is that food is medicine and information for your body. Food is for real hunger, not boredom. Each patient is unique and any advice will need to be medically tailored.

Hara Hachi bu (腹八分目) is a Japanese phrase that translates to, “Eat until you are eight parts (out of ten) full” or “belly 80 percent full.”  You can make simple changes in everyday habits to learn to eat until you are only 80 percent full.

First, eat more slowly. Eating faster results in eating more.  Slow down to allow your body to respond to cues, which tell us we are no longer hungry. You should also focus on food.  Turn off the TV and the computer.  If you’re going to eat, just eat.  You’ll eat more slowly, consume less, and savor the food more.

Second, use small dishes.  Choose to eat on smaller plates and use tall, narrow glasses. You’re likely to eat significantly less without even thinking about it. Ten minutes before eating a meal, drink a large glass of cold water with lemon, and do so again 10 minutes after finishing a meal. Don’t snack, and don’t have anything in the house that you should not eat.

There are more steps you can take to make yourself healthier:

Step Step Step: Walk for 10 minutes after every time you eat or drink anything, even if it’s just water.

Step 1: Stop all vegetable oils — no canola, corn, soybean oil, Crisco, or margarine. Vegetable oils are also called industrial seed oils and were originally industrial waste products. Look at all food labels, and do not eat food with any vegetable oils listed. Do not use any spray-on oil. Instead, eat healthy oils and fats such as olive oil, coconut oil, butter, avocado, and duck fat.

Step 2: Eliminate all sugars and artificial sweeteners, or anything that is sweet on your tongue. Eliminate all refined sugars (juices, soda, diet soda, candy, chips).

Step 3: Sleep well and get at least 7 hours of uninterrupted sleep every night. Do not use your TV, phone, or computer in bed.

Step 4: Supplement with 4-6 grams of Krill or Fish Oil per day. Consider adding minerals like magnesium and salts as well. Ketone supplements may also play a role.

Step 5: Decide if you need a Cleanse Protocol or the Live Health Protocol. The purpose of either is NO vegetable oils, NO refined carbohydrates, and getting restorative sleep.

Cleanse Protocol: If you are starting out and are uncertain if specific foods may be contributing to your inflammation, or if you have weight to lose and are stuck, the cleanse protocol may be appropriate. You should only eat twice a day. During this time, you can eat as much beef, chicken, or fish as you like, and you can add butter and spices. That’s it for the next 4 weeks, then re-add one item per week that you might be sensitive to, as long as it still fits under the Live Health Protocol. Drink only water.

Live Health Protocol: This protocol helps you to live healthily and reduce your pain and inflammation. You should eat real food, such as meat (beef, pork, chicken, and fish), whole real eggs, green leafy vegetables, and seeds and tree nuts (almonds, macadamia). Drink only water, coffee, and unsweetened tea.

• Don’t eat fake industrial foods, carbohydrates or sugars (grains, cereals, grits, oatmeal, rice, rice cakes, pasta, potatoes, bread), fruits, or nuts from the soil (peanuts, cashews). Don’t drink soda, juice, diet soda, or creamers in coffee.

Bonus points:
Eat one to two tbsp of psyllium fiber dissolved in warm water 30 minutes before bed.
The ultimate health supplement is to skip one meal per day and eat only twice a day, in a short 6 to 8-hour feeding window.
No caffeine after 3 p.m.

Am I on the right track?
Some patients need immediate feedback, and this can be done by measuring ketones as a marker of fat loss.

Don’t make this complicated.  Eat the same thing every day for the first few weeks, and choose between 4-5 different meals.  You should feel full after the meal.  Don’t snack. It’s a process that will take a few weeks to learn.

Don’t think of this as not having something, look at what you can have and eat until you are satisfied.

The more vegetable oil and sugar you eat, the worse your pain and inflammation will be. You may have to increase your salt intake if you feel fatigued or get muscle cramps. Medications may have to be adjusted.

It’s about reducing your sugar intake and increasing protein and healthy fats, and the rest will take care of itself.

It’s a way of living, not a diet.  This is a process: you will fail a few times, but each time you fail you learn. Don’t try, just do.
For more information

Reversediabetes.md

Related reading

• How to Reduce Gut Inflammation
• Why We Don’t Count Calories
• Eating your way to true health
• Diet to Prevent Type 2 Diabetes

Sources

1. Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ. 2016. PMID 27071971
2. Swaminathan S, Dehghan M, Raj JM, et al. Associations of cereal grains intake with cardiovascular disease and mortality across 21 countries in Prospective Urban and Rural Epidemiology study: prospective cohort study. BMJ. 2021. PMID 33536317
3. Hall KD, Ayuketah A, Brychta R, et al. Ultra-processed diets cause excess calorie intake and weight gain: an inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism. 2019. PMID 31105044

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 17, 2026

  Reverse Diabetes MD Presentation | Reverse Diabetes MD from Gurpreet Padda on Vimeo. Using an addiction model for obesity may be a more accurate way to view it. Obesity is more complex than the simple calories in, calories out model. Obesity is more than eat less, move more. It is shaped by an underlying response system in the brain and hormones. That system hijacks the endorphin (feel-good) system. The result is a disorder much like substance use. Obesity will not be solved by the “eat less, move more” mantra when the hardwired response is a dopamine reward system. No amount of habit building can steer the patient away from a dopamine rush. This is an itch that demands to be scratched. Treatment requires shutting off cues, providing satiety (the feeling of being full), and for a time swapping in other behaviors. Here is how the problem works. Obesity is not the problem. Obesity is the result of harmful behavior that engineered food keeps reinforcing. Obesity is just the most visible sign of the problems underneath. Food turns on two distinct systems: nutrient set points and the endorphin system. The human brain has set points for how much food and liquid to take in, and they are based on nutrients. Foods packed with nutrients turn on the reward system. That helped early humans survive by storing fat fast. This reward switches on the primitive endorphin system. It works by making dopamine in the nucleus accumbens (the brain’s reward center). That is similar, but not exactly the same, as other addictive substances. Here is the brain science of eating. Some foods (those high in fat, sugar, and salt, when combined with flavor enhancers) have an abuse potential like manufactured, concentrated substances. Think cocaine, alcohol, and opiates. Compulsive overeating is a more classically recognized addiction disorder. Dopamine is the known brain chemical for classic substance abuse disorders. It also governs food reward and the pleasure side of appetite. The classic addiction model does not fully explain obesity, however. We agree with the Nature article that looked at the food addiction model as it relates to obesity. It stated that the model is “misleading”, with supporting evidence described as “inconsistent and weak.” Obesity and the brain: how convincing is the addiction model? Nature Rev. Neurosci. 13, 279–286 (2012). According to the Yale Food Addiction Scale, not all obese people show food addiction. The scale applies the criteria for substance dependence to eating. By those criteria, 25% to 37.5% of obese people qualify. This is 200-300% greater in obese versus lean groups. The rate of food addiction is 500% greater in obese people with binge-eating disorder. Meule, A. How prevalent is “food addiction”? Front. Psychiatry 2, 61 (2011). Davis, C. et al. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite 57, 711–717 (2011). Gearhardt, A. N. et al. An examination of the food addiction construct in obese patients with binge eating disorder. Int. J. Eat. Disord. 30 Aug 2011 (doi:10.1002/eat.20957). The more likely mechanism is eating too much food. Overeating is like goal‐directed drug-taking. At first the ventral striatal and prefrontal areas of the brain control it. Then it becomes habitual and compulsive, driven mostly by the dorsal striatum, and executive control is lost. Acute (one-time) use of the drug of abuse raises dopamine in the accumbens. Then the mesolimbic dopamine systems become sensitized. That leads to stronger salience (attention), and so to more motivation toward drug‐related cues. Development of addiction is associated with a drop in striatal D2 receptors. This is linked to a reward deficiency syndrome, where more of the drug is taken to get the same reward. Rodents were exposed to high‐sugar diets, high‐fat diets, and a combination of high‐sugar high‐fat diets. They develop behaviors that resemble addiction, such as binge eating, compulsive food‐seeking, and withdrawal symptoms. Sugar addiction models have shown an opiate‐mediated withdrawal syndrome (one run by the body’s opioid system). Compulsive food‐seeking keeps going even against painful foot shocks. Opioid circuits in both the nucleus accumbens and the ventral pallidum control taste reactions to tasty foods. Turning on mu opioid receptors in the ventral striatum and amygdala causes hyperphagia (overeating). It’s the hyperpalatable foods that produce an addiction‐like syndrome. Animals given either high‐sugar or high‐fat diets eat too much. But they do not gain weight, because they make up for it by eating less chow. Only the high fat and sugar combination causes weight gain. We believe the obese patient’s relationship to food is more like a behavioral addiction, such as pathological gambling, than a classic substance addiction. But there is no clear-cut withdrawal mechanism.  According to the National Institutes of Health, there is a “harmful use that is maladaptive but does not meet the criteria for dependence.” External cues, anticipation clues, pancreatic training, and loss of fat-burning adaptation drive the refeeding cycle. Specific nutrients do cause endorphin activation and a chemical effect in the brain. Big Food’s push to grow more food results in fewer micronutrients. Megafarms use monocropping (one crop on the same land, year after year). That strips the soil of helpful microelements to maximize production. By 1967, American corn farms were growing nearly three times as much corn as they had thirty years earlier. The surplus from monocropping went to livestock to boost production. The average dairy cow now produces more than 70 pounds of milk per day. The top Holsteins produce two hundred pounds per day. That is a 1,200 percent increase over the 1948 average. In the same way, a typical potato farmer grew about 63 sacks of potatoes for every acre in the 1930s. By the mid-1960s, it was up to two hundred sacks. But fewer micronutrients make food bland. Maximizing food quantity cost nutrient density, and food began to get blander. The fix for bland, high-output food was processing after harvest. Makers added engineered flavoring to fake taste. The field of flavor engineering combines organic chemistry with engineering, neuroscience, psychography, psychophysics, ethnography, demography, molecular biology, finance, botany, economics, and physiology. The goal is flavors that specifically increase cravings. Eating is a behavior driven by an expectation of pleasure. We crave flavors. Food makers design hyperpalatable (tasty), highly processed foods to turn on the reward system and make you eat more.  The constant stream of signals promotes grazing. Sadly, fake flavors distort the brain’s read of nutrient value. The patient ends up eating too many manufactured carbs and manufactured fats. That mix is highly obesogenic (it drives obesity). Food palatability (engineering and variety) stirs up appetite. It cuts satiety. It promotes taking in too much energy. More variety and palatability also cause weight gain in animal models. Food combinations high in sugar, fat, and flavor are hyperpalatable. Highly palatable meals were 44% larger than the average meal. That can turn on the brain’s pleasure-seeking pathways. Over time, a highly palatable diet may lead to a weaker reward response in the brain. Processed food contains mostly polyunsaturated fatty acids (PUFA) Omega-6 vegetable oils. The human palate has a hard time tasting rancidity in vegetable oils. So the shelf life of processed foods can be stretched. The standard American diet has a greater than 20:1 ratio of unhealthy Omega-6 to healthy Omega-3. This skewed ratio is associated with many brain and mood problems, including profound anxiety. Restoring a healthy ratio of 4:1 (even by supplementing Omega 3) seems to reduce this profound anxiety.   Buydens-Branchey, L., & Branchey, M. (2007). Long-chain n-3 polyunsaturated fatty acids decrease feelings of anger in substance abusers. Psychiatry Research, 157(1-3), 95–104. doi:10.1016/j.psychres.2007.01.004 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2225526/ Sucrose (table sugar) is a disaccharide (a double sugar) made of 50% fructose and 50% glucose. It is broken down mainly in the small intestine, which releases equal parts glucose and fructose. Glucose causes insulin release. Insulin-dependent channels clear it from the blood fast. But fructose does not depend on insulin. The liver takes it up fast in a first-pass effect, and it is preferentially stored as fat. Glucose and fructose have different effects on the addiction centers in the brain. Fructose produced activation in the brain’s ‘reward circuit,’ and increased the desire for food. Glucose, meanwhile, does not directly activate the reward center. American College of Neuropsychopharmacology. “Fructose and glucose: Brain reward circuits respond differently to two kinds of sugar.” ScienceDaily. ScienceDaily, 10 December 2014. www.sciencedaily.com/releases/2014/12/141210080734.htm By contrast, high-fructose corn syrup has a ratio of 55:45 fructose to glucose. High-fructose corn syrup was invented in the early 1970s. It began to replace regular sugar in prepared foods around 1975. The start of the obesity epidemic lines up with the use of HFCS. Today’s sweetened drinks made with HFCS have a fructose-to-glucose ratio of about 60:40. That is 50% more fructose than glucose. According to Science Daily, “Several major brands appear to be produced with HFCS that is 65% fructose. Finally, the sugar profile analyses detected forms of sugar that were inconsistent with what was listed on the food labels.” https://www.ncbi.nlm.nih.gov/pubmed/20948525 University of Southern California – Health Sciences. “Soda consumers may be drinking more fructose than labels reveal.” ScienceDaily. ScienceDaily, 4 June 2014. The deliberate, unlabeled rise in fructose seems strange. Sugar content varied widely from the amounts on labels. On average, the drinks had 18% more fructose than expected. HFCS is supposed to be 55% fructose, compared to the 50% in table sugar. Most foods and drinks are supposed to use HFCS that is 42% fructose. Beverages that contain 65% fructose were Coke, Pepsi, and Sprite. Beverages that contain 60% fructose were Dr. Pepper, Gatorade, and Arizona Iced Tea. http://goranlab.com/pdf/Ventura%20Obesity%202010-sugary%20beverages.pdf Americans drink about 50 gallons of soda every year (with 34 pounds of sugar). But soda drinkers are taking in far more fructose than anyone knew.  Fructose specifically turns on the reward center. Could it be that the soda companies know fructose turns on the reward system, which creates more urge to buy? The side effect is too much fat building up in the liver. That feeds our epidemic of NAFLD, Metabolic Syndrome, Prediabetes, Type 2 Diabetes. Could the priming of the opioid epidemic also be associated? Treatment from an addiction approach:

• Shutting off the cues that come first
• Temporal substitution
• Satiety

Effects on the neuroendocrine systems:

• Calming neuroinflammation by adding omega-3
• Easing insulin resistance by emptying the liver
• Time-limited feeding

Frequently asked questions

Is food addiction the same as drug addiction?

Close, but not identical. Hyperpalatable food drives dopamine release in the nucleus accumbens. That is the same reward center that drugs of abuse hit. Rodents fed high-sugar, high-fat diets binge, seek food compulsively and show withdrawal. We see an obese patient’s relationship with food as closer to a behavioral addiction, like pathological gambling, than to a classic substance addiction.

What is the most common food addiction?

Food engineered to combine sugar, fat and salt with flavor enhancers. Sugar alone or fat alone makes animals overeat without gaining weight. The combination of high fat and high sugar causes weight gain. Fructose adds a second hook. It turns on the brain’s reward circuit and raises the desire for food, while glucose does not. Sodas made with high-fructose corn syrup deliver it in bulk.

What causes food addiction?

Engineered food. Megafarms raised yields at the cost of micronutrients, and the food turned bland. Makers fixed the blandness with engineered flavoring built to increase cravings. Hyperpalatable, highly processed foods are designed to turn on the reward system and make you eat more. Synthetic flavors also distort the brain’s read of nutrient value. The result is overeating manufactured carbohydrate and fat.

How do I stop my urge to eat?

Treat it as an addiction, not a willpower problem. Eat less, move more fails against a dopamine reward system. Treatment shuts off the cues that trigger eating. For a time, it swaps in other behaviors. It provides real satiety. On the body side, it adds omega-3 to reduce neuroinflammation (inflammation in the brain and nerves). It empties the liver to improve insulin resistance. And it uses time-limited feeding.

References:

Pro v Con Reviews: Is Food Addictive?  Is food addiction a valid and useful concept? H. Ziauddeen, P. C. Fletcher. 12 October 2012 https://onlinelibrary.wiley.com/doi/full/10.1111/j.1467-789X.2012.01046.x http://goranlab.com/pdf/Ventura%20Obesity%202010-sugary%20beverages.pdf

Related reading

• The Secret to a Healthy Weight: Insulin, Not Calories
• Energy Balance Theory 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 June 17, 2026

  Why Treat Obesity and Prediabetes | Reverse Diabetes MD from Gurpreet Padda on Vimeo. It’s important to treat obesity and prediabetes before diabetes can develop. That is because obesity is the leading indicator in developing diabetes. Data from the National Health and Nutrition Examination Survey shows that under 12.2 percent of American adults were metabolically healthy in 2009–2016. Under 7 percent are, on the tighter criteria applied after 2021.  Eighty-six million adults in the U.S. have prediabetes (HbA1c ranging from 5.7–6.4%). Up to 70 percent of these people will eventually develop diabetes. Obesity is the main factor in the progression of prediabetes to diabetes. Almost all patients who come to our clinics have significant issues associated with pain. Pain is one of the hallmarks of metabolic inflammation.  The vast majority of patients who come to our clinics are also overweight. When we check their biochemical markers, they have prediabetes and metabolic inflammation. Prediabetes is known to be a condition that comes before type 2 diabetes (T2D). Changes in immune cell levels and function can cause more of these inflammatory cells to move into tissue that is already inflamed. There is also upregulation of cytokines (immune signal proteins get turned up). This immune activation begins during the pre-diabetic state. The HbA1c has a significant tendency to miss cases of diabetes. Compared to the oral glucose-tolerance test (OGTT), HbA1c will under-diagnose diabetes in 73 percent of adults. HbA1c has a sensitivity of 26.93 percent and specificity of 99.39 percent. The 2019 American Diabetes Association Standards of Medical Care in Diabetes recommends at least yearly screening for those with high risk of prediabetes. It states that patients with “A1C 5.7−6.4% (39−47 mmol/mol)…are ideal candidates for diabetes prevention efforts”. It also states that “lifestyle/behavioral therapy featuring an individualized reduced calorie meal plan is highly effective in preventing type 2 diabetes and improving other cardiometabolic markers (such as blood pressure, lipids, and inflammation).”

• Weight loss using coaching, dietary change, self-efficacy (belief in your own ability to change), and more physical activity can help as well. The recommendation is to “achieve and maintain 7% loss of initial body weight and increase moderate-intensity physical activity (such as brisk walking) to at least 150 min/week.” Also, “Metformin therapy for prevention of type 2 diabetes should be considered in those with prediabetes, especially for those with BMI ≥35 kg/m2, those aged <60 years, and women with prior gestational diabetes mellitus.”

They also state that “Prediabetes is associated with heightened cardiovascular risk; therefore, screening for and treatment of modifiable risk factors for cardiovascular disease is suggested.” Prevention or Delay of Type 2 Diabetes: Standards of Medical Care in Diabetes—2019; American Diabetes Association. Diabetes Care 2019 Jan; 42(Supplement 1): S29-S33. https://doi.org/10.2337/dc19-S003 Type 2 diabetes is marked by both peripheral insulin resistance (the body’s tissues stop responding well to insulin) and too little insulin production. Insulin resistance has been associated with high levels of free fatty acids and proinflammatory cytokines in plasma. It also leads to less glucose transport into muscle cells. For Type 2 Diabetes to occur, insulin resistance and too little insulin secretion must both be present. For example, overweight people may have insulin resistance. But diabetes only develops in those who cannot raise insulin secretion enough to make up for their insulin resistance. Unfortunately, this period of prediabetes allows significant tissue damage. Increased cardiovascular risk begins before persistent hyperglycemia (blood sugar that stays high) develops. This is due to insulin resistance (Stern, 1996; Haffner and D’Agostino, 1999). Macrovascular damage (to large blood vessels) has already occurred with the onset of insulin resistance. Microvascular damage (to small blood vessels) increases once hyperglycemia starts. The United Kingdom Prospective Diabetes Study (UKPDS) analyzed more than 4,000 type 2 diabetes patients. They were aggressively treated and followed for up to 15 years. Those in the intensely treated group had a significantly lower rate of progression of microvascular complications than patients getting standard care. Rates of macrovascular disease were only reduced in the metformin-monotherapy arm (metformin alone). In that arm, the risk of myocardial infarction (heart attack) was significantly decreased. In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, there was a 66 percent increase in mortality per 1 percent increase in HbA1c. The best outcome was for patients keeping HbA1c below 6.0.   Early intervention in the atherogenic (plaque-building) prediabetic state, while HbA1c is still in the prediabetic range (5.7-6.4%), matters. It reduces the 200 to 400 percent increased risk of cardiovascular events and plaque formation.  This intervention is cost-effective, low-risk, and disease-modifying if it uses both lifestyle change and metformin. Delaying early intervention (when HbA1c > 6.5) increases the glycocalyx and endothelial damage (damage to the inner lining of blood vessels). It also increases irreversible diabetes-specific microvascular complications. We readily admit that overly strict blood glucose control may have a negative outcome if multiple hypoglycemic agents are used in addition to metformin. However, metformin is tolerated very well if the dose is raised slowly. Our early intervention focuses on lifestyle change and metformin monotherapy (metformin alone). We use these lifestyle changes:

• reducing gastrointestinal permeability (how leaky the gut is) from gluten and gliadin, which lowers the inflammatory load
• reducing carbohydrate loading, specifically fructose, to reduce insulin resistance and fat build-up in the liver
• restoring an appropriate omega-6:3 ratio by removing industrial seed oils and supplementing with omega-3 fish oil
• improving insulin sensitivity by reducing insulin release, using time-restricted feeding, and reducing the overall glycemic load

Metformin

• Metformin has long been considered a first-line drug in the treatment of type 2 diabetes. It has a very low side effect profile, except for people with renal compromise (reduced kidney function). Even with how widely metformin is used, its mechanism of action remains unclear. The following are possibilities when considering how metformin works:
• antibiotic, changing the gut microbiome ratio to a lower proinflammatory load
• effect on the mTOR pathway, which may independently reduce neuropathic pain and is associated with cancer suppression as well as life-lengthening
• change in vagal tone, reducing sympathetic tone and cortisol secretion
• enhances insulin sensitivity at the receptor and lower blood level of insulin
• reduces the formation of advanced glycation end-products
• inhibits the liver’s ability to release glucose into the bloodstream
• inhibits the mitochondrial respiratory chain in the liver, which leads to activation of AMPK. This enhances insulin sensitivity (via effects on fat metabolism) and lowers AMP. That reduces the expression of gluconeogenic enzymes (enzymes that make new glucose)
• inhibition of fructose-1,6-bisphosphatase by AMP in the liver

The longer we can delay progression to Type 2 Diabetes, even if using oral hypoglycemics, the more cost-effective it is. Below is a cost analysis. It compares early intervention with metformin to delaying treatment until insulin is needed due to beta-cell fatigue (tired insulin-making cells). It assumes similar lifestyle management:

• The average wholesale cost of generic Metformin is less than $0.05/tablet 1,000 mg. That makes a 30-day supply $6.00 per month. https://www.goodrx.com/metformin?dosage=1000mg&form=tablet&label_override=metformin&quantity=60
• For an average wholesale insulin cost, a combination of both long-acting and short-acting insulin is prescribed.

Long-acting insulin, Lantus, costs $431/month. The short-acting insulin, Humalog, costs $533/month. The combined cost is $964/month, not counting injection supplies. https://www.goodrx.com/insulins Someone could pay for 160 months of metformin therapy for the same cost as 1 month of insulin therapy. Metformin keeps reducing the likelihood of developing type 2 diabetes among those at high risk for it over 15 years. This is particularly true among those with higher baseline glycemia (starting blood sugar levels).  Metformin prevents diabetes. That is important because diabetes leads to vision loss, renal failure (kidney failure), amputations, and heart disease. Preventing or delaying or reducing the risk for diabetes is important in and of itself. Metformin is cheap and well-tolerated, with a powerful effect. Diabetes prevention seen at 15 Years, regardless of analytic method. Long-term Effects of Metformin on Diabetes Prevention: Identification of Subgroups That Benefited Most in the Diabetes Prevention Program and Diabetes Prevention Program Outcomes Study. Diabetes Prevention Program Research Group. Diabetes Care Apr 2019, 42 (4) 601-608; DOI: 10.2337/dc18-1970 Using early intervention to return glucose regulation to normal, with reversal of insulin resistance, prevents progression of prediabetes to diabetes.  Normal glucose regulation is an indicator of disease modification. It comes with measurably lower all-cause mortality (death from any cause). Our goal is to reduce metabolic inflammation and avoid the preventable complications of insulin resistance.

Frequently asked questions

What is the A1C level for prediabetes?

Prediabetes is an HbA1c of 5.7% to 6.4%. The American Diabetes Association calls people in that range ideal candidates for diabetes prevention. The A1C test has a blind spot, though: compared with the oral glucose-tolerance test, it under-diagnoses diabetes in 73 percent of adults. A normal-looking A1C does not rule out a problem.

What should I do if I am diagnosed with prediabetes?

Treat it now, before it becomes diabetes. Up to 70 percent of people with prediabetes eventually develop diabetes, and blood vessel damage starts with insulin resistance, before blood sugar stays high. Our early intervention pairs lifestyle change with metformin alone: less carbohydrate, especially fructose, less gluten, no industrial seed oils, omega-3 fish oil and time-restricted feeding.

What foods should a prediabetic avoid?

Cut the carbohydrate load, especially fructose, which drives insulin resistance and fat build-up in the liver. Remove gluten and gliadin to lower gut permeability and the inflammatory load. Remove industrial seed oils to restore a healthy omega-6 to omega-3 ratio, and add omega-3 fish oil. Time-restricted feeding then lowers insulin release and the overall glycemic load.

Is metformin used to treat prediabetes?

Yes. The American Diabetes Association says metformin should be considered in prediabetes, especially with a BMI of 35 or higher, age under 60, or prior gestational diabetes. Metformin is cheap and well tolerated when the dose is raised slowly. Generic metformin runs about $6 a month, so 160 months of it costs the same as one month of insulin.

References for additional reading: Prevalence of optimal metabolic health is remarkably low among U.S. adults, with one in eight Americans achieving optimal levels of the five traditional cardiometabolic risk factors without medication. Joana Araújo, Jianwen Cai, and June Stevens. Metabolic Syndrome and Related Disorders. Feb 2019. http://doi.org/10.1089/met.2018.0105 ENDO 2019: The Endocrine Society Annual Meeting. https://www.endocrine.org/news-room/2019/endo-2019—a1c-test-misses-many-cases-of-diabetes Prescrire Int. 2014 Nov;23(154):269-72.  https://www.ncbi.nlm.nih.gov/pubmed/25954799 N Engl J Med 2008; 358:2545-2559 https://www.nejm.org/doi/full/10.1056/nejmoa0802743 “Patients allocated metformin, compared with the conventional group, had risk reductions of 32% (95% CI 13-47, p=0.002) for any diabetes-related endpoint, 42% for diabetes-related death (9-63, p=0.017), and 36% for all-cause mortality (9-55, p=0.011).” Lancet. 1998 Sep 12;352(9131):854-65.  https://www.ncbi.nlm.nih.gov/pubmed/9742977 “The increased risk of adverse cardiovascular outcomes associated with type 2 diabetes does not begin at the diagnostic cutoff for plasma glucose (or HbA1c) at which the condition is diagnosed. Rather, there appears to be a continuum of increased microvascular and macrovascular risk that extends to levels of glycaemia well below these cutoffs. While it seems reasonable to hypothesize that correction of prediabetic dysglycemia might also reduce the future risk of adverse cardiovascular outcomes, further evidence from clinical trials is needed to demonstrate improved long-term outcomes in this setting.” Hopper I, Billah B, Skiba M, Krum H. Prevention of diabetes and reduction in major cardiovascular events in studies of subjects with prediabetes: meta-analysis of randomized controlled clinical trials. Eur J Cardiovasc Prev Rehabil. 2011;18:813–823. [PubMed] Metformin to be considered in IGT, IFG, HbA1c of 5.7–6.4 %, especially in BMI >35 kg/m², age <60 years or prior GDM American Diabetes Association Standards of medical care in diabetes—2014. Diabetes Care. 2015;38(Suppl 1):S31–S33. “As most individuals with prediabetes will eventually go on to develop type 2 diabetes, the large number of people with prediabetes worldwide implies a reservoir of new type 2 diabetes cases to come. Optimizing the management of prediabetes, with the aim of delaying diabetes onset for as long as possible, is therefore an urgent global clinical priority.” “In the Diabetes Prevention Study (DPS), for example, no patient who achieved at least four of the five lifestyle goals (weight reduction, total fat intake, saturated fat intake, fiber intake, exercise) went on to develop diabetes during the period of follow-up.” Diabetes Prevention Program Research Group. The 10-year cost-effectiveness of lifestyle intervention or metformin for diabetes prevention: an intent-to-treat analysis of the DPP/DPPOS. Diabetes Care 2012;35:723–730 “The Diabetes Prevention Program (DPP), a randomized controlled clinical trial, demonstrated that compared with the placebo intervention (placebo), the intensive lifestyle intervention (lifestyle) reduced the incidence of type 2 diabetes by 58%, and the metformin intervention (metformin) reduced the incidence of type 2 diabetes by 31% over 2.8 years” Diabetes Prevention Program Research Group. Long-term safety, tolerability, and weight loss associated with metformin in the Diabetes Prevention Program Outcomes Study. Diabetes Care 2012;35:731–737 Balk EM, Earley A, Raman G, Avendano EA, Pittas AG, Remington PL. Combined diet and physical activity promotion programs to prevent type 2 diabetes among persons at increased risk: a systematic review for the Community Preventive Services Task Force. Ann Intern Med 2015;163:437–451 Knowler WC, Barrett-Connor E, Fowler SE, et al.; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393–403

Related reading

• Treat Addiction, Pain and Diabetes
• Reverse Diabetes MD presentation for providers

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 17, 2026

GGT (gamma-glutamyl transferase) is a liver enzyme that climbs with oxidative stress (cell damage from unstable oxygen). That stress comes from excess carbohydrates, processed food, vegetable oil or alcohol. It burns through glutathione, your master antioxidant. Once GGT rises above the lowest 25% to 35% of the normal range, the risk of type 2 diabetes, stroke, cancer and death rises with it.

About GGT (Oracle of Death or The final common Pathway) | Reverse Diabetes MD from Gurpreet Padda on Vimeo. Excess processed foods and carbohydrates can also lead to more liver damage. People don’t think about GGT when they think about health risks. But it could be called the “oracle of death” or “the final common pathway” because of how it predicts liver damage and the disease that follows. Gamma-glutamyl transferase (GGT) is an enzyme found in high amounts in the liver. It is elevated in diseases that damage the liver. GGT is a transferase. That is an enzyme that moves a part of one molecule to another. It moves gamma-glutamyl groups from molecules such as glutathione (GSH) to an acceptor. That acceptor may be any amino acid, a peptide, or water. GSH removes free radical toxins. It gives natural protection against harmful oxidative stress. The normal job of GGT is to rebuild glutathione, the body’s master antioxidant. GGT is the only enzyme of the GSH cycle that sits on the outer surface of the plasma membrane (the cell’s outer skin). It breaks down GSH outside the cell. That provides cysteine, the rate-limiting building block, so the cell can make new GSH inside. When GGT levels are above “low-normal” ranges, excess GGT can catabolize (degrade) GSH. That causes critical depletion of this antioxidant. When GSH runs low, oxidative stress and damage start to occur. This leads to a cycle of irreversible cell, tissue, and DNA damage. Organ function becomes severely impaired. Elevated GGT indicates that you are demanding more GSH. It shows there was not enough GSH in the system to handle an oxidative insult. During oxidative stress, GGT gene expression goes up. This is an adaptation to stress. Say you eat excess carbohydrates, processed foods, vegetable oil, alcohol, or other liver toxins. Then the liver can become insulin resistant. That results in a high insulin level. High insulin is a metabolic switch. It causes fat to build up in the liver. Hyperinsulinemia (excess insulin) drives insulin resistance, and insulin resistance encourages more hyperinsulinemia. As fat builds up in the liver, the liver gets more insulin resistant. At the same time it goes through more oxidative stress. That drains glutathione. Rising GGT shows the drain.   GGT data was first collected by the smartest guys in the room (life insurance actuaries). They first measured it because it could mark alcohol abuse in life insurance applicants. The life insurance industry collected this data for many years. The result was biometric stratification of mortality risk. That means sorting people into risk-of-death groups by body measures. It is now central to how life insurers predict all causes of death. Palmier J., Dixon A., Lanzrath B. Leading Contributors to Mortality Risk in Life Insurance Applicants. Schaumburg, Ill, USA: Society of Actuaries; 2012. (Smalltalk Issue 38). Palmier J., Lanzrath B. J. Laboratory and biometric predictors of cancer-related mortality in an insured population. Journal of Insurance Medicine. 2012;43(3):162–168   In the past, elevated GGT has been associated with liver problems, most often from drinking too much alcohol. Other drugs that can raise GGT include barbiturates, phenytoin, anti-inflammatory drugs (including aspirin), St. John’s Wort, and kava. We now believe that elevated GGT is an early warning sign of other health risks. These include atherosclerosis, stroke, type 2 diabetes, kidney disease, cancer, metabolic syndrome (MetS), and all-cause mortality (death from any cause). GGT doesn’t have to be above a lab’s normal levels for risk to go up. When GGT levels pass the lowest 25% to 35% of normal population ranges, disease risks grow in step with GGT. This “dose-response” rise in GGT indicates a greater risk of future disease and death. That holds even when GGT levels are within “normal” ranges. Even high-normal GGT carries a significant rise in risk: Normal low

• < 9 U/l for women
• < 14 U/l for men

Moderately high with increased risk

• 18 U/L for women
• 28 U/L for men

High levels of normal with significant increase in risk

• >36 U/L for women
• >56 U/L for men

According to the National Institutes of Health, “GGT levels measured in the Framingham Offspring Study (FOS), only moderately elevated GGT, starting at levels just above population GGT medians, and often measured one or two decades in advance of disease endpoints or mortalities, established GGT as an early predictive marker of MetS, CVD, heart failure, and all-cause mortality.”   Gamma-Glutamyltransferase: A Predictive Biomarker of Cellular Antioxidant Inadequacy and Disease Risk Gerald Koenig, Stephanie Seneff. Dis Markers. 2015; 2015: 818570. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4620378/ GGT predicts future death. In the general population, about 21% of men and 15.6% of women have elevated GGT. Elevated GGT, even within normal lab ranges, carries significant added risks. Patients with high-normal GGT have more than a 1.5-fold risk of dying from cardiovascular diseases. That is compared to people with low-normal GGT. Look at all-cause mortality. Elevated GGT in the upper fifth of the population gives a 2x higher risk for all-cause mortality (death from any cause). It gives a 1.7x higher risk of cardiovascular death, and a 2.3x higher risk for cancer and death. Now look at liver cancer. Elevated GGT in the upper fifth of the population (not even the top 1%) gives a 15 to 18 times higher risk of hepatic cancer and death from liver cancer. Hazard ratios According to Clinical Chemistry, “GGT above the reference category (GGT ≥9 U/L in women, ≥14 U/L in men) was significantly (P <0.001) associated with all-cause, cancer, hepatobiliary, and vascular mortalities.” Gamma Glutamyltransferase and Long-Term Survival: Is It Just the Liver? Lili Kazemi-Shirazi et al. DOI: 10.1373/clinchem.2006.081620 Published April 2007. http://clinchem.aaccjnls.org/content/53/5/940 High levels also raise the risk of atherogenic dyslipidemia (a blood fat pattern that builds plaque). It predicts coming heart disease. Dyslipidemia reflects insulin resistance. When your liver becomes insulin resistant, it will tend to cause visceral fat (the fat packed around your organs) to build up in your organs.  Visceral fat buildup is most clearly seen as a larger waist than expected, or a “beer belly,” even a small one in women. Many people look slim, but they are TOFI (thin outside, fat inside). Dyslipidemia is a mix of high LDL, low HDL, high triglyceride, high particle count of LDL

• LDL:HDL Triglyceride:HDL LDL-P Oxidized LDL GGT

  Most idiopathic or essential hypertension (high blood pressure with no known cause) is related to hyperinsulinemia. The extra insulin makes blood vessels stiff and thick. Reversing hypertension may be as simple as reducing insulin. GGT correlates with plaque forming in arteries (atherosclerotic plaque). That plaque is associated with an inflammatory disease, metainflammation. GGT activity also shows up in the same spot as oxidized LDL in the plaque, as seen below. Circulating Markers of Liver Function and Cardiovascular Disease Risk. Arterioscler Thromb Vasc Biol. 2015 Nov;35(11):2290-6. doi: 10.1161/ATVBAHA.115.305235. Epub 2015 May 14. https://www.ncbi.nlm.nih.gov/pubmed/25977566 Risk for future diabetes: If your BMI is low and your GGT is low, you have a baseline risk of 1.0. Say you have a low BMI below 25 and a high GGT (in the top quarter of the population). Then you have a 3x risk of diabetes within 3-5 years. Say you have a moderate-high BMI greater than 30 and a high GGT (in the top quarter of the population). Then you have a 15x risk of diabetes within 3-5 years. Say you have a high BMI greater than 35 and a high GGT (in the top quarter of the population). Then you have a 19x risk of diabetes within 3-5 years. Obesity is one factor that predicts future diabetes, but GGT may be more accurate. Once you adjust obesity for GGT, obesity doesn’t predict diabetes. GGT predicts diabetes better. That is because it shows liver insulin resistance and liver inflammation.

Our treatment protocols for elevated GGT encourage:

• Squeeze the fat out of the liver with either time-restricted feeding or fasting
• Cut out vegetable oil and take fish or krill omega-3 oil
• Switch to natural fats, such as butter and tallow
• Cut out processed foods, including refined grains and acellular carbohydrates
• Metformin to boost insulin sensitivity in the liver
• Drinking moderate to high amounts of coffee has been universally shown to reduce GGT

Related reading

• 3 Reasons Trans Fats Are Bad for You
• Insulin Resistance 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 June 17, 2026

Reverse Diabetes MD Presentation | Reverse Diabetes MD from Gurpreet Padda on Vimeo.

It’s time to look harder at the root causes of obesity, prediabetes and type 2 diabetes, because of what they mean for future public health. Reversing the obesity, prediabetes and type 2 diabetes epidemic is today’s most important public health challenge. Nearly 70% of the population is insulin resistant, prediabetic or frankly diabetic.

Kraft, J.R.:” Glucose Insulin Tolerance. A routine Clinical Laboratory Tool Enhancing Diabetes Detection”. In O.B. Hunter. Jr. (ed): Radio assay: Clinical Concepts. Skokie, IL. Professional Education Dept. G.D. Searle & Co., 1974. Pp 91-106

Data from the National Health and Nutrition Examination Survey 2009-2016 found that less than 12.2% of the US population was metabolically healthy. On the tighter criteria applied after 2021, that share fell below 7%.

“Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009-2016,” was published online Nov. 28 in the journal Metabolic Syndrome and Related Disorders.

Almost all the patients who come to our clinics are overweight. When we check their blood markers, they have prediabetes and metabolic inflammation. Pre-diabetes is known to come before type 2 diabetes (T2D). Changes in the number and function of immune cells can cause more of these inflammatory cells to move into tissue that is already inflamed. Cytokines (immune signaling proteins) are also turned up. This immune activation begins in the pre-diabetic state.

Studies published in a European journal on preventing heart disease put it this way: “The increased risk of adverse cardiovascular outcomes associated with type 2 diabetes does not begin at the diagnostic cutoff for plasma glucose (or HbA1c) at which the condition is diagnosed. Rather, there appears to be a continuum of increased microvascular and macrovascular risk that extends to levels of glycemia well below these cutoffs.”

Hopper I, Billah B, Skiba M, Krum H. Prevention of diabetes and reduction in major cardiovascular events in studies of subjects with prediabetes: meta-analysis of randomized controlled clinical trials. Eur J Cardiovasc Prev Rehabil. 2011;18:813–823. [PubMed]

A 2015 global survey by Credit Suisse found a substantial level of misinformation among doctors and nutritionists:

• 92% believed that fat consumption could lead to cardiovascular issues
• 87% believed that fat consumption could lead to obesity
• 54% of doctors and 40% of nutritionists thought that eating cholesterol-rich foods raised blood cholesterol
• 83% of doctors believed butter was worse than margarine
• 66% of doctors believed vegetable oils are beneficial to health.

Fat; The New Health Paradigm – Credit Suisse 2015

Prescription drugs are now the third most common cause of death worldwide, after heart disease and cancer. That should alarm us. The Academy of Medical Royal Colleges and the BMJ offer a blueprint to reduce the harms of “too much medicine” as part of the Choosing Wisely campaign. They recommend teaching the public to ask their medical professionals whether there are “simpler or safer options” to taking a medication.

Malhotra A, Maughan D, Ansell J, Lehman R, Henderson A, Gray M et al. Choosing Wisely in the UK: The Academy of Medical Royal Colleges’ initiative to reduce the harms of too much medicine BMJ 2015; 350 :h2308.

The root causes of obesity, prediabetes and type 2 diabetes are built into the food environment. Legislative efforts that push people to eat fewer processed foods and drink fewer sugary drinks will help significantly reduce the burden of diet-related disease. Diet-related disease now contributes to more disease and death worldwide than physical inactivity, smoking and alcohol combined.

Newton JN, Briggs AD, Murray CJ, Dicker D, Foreman KJ, Wang H, et al. Changes in health in England, with analysis by English regions and areas of deprivation, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015. doi:10.1016/S0140-6736(15)00195-6.

Processed foods labeled as “low-fat” or “proven to lower cholesterol” should be avoided. The flawed science behind the 1977 Dietary Guidelines pushed people to eat less fat. That opened the door to eating more carbohydrates. This shift away from natural food with animal products and fats led people to eat more processed food rich in carbohydrates, processed grains and industrial seed oils. In the United States between 1961-2011, 90% of the added calorie intake came from carbohydrates and polyunsaturated vegetable oils.

Select Committee on Nutrition and Human Needs. Dietary goals for the United States. First ed. Washington: U.S. Govt. Print. Off., February 1977.

CreditSuisse.Fat: The New Health Paradigm: Research Institute, 2015: 76

 

Obesity rose after these guidelines. That suggests they may be a root cause of the problem. Nutrition science was first built on human correlational studies, which are often flawed. That science has also been corrupted by commercial influence. The food industry’s undue influence on official guideline bodies and politicians has posed a significant threat to public health. “Nutritional epidemiology is a scandal. It should just go to the waste bin,” claims professor John Ioannidis, professor of medicine, health research and policy, and statistics at Stanford University School of Medicine and School of Humanities and Sciences.

Max Planck also said, “Science progresses one funeral at a time.” Nearly 50 years passed between the first published evidence linking smoking and lung cancer and effective rules to curb tobacco use. Big tobacco companies used a strategy of denial. They planted doubt, muddied the facts and even bought the loyalty of scientists. The recent likeness to big food and big pharma is uncanny.

Brownell KD, Warner KE. The perils of ignoring history: big tobacco played dirty and millions died. How similar is big food? Milbank Q 2009;87: 259–94.

The food industry has a fiduciary duty to make profit for its shareholders. Sadly, the food industry’s downstream cost to public health is bankrupting most Western societies. Sadly, academics, institutions and journals whose first duty is to patients and scientific integrity have at times colluded with industry for money. It is not credible to suggest that eating 22 teaspoons of sugar daily falls within recommended guidelines. This is despite the known science: for optimum health, the human diet has no dietary or biological need for sugar.

Malhotra, A. (2013) The dietary advice on added sugar needs emergency surgery. BMJ, 346, f3199.

 

Evidence from multiple randomized controlled trials shows that a higher-fat, lower-carbohydrate diet beats a low-fat diet for weight loss and for lowering cardiovascular disease risk. The Harvard School of Public Health ran a meta-analysis of 53 randomized controlled trials with 68,128 participants. It concluded that “when compared with dietary interventions of similar intensity, evidence from randomized controlled trials does not support low-fat diets over other dietary interventions for long-term weight loss. In weight loss trials, higher-fat weight loss interventions led to significantly greater weight loss than low-fat interventions.”

Sackner-Bernstein J, Kanter D, Kaul S. Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A Meta-Analysis. PLoS One 2015;10(10):e0139817 DOI: 10.1371/journal.pone.0139817.

Bazzano LA, Hu T, Reynolds K, et al. Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial Effects of Low-Carbohydrate and Low-Fat Diets. Ann. Intern. Med. 2014;161(5):309-18 DOI: 10.7326/M14-0180.

Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomized controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2(1) DOI: 10.1136/openhrt-2014-000196.

 

The Women’s Health Initiative is one of the largest randomized controlled diet trials ever done. It used 48,835 post-menopausal women, with a mean follow-up of 8.1 years. They were randomized to either a standard western diet or a low-fat, calorie-reduced diet with more exercise. The authors had expected the low-fat, calorie-reduced diet with more exercise to reduce cardiovascular disease. The intervention lowered total fat intake by 8.2% of energy and saturated fat intake by 2.9% of energy. But it did not reduce the risk of CHD (coronary heart disease) or stroke. Lowering dietary fat and total daily calories (361 calories/day reduction) failed to produce any significant weight loss over the study. So the study rejected the idea that the low-fat diet helps either cardiovascular disease or weight loss.

Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006;295(6):655-66 doi: 10.1001/jama.295.6.655.

By contrast, eating fat makes you feel full. Compared with protein and carbohydrates, fat has the least impact on blood glucose and insulin output. Making too much insulin, and the insulin resistance that follows, is the forerunner of type 2 diabetes. A meta-analysis of the evidence available before the 1977 US change in dietary guidelines did not support limiting dietary fat. There was no scientific consensus. Even so, these guidelines advised limiting total fat to 30% of calorie intake and saturated fat to 10% of calorie intake. That created the low-fat craze and a national experiment in diet-induced metabolic dysfunction.

Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomized controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2(1) doi: 10.1136/openhrt-2014-000196.

 

Thirty years later, in 2014, a meta-analysis of 76 studies covered over 600,000 participants from 18 countries. It concluded that “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann. Intern. Med. 2014;160(6):398-406 doi: 10.7326/M13-1788.

 

A study published in the BMJ (British Medical Journal) found that “Saturated fat intake was not associated with all- cause mortality, CVD mortality, total CHD, ischemic stroke, or type 2 diabetes.”

de Souza RJ, Mente A, Maroleanu A, et al. Intake of saturated and trans unsaturated fatty acids and risk of all-cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ 2015;351 doi: 10.1136/bmj.h3978.

 

Also, The American Journal of Clinical Nutrition found that “diets with cheese and meat as primary sources of saturated fatty acids cause higher HDL cholesterol and apo A-1 and, therefore, appear to be less atherogenic than is a low-fat, high- carbohydrate diet.”

Thorning TK, Raziani F, Bendsen NT, Astrup A, Tholstrup T, Raben A. Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial. The American journal of clinical nutrition 2015 doi: 10.3945/ajcn.115.109116.

 

Full-fat dairy may protect against obesity.  A 2014 study concluded: “Participants in the highest tertile of whole-fat dairy intakes (milk, cheese, yogurt) had significantly lower odds for being obese. “

Crichton GE, Alkerwi Aa. Whole-fat dairy food intake is inversely associated with obesity prevalence: findings from the Observation of Cardiovascular Risk Factors in Luxembourg study. Nutrition Research 2014;34(11):936-43 doi: 10.1016/j.nutres.2014.07.014.

 

Cohort studies confirm that plasma saturated fatty acids from dairy sources such as cheese and yogurt are inversely related to the incidence of type 2 diabetes. By contrast, the plasma saturated fat palmitic acid, linked to the consumption of starch, sugar and alcohol, is strongly associated with the development of type 2 diabetes.

Mozaffarian D. Saturated fatty acids and type 2 diabetes: more evidence to re-invent dietary guidelines. Lancet Diabetes Endocrinol 2014;2:770–2

Natural, non-processed, non-refined food (meat, fish, eggs, nuts, seeds, olive, avocados) contains high levels of saturated fat. These natural foods are a portion of the ancestral human diet.  People have eaten as much as they want to of these foods without adverse health consequences since paleolithic times, until 1977 when the Dietary guidelines demonized saturated fat of omnipresent natural fat, driving people away from highly nourishing, wholesome and health-promoting foods.

Reducing dietary saturated fats does not reduce cardiovascular events and death. Improvements in cardiovascular outcomes are independent of direct cholesterol lowering. Dietary trials that provide abundant natural fats such as α-linolenic acid, polyphenols and Ω-3 fatty acids found in nuts, olive oil, oily fish and vegetables exert a positive health effect, likely by reducing inflammation, atherosclerosis and thrombosis.

Chakrabarti S, Freedman JE. Review: nutriceuticals as antithrombotic agents. Cardiovasc Ther 2010;28:227–35.

Interestingly, replacing saturated fat with Ω-6 containing vegetable oils (highly processed and refined industrial seed oil) does lower LDL cholesterol but does not actually improve cardiovascular mortality, and may actually increase mortality.

Veerman J Lennert. Dietary fats: a new look at old data challenges established wisdom BMJ 2016; 353 :i1512

Total and LDL cholesterol are a poor marker of cardiovascular health.  Cholesterol profile of elevated triglycerides and low HDL is a more predictive marker of cardiac risk and a reliable marker of insulin resistance. In fact, the QRISK calculator, used to estimate the 10-year risk of CVD, does NOT use LDL cholesterol, but uses total cholesterol/HDL ratio instead.

Preventing insulin resistance in young men would prevent 42% of myocardial infarctions, a larger reduction than correcting hypertension (36%), low high-density lipoprotein cholesterol (31%), body mass index (21%) or low-density lipoprotein cholesterol (16%).

Eddy D, Schlessinger L, Kahn R, Peskin B, Schiebinger R. Relationship of insulin resistance and related metabolic variables to coronary artery disease: a mathematical analysis. Diabetes Care. 2009;32(2):361–6.

 

Refined Carbohydrates:

Prediabetes and Type 2 diabetes are diseases of insulin resistance with initial excessive insulin production, which display the symptom of elevated blood glucose levels as the disease progresses. Treating the root cause of the disease, instead of the symptom, is the key. Eliminate all refined carbohydrates to reverse obesity, prediabetes, and type 2 diabetes.

Refined carbohydrates are known to increase blood glucose levels, increase requirements for medications and result in weight gain. It is disturbing that dietary guidelines prioritize the consumption of starchy carbohydrates for type 2 diabetics, to nearly 55% of their daily macronutrient consumption. Such diets will potentially lead to progressive worsening of disease with all its attendant complications, such as blindness, kidney failure, nerve damage, peripheral vascular disease, heart disease and stroke.

Added sugar has no nutritional value whatsoever. There are no biochemical reactions in the human body that require dietary fructose. No single study exists that demonstrates benefit associated with its consumption.

Credit Suisse – Sugar Consumption at a crossroads

Dietary carbohydrate restriction is the “single most effective intervention for reducing all of the features of the metabolic syndrome” according to Credit Suisse. It should be the first approach in diabetes management. A ketogenic diet is one that gets less than 10 percent of its calories from carbohydrates. It produces the greatest falls in HbA1C and the biggest cuts in medication use. These benefits come independently of weight loss.

Feinman RD, Pogozelski WK, Astrup A, et al. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition 2015;31:1–13.

Sugar+veg oil+grain=obesity→PreDM→T2D

Dietary sugar is strongly associated with higher risk of type 2 diabetes, hypertension and cardiovascular disease. This holds independent of its calories or its effects on body weight.

Lustig RH: Sickeningly sweet: does sugar cause type 2 diabetes? YES. Can J Diab (in press).

Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome. Lustig RH, Mulligan K, Noworolski SM, Tai VW, Wen MJ, Erkin-Cakmak A, Gugliucci A, Schwarz JM. Obesity (Silver Spring). 2016 Feb;24(2):453-60. doi: 10.1002/oby.21371. Epub 2015 Oct 26.

Added sugar intake and cardiovascular diseases mortality among US adults. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. JAMA Intern Med. 2014 Apr;174(4):516-24. doi: 10.1001/jamainternmed.2013.13563.

 

Vegetable Oil:

Humans have at least 2-3 million years of history. Yet only since 1917 have industrial seed oils been a significant part of the human diet, with a major jump in use in the late 1970s. Linoleic acid (the Ω-6 fat in these vegetable oils) oxidizes very easily. That makes foods rancid, and it also oxidizes in the body. In non-processed whole food (seeds, nuts, fish and eggs), linoleic acid comes packed with vitamins, minerals and antioxidants. Those protect this fragile polyunsaturated fat.

Free Radic Biol Med. 2001 Dec 1;31(11):1388-95. The stomach as a bioreactor: dietary lipid peroxidation in the gastric fluid and the effects of plant derived antioxidants. Kanner J, Lapidot T.

Curr Atheroscler Rep. 2009 Nov;11(6):403-10. Impact of circulating esterified eicosanoids and other oxylipins on endothelial function. Shearer GC, Newman JW.

A meta-analysis of almost 10,000 patients confirmed that high intake of Ω-6 oils (from vegetable oils/margarines) increases the risk of death and heart disease compared to saturated fat plus trans fat. Human research data suggest that we should remove these vegetable oils from our food supply for optimal health.

29.BMJ. 2013 Feb 4;346:e8707. doi: 10.1136/bmj.e8707. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. Ramsden CE1, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR.

Older data was confounded because it lumped in Ω- 3 polyunsaturated fatty acid intake. This misrepresented the health benefits of Ω–6. Other studies, such as the Anti-Coronary Club trial, confirm that Ω–6 PUFA increases death and coronary heart disease compared to animal fat.

Christakis G, Rinzler SH, Archer M et al. Effect of the anti-coronary club program on coronary heart disease. Risk-factor status. JAMA 1966;198:597–604

The LA Veterans trial found that cancer deaths rise with the use of Ω–6 rich vegetable oils.

Pearce ML, Dayton S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1971;1:464-7.

Animal studies have also found that Ω–6 PUFA promotes the growth of experimentally induced cancers, while Ω–3 holds back their growth. Ω–6 rich vegetable oil ( such as sunflower and corn oil) is linked to a higher risk of death, coronary heart disease and cancer in humans. It is also linked to the growth of cancer in animal models.

Am J Epidemiol. 1998 Feb 15;147(4):342-52. Adipose tissue Ω–3 and Ω–6 fatty acid content and breast cancer in the EURAMIC study. European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Breast Cancer. Simonsen N1, van’t Veer P, Strain JJ, Martin- Moreno JM, Huttunen JK, Navajas JF, Martin BC, Thamm M, Kardinaal AF, Kok FJ, Kohlmeier L.

Cancer Res. 1988 Dec 1;48(23):6642-7. Effect of different levels of Ω–3 and Ω–6 fatty acids on azoxymethane-induced colon carcinogenesis in F344 rats. Reddy BS, Sugie S.

 

Why eat less, move more fails:

A calorie is a calorie only if it is burned in a bomb calorimeter and the heat given off is measured. Calories from different foods have entirely different metabolic effects on the human body. Equal calorie portions of sugar, alcohol, meat or olive oil act very differently on hormone systems. These include insulin and fullness signals such as cholecystokinin or peptide YY. It does not matter how many calories a portion of food on a plate contains. What matters is how our body responds to taking in and absorbing those calories. It matters how they are metabolized and how full we end up feeling.

The calorie-cutting plans pushed for weight loss today do not work. The standard calorie-cutting approach gives a 1 in 167 chance of reaching a normal weight. That is a greater than 99% failure rate.

Fildes A et al. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015;105: e54–e59

People wrongly assume that eating too many calories is the root cause of obesity. A calorie of food energy has different fates in the body depending on hormone signals. That same calorie may be used to make body heat or stored as body fat. Obesity is a disease of failed energy partitioning (how the body splits energy between burning and storing), not one of total energy intake. The main driver of this partitioning is the hormone insulin. Insulin is specifically a fat storage growth hormone.

Focusing on calories in and calories out builds in a bias against high-fat food. Yet high-fat food may protect against obesity and related diseases. This simple calorie focus leads to a dietary guideline that swaps fat for starch and sugar. That swap promotes insulin resistance.

We hope that shifting focus away from calories will reduce obesity, related diseases and cardiovascular risk. That means stressing a way of eating built on food quality rather than quantity.

Malhotra A, DiNicolantonio JJ, Capewell S. It is time to stop counting calories, and time instead to promote dietary changes that substantially and rapidly reduce cardiovascular morbidity and mortality. Open Heart 2015;2(1) doi: 10.1136/openhrt-2015-000273.

Yo-yo dieting, with fast weight loss and regain from fad diets, harms health. This ‘weight cycling’ adds to hypertension, insulin resistance and dyslipidemia (unhealthy blood fats). The result is a higher risk of death and worse cardiovascular outcomes.

Mann T, Tomiyama AJ, Westling E, et al. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol 2007;62:220–33.

LC + exercise ≠ health

In the Action for Health in Diabetes trial, no cardiovascular benefits were found from a low-calorie diet plus more physical activity in type 2 diabetic patients.

(Despite the significant weight loss, even up to the longest follow-up of 13.5 years, no health benefits could be found. )

Wing RR, Bolin P, Brancati FL, et al. Look AHEAD Research Group. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med 2013;369:145–54.

 

Exercise is not the solution:

The public and media widely accept that eating more calories than we burn causes the obesity epidemic. So they believe the solution is to just exercise more.

Food and drink companies have pushed this exercise message to clear their own name. The very companies selling processed and highly refined foods linked to the obesity epidemic have sponsored major sporting events. This association of ultra-processed food and soft drinks with sport is troubling. Celebrity endorsements send the wrong message, especially to children.

Regular physical activity does have health benefits, but weight loss is not one of them. In fact, our levels of physical activity have changed little in the past three decades, while obesity has risen.

Luke A, Cooper RS. Physical activity does not influence obesity risk: time to clarify the public health message. Int J Epidemiol 2013;42:1831–6.

It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet . A Malhotra, T Noakes, S Phinney Br J Sports Med bjsports- 2015-094911Published Online First: 22 April 2015 doi:10.1136/bjsports-2015- 094911

 

The time spent not eating is more important than the time spent eating. Snacking will make you fat. The cause is the chronic high insulin from constant feeding.

There have been two major changes in our eating habits since the 1970s, before the obesity epidemic began. The first is the switch to a high-carbohydrate, low-fat diet. It is well documented and has played an important role in causing obesity. But the rise in how often we eat plays an equal if not larger role, and it has been largely ignored. In the 1970s, people ate an average of three times a day: breakfast, lunch and dinner. By 2005, that number had almost doubled. Now we eat breakfast, snack, lunch, snack, dinner and snack. More often than not, each of these contains refined carbohydrates.

Cameron JD. 6 meals per day does not result in greater weight loss. Br J Nutr. 2010 Apr;103(8):1098-101

Popkin BM. Does hunger and satiety drive eating anymore? Am J Clin Nutr 2010;91:1342–7

 

Eating almost nonstop from the moment we wake to the moment we sleep gives the body a chance to store food energy without a chance to burn it. Eating six times a day does not cause weight loss. It tends to increase how much food we eat overall. Snacks are made for convenience and long shelf life. They are filled with refined carbohydrates and often have Ω–6 vegetable oil added.  Heavy processing of food raises its glycemic index. Grazing all day keeps insulin, the fat storage hormone, high all the time.

Eating fewer meals and cutting out snacks are simple ideas. People practiced them widely before the obesity epidemic.

 

Frequently asked questions

What is the biggest contributor to type 2 diabetes?

The root cause sits in the food environment. Sugar, industrial seed oils and refined grains drive obesity, then prediabetes, then type 2 diabetes. Type 2 diabetes is a disease of insulin resistance. It begins with the body making too much insulin, and high blood sugar shows up later. Eating all day, snacks included, keeps insulin high around the clock.

Can type 2 diabetes go away?

Yes, when you treat the root cause instead of the symptom. Eliminating refined carbohydrates reverses obesity, prediabetes and type 2 diabetes. Cutting dietary carbohydrates should be the first approach in diabetes management. A ketogenic diet gets under 10 percent of calories from carbohydrates. It produces the greatest falls in HbA1c and the biggest drop in medications, independent of weight loss.

What is the worst food for blood sugar?

Refined carbohydrates and added sugar. Refined carbohydrates raise blood sugar, increase the need for medication and cause weight gain. Added sugar has no nutritional value. No reaction in the human body requires dietary fructose. Dietary sugar is tied to higher risk of type 2 diabetes, high blood pressure and heart disease, regardless of its calories or its effect on weight.

Can a healthy person get type 2 diabetes?

Most people who feel healthy are not metabolically healthy. Less than 12.2% of Americans met the bar for metabolic health in NHANES 2009-2016 data. Fewer than 7% meet it on the tighter criteria applied after 2021. Nearly 70% are insulin resistant, prediabetic or diabetic. Heart and blood-vessel risk climbs well before blood sugar reaches the diagnostic cutoff.

Why doesn’t eating less and moving more work for weight loss?

Calories from sugar, alcohol, meat or olive oil act on your hormones differently. Insulin decides whether food energy is burned or stored as fat. Standard calorie cutting gives an obese person a 1 in 167 chance of reaching a normal weight. Exercise has real health benefits, but weight loss is not one of them: you cannot outrun a bad diet.

Additional references for RCTs comparing low carb and low fat for weight loss

• Shai I, et al. Weight loss with a low-carbohydrate, mediterranean, or low-fat diet. N Engl J Med 2008;359(3);229–41.
• Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The A to Z Weight Loss Study: A Randomized Trial. JAMA. 2007;297:969–977.
• Brehm BJ, et al. A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. J Clin Endocrinol Metab 2003;88:1617–1623.
• Samaha FF, et al. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. N Engl J Med 2003;348:2074–81.
• Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr. 2003 Mar;142(3):253–8.
• Aude YW, et al. The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial. Arch Intern Med. 2004;164:2141–2146.
• Volek JS, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism 2004, 1:13.
• Yancy WS Jr, et al. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial. Ann Intern Med. 2004;140:769–777.
• Nickols-Richardson SM, et al. Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet. J Am Diet Assoc. 2005;105:1433–1437.
• Krebs NF, et al. Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents. J Pediatr 2010;157:252-8.
• Summer SS, et al. Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet. Obesity (Silver Spring). 2011 Mar 31. [Epub ahead of print]
• Daly ME, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial. Diabet Med. 2006 Jan;23(1):15–20.
• Westman EC, et al. The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr. Metab (Lond.)2008 Dec 19;5:36.
• Halyburton AK, et al. Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive performance. Am J Clin Nutr 2007;86:580–7.
• Dyson PA, et al. A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects. Diabet Med. 2007 Dec;24(12): 1430-5.
• Keogh JB, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. Am J Clin Nutr 2008;87:567–76.
• Volek JS, et al. Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet. Lipids 2009;44:297–309.
• Partsalaki I, et al. Metabolic impact of a ketogenic diet compared to a hypocaloric diet in obese children and adolescents. J Pediatr Endocrinol Metab. 2012;25(7-8):697-704.

Related reading

• Why treat obesity and prediabetes
• What Is Diabesity? How to Reverse It

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 31, 2026

Time-restricted feeding works in four steps. Talk to your doctor about your conditions and medications. Stop sugars, artificial sweeteners, processed foods and vegetable oils. Build meals on protein and healthy fats. Then start with an 8-hour eating window and narrow it by about one hour a week.

Time Restricted Feeding | Reverse Diabetes MD from Gurpreet Padda on Vimeo.

What is time-restricted feeding?

Time-restricted feeding can help people move into a healthier lifestyle. It can help reverse insulin resistance and keep a healthy weight. Most people eat from the time they wake up until the time they go to bed. Typically, they eat three main meals, many snacks, and often soda in between. This pattern leads to chronic high insulin production, which wears out the insulin receptors. Also, insulin is a fat storage hormone. High insulin levels lead to fat building up in the liver, which creates metabolic inflammation.

Your metabolism has two states: the “fed” (insulin high) state and the “fasted” (insulin low) state. Either we are storing food energy (adding to storage), or we are burning stored energy (shrinking storage, or fat lysis). Say we start eating the minute we roll out of bed and do not stop until we go to sleep. Then we spend almost all our time in the fed state. Over time, we gain weight, because we have not given our body time to burn stored food energy.

Time-restricted feeding shortens the time window when a patient eats. That shortens the “fed” state and lengthens the “fasted” state. This lowers the total amount of insulin made in a day. Insulin is a fat-storage hormone, and a high level of insulin production leads to insulin resistance. Time-restricted feeding is a type of fasting. It has extraordinary benefits, including weight and body fat loss, and lower blood insulin and sugar levels. It also brings a reversal of type 2 diabetes. Other possible benefits include clearer thinking and focus, and a lower risk of Alzheimer’s disease. It may also turn on cellular cleansing by stimulating autophagy, and reduce inflammation.

Time-restricted feeding is a type of fasting. It is not starvation. Starvation is the involuntary absence of food for a long time. It leads to severe suffering or even death. Starvation is not planned or controlled. Fasting is choosing not to eat. It is done by someone who is not underweight, so they have enough stored body fat to live off. When done right, intermittent fasting should not cause suffering. Food is easy to get, but you choose not to eat it. You may begin a fast at any time you choose, and you may end it at will, too. You can start or stop a fast for any reason or no reason at all. Any time that you are not eating, you are intermittently fasting. For example, you may fast between dinner and breakfast the next day. That is about 12-14 hours. In that sense, intermittent fasting should be seen as part of everyday life.

Just having insulin present increases fat storage. When insulin is absent, the body can use lipolysis, or burning fat as energy.

Lifestyle changes are key to managing obesity and Type 2 Diabetes. But by themselves they don’t always control blood glucose levels. Bariatric surgery (gastric band or bypass) works but has significant risk. Drugs often manage the symptoms and may stave off complications, but they don’t reverse the disease.

Time-restricted feeding has the potential to fill this gap in obesity and diabetes care. It provides calorie restriction and the hormonal benefits of bariatric surgery, without invasive surgery. Time-restricted feeding means the controlled and voluntary choice to skip all food and drinks with calories for a set period of time. During the fasting periods, patients may drink unlimited amounts of very-low-calorie fluids. These include water, coffee, tea, and even bone broth. A general multivitamin is encouraged to provide enough micronutrients.

Metabolic flexibility:

Time-restricted feeding, or meal-timing strategy, reduces swings in hunger. It changes how the body burns fat and carbs, which may help with losing weight and improving insulin sensitivity. It does not necessarily change how many total calories patients burn. But it reduces the daily hunger swings and increases fat burning at night. It improves metabolic flexibility, which is the body’s ability to switch between burning carbs and burning fats. Metabolic flexibility is how easily the body moves between two opposite states, “fed” and “fasted,” without cravings or hunger pangs.

During feeding, insulin is high, which tells your body to store extra calories as fat. When insulin is present, fat burning stops, and the body burns glucose instead. In the fasted state, insulin is low, while glucagon and growth hormone rise. So the body pulls stored body fat from your fat cells and burns this fat for energy (instead of glucose). You can only burn stored body fat while in the fasted state. And you can only store more body fat while in the fed state.

Most overweight patients live in a constant fed state, and rarely in a fasted state. Their cells keep burning glucose rather than fat. They have insulin resistance, caused by chronically high insulin levels. These high levels promote fat storage and block fat from being released.

Overweight “sugar burners” may stop eating for even a few hours. When they do, they quickly run out of glucose from their last meal, instead of moving to the fasted state and burning stored body fat. This causes acute brain signals of hunger and cravings for sugar right away. They spend most of the day trapped in a cycle. They eat every few hours, spike glucose, and then get hungry when blood sugar drops.  They may even get low blood sugar and feel jittery. This is called reactive hypoglycemia. It is a big clue that a patient lacks metabolic flexibility.

Fat-adapted energy use:

Your metabolic flexibility is set by your mitochondria, the tiny energy factories inside the cells. The mitochondria can burn either glucose (sugar) or fat for fuel. Over time they will prefer one over the other. “Sugar burners” have built up the pathways in the mitochondria that burn glucose and decreased the pathways for burning fat. As you become more metabolically flexible, the fat burning pathways will take over, and you will become “fat adapted.”

Becoming fat adapted takes time and practice. Your body has to do a number of things to slowly up-regulate (or increase) your fat-burning pathways. It must improve insulin sensitivity to lower insulin and help release fat as free fatty acids. It must also upregulate the fat-burning pathways at the cellular level (in the mitochondria).

Ways to improve fat adaptation include:

• Low-carbohydrate diets: A low-carb, high-fat (LCHF) diet helps the body use fat for energy rather than glucose. That is because there is more fat and less glucose, even in the fed state.
• Exercise: High-intensity exercise uses up glucose and glycogen fast. This forces the body to switch to fat for fuel. Exercise also improves insulin sensitivity.
• Caloric restriction: Eating fewer calories also means less glucose for fuel. This forces the body to rely on stored body fat for fuel.
• Intermittent fasting makes the body spend more time in the fasted state. This gives the body more “practice” at burning fat.
• Supplementation: Ketone supplements may be useful when first starting out. Ketones are breakdown products of fat. When you first start out, ketones can reduce your hunger and give energy to your mitochondria.

Patient education and engagement is the key to remission and to cutting back on drugs. Morrison et al. also found that more frequent contact with a provider led to markedly rapid drops in serum glucose, HbA1C, and low-density lipoprotein cholesterol levels. This was in patients who followed up with the treating physician on average every 2 weeks.

How to do time-restricted feeding:

Our protocol can reverse obesity and Type 2 Diabetes in people who can still make some insulin. It does this by resensitizing the insulin receptor and restoring normal cyclical insulin production. We restore the normal ebb and flow of insulin, so the receptors are re-sensitized. The constant high level of insulin in the blood drops, which reduces insulin’s fat storage action.

Time-restricted feeding is a type of intermittent fasting. It limits your eating to a certain number of hours each day. Here is an example. You choose to eat all your food for the day in an 8-hour period, such as from 11 a.m. to 7 p.m. That gives an 8-hour feeding window. The other 16 hours are the fasting period, when you eat no calories. You repeat the same schedule every day.

Limit feed times to a shorter window each day. Start at 8 hours/day and reduce by 1 hour per week down to 4-6 hours/day. This is highly effective in reversing diabetes and producing weight loss. Medications must be adjusted by a clinician to prevent glucose levels that drop too low by accident, or changes in blood pressure. These can be life-threatening. To succeed with this technique, prevent cravings. Feeling full is the key. You should not be hungry, or this will not last. Food choice drives feeling full.

Steps to success

Step 1

Before you start a time-restricted feeding schedule, talk to your doctor or health care provider. Get medical advice from a professional who shares your health goals.

You may have medical conditions that need close monitoring. You may also be on medications that may need to be adjusted. Before you start a fasting program, it is important to understand your medical history and the medications you take. Please talk to your doctor or healthcare provider.

Step 2

Stop all sugars, including all artificial sweeteners. Many sugars and processed carbs just don’t fill you up. Stop all sugar and artificially sweetened drinks. Before you start your protocol, remove sugars and processed carbohydrates.

Stop all sources of vegetable oil. Replace them with healthy natural oil and real butter. Swapping industrial seed oil for real oils is easy if you are not eating processed foods. It even makes the food taste better.

Stop all processed foods. Processed foods are built to make you eat again and again and again, every 2-3 hours.

Step 3

Focus on protein and healthy fats. Choose meals that are rich in protein and healthy fats. Eat all types of meat like beef, fish, chicken, eggs, lamb, and seafood. Yogurt and cheeses are also nutritious and filling. Fill up on low-sugar vegetables like olives, peppers, cucumbers, and avocado. Eat as many green leafy vegetables as you please. This helps your body adapt to burning fat and may make fasting easier to start.

Step 4

Start slow. This metainflammation didn’t happen in one day, and it won’t go away in a day. Try a generous 8-hour eating window on your first day to see how it feels. Eat as you please during your 8-hour time frame. Then see how your body and appetite feel for the rest of the day.

Then, slowly narrow your eating window. As you get better at judging your hunger and understanding hunger pangs, you can slowly shrink your daily feeding window. Try cutting by one hour a week, until you reach a 4-hour window.

Things to think about:

You may notice hunger pangs if you haven’t first changed your diet to include more filling foods. These are foods full of protein, healthy fat and fiber. If you have hunger pangs, try drinking some hot tea, coffee, water or seltzer. This will fill your stomach up. It gives you enough time to realize that maybe you really aren’t as hungry as you first thought. Some people use lemon in seltzer water.

This should be a fun experience, not a miserable one. If you are miserable, something has been overlooked. Remember that time-restricted feeding is a great way to limit snacking. Eating filling real food during your eating window will restore and realign your hormone system.

Patients can reverse their diseases without worrying about the side effects and cost of many pharmaceuticals. They also avoid the unknown long-term risks and uncertainty of surgery. They do it all by means of time-restricted feeding.

Some practical tips:

• Don’t use time-restricted feeding as an excuse to eat junk food when you are eating. Keep avoiding processed foods.
• When you first start time-restricted feeding, you might have to use a fast-mimicking substance like a ketone supplement.
• Check with your doctor before starting time-restricted feeding, especially if you are diabetic and on diabetes medications!
• You can generally take any vitamins or supplements you want while fasting, as long as they don’t have calories. But you don’t need any supplements, because you will be eating plenty of nutrient-dense foods every day. You may have to eat more salt.
• You don’t have to worry about losing muscle from lack of protein during your fast. Just eat enough protein at the meals before and after fasting. An LCHF (low-carb, high-fat) diet pairs nicely with intermittent fasting, as both improve fat adaptation a great deal.
• You can exercise with time-restricted feeding, either cardio or lifting weights. Lifting weights is better. You will not lose muscle while fasting as long as you exercise regularly.
• Drink plenty of water and non-caloric drinks while fasting. Coffee and tea in the morning make fasting much more enjoyable. They also bring health and fat-burning benefits, and are highly recommended.
• Skipping your morning meal gives your body more time to burn fat for energy. Hunger is lowest in the morning, so it may be easiest to skip it and break your fast later in the day.

Time-restricted feeding has many benefits but remains controversial. Diabetes medications will need to be adjusted. Discuss any changes in medication and related lifestyle changes with your doctor. Some people should not use time-restricted feeding. These include those who are underweight or have eating disorders, pregnant or breastfeeding women, and children under the age of 18.

Need more help? We have more to offer.

Frequently asked questions

Is time-restricted feeding the same as intermittent fasting?

Time-restricted feeding is one type of intermittent fasting. It limits all food to a set number of hours each day and repeats the same schedule daily. Intermittent fasting is the broader term. Any time you are not eating, you are fasting, such as the 12 to 14 hours between dinner and the next breakfast. Fasting is voluntary, and it is not starvation.

What are the best hours for time-restricted eating?

A common start is an 8-hour window, such as 11 a.m. to 7 p.m., with a 16-hour fast. Skipping the morning meal works well. That is because hunger is lowest in the morning, and it gives your body more time to burn fat. From there, shorten the window by one hour a week until you reach 4 to 6 hours a day.

What are common mistakes with 16:8 fasting?

The big one is using the eating window as an excuse to eat junk food. Keep avoiding processed foods. Skipping protein and healthy fats leaves you with hunger pangs. Starting without your doctor adjusting diabetes or blood pressure medication can be life-threatening. Forgetting water and non-caloric drinks also makes fasting harder. So does not adding salt when you need it.

What should you eat during your eating window?

Build your meals on protein and healthy fats. Eat all types of meat, including beef, fish, chicken, lamb and seafood, plus eggs. Yogurt and cheese are nutritious and filling. Add low-sugar vegetables like olives, peppers, cucumbers and avocado. Eat as many green leafy vegetables as you like. This helps your body adapt to burning fat, which makes fasting easier.

How many hours should your eating window be?

Start with a generous 8-hour eating window. Eat as you please during those 8 hours. Notice how your body and appetite feel for the rest of the day. As you get used to hunger, shrink the window by about one hour a week until you reach a 4-hour window. Go slow: the metainflammation did not happen in a day.

What can you drink during the hours you are not eating?

Hot tea, coffee, water and seltzer all help when hunger pangs hit. They fill your stomach and give you time to notice that you may not be as hungry as you first thought. Some people add lemon to their seltzer. Leave out sugar-sweetened drinks and artificial sweeteners. They have no place in this plan.

Additional references:

Sutton EF, Beyl R, Early KS, et al. Early time-restricted feeding improves insulin sensitivity, blood pressure, and oxidative stress even without weight loss in men with prediabetes. Cell Metabolism. 2018. PMID 29754952

Suleiman Furmli, Rami Elmasry, Megan Ramos, Jason Fung. Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. BMJ Case Reports, 2018; bcr-2017-221854 DOI: 10.1136/bcr-2017-221854

Morrison F , Shubina M , Turchin A . Encounter frequency and serum glucose level, blood pressure, and cholesterol level control in patients with diabetes mellitus. Arch Intern Med 2011;171:1542–50.doi:10.1001/archinternmed.2011.400

Duke S-AS , Colagiuri S , Colagiuri R . Cochrane Metabolic and Endocrine Disorders Group. Individual patient education for people with type 2 diabetes mellitus. Cochrane Database Syst Rev 2009;22.doi:10.1002/14651858.CD005268.pub2

Brethauer SA , Aminian A , Romero-Talamás H , et al . Can diabetes be surgically cured? Long-term metabolic effects of bariatric surgery in obese patients with type 2 diabetes mellitus. Ann Surg 2013;258:1.doi:10.1097/SLA.0b013e3182a5034b

Pucher PH , Lord AC , Sodergren MH , et al . Reversal to normal anatomy after failed gastric bypass: systematic review of indications, techniques, and outcomes. Surg Obes Relat Dis 2016;12:1351–6.doi:10.1016/j.soard.2016.01.030

Shoar S , Nguyen T , Ona MA , et al . Roux-en-Y gastric bypass reversal: a systematic review. Surg Obes Relat Dis 2016;12:1366–72.doi:10.1016/j.soard.2016.02.023

The University of Alabama at Birmingham. “Time-restricted feeding study shows promise in helping people shed body fat.” ScienceDaily. ScienceDaily, 6 January 2017. www.sciencedaily.com/releases/2017/01/170106113820.htm

Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? K. A. Varady. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1467-789X.2011.00873.x

Moro, T., Tinsley, G., Bianco, A., Marcolin, G., Pacelli, Q. F., Battaglia, G., … Paoli, A. (2016). Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males. Journal of translational medicine, 14(1), 290. doi:10.1186/s12967-016-1044-0. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064803/

Gabel, K., Hoddy, K. K., Haggerty, N., Song, J., Kroeger, C. M., Trepanowski, J. F., … Varady, K. A. (2018). Effects of 8-hour time restricted feeding on body weight and metabolic disease risk factors in obese adults: A pilot study. Nutrition and healthy aging, 4(4), 345–353. doi:10.3233/NHA-170036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004924/

Related reading

• Eat More Protein to Lose Weight?
• Eating your way to true health
• Bedtime Psyllium for Gut Irritation

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 17, 2026