What You Eat Influences Metabolic Syndrome
Metabolic syndrome (MetS) and inflammation are linked
MetS is a cluster of disruptions in the body's metabolism that affect energy generation and use. This can cause hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia. Atherogenic dyslipidemia has abnormal blood lipids. Namely, high amounts of triglycerides and small, low-dense lipoprotein (LDL) particles with low amounts of high-density lipoprotein (HDL) (Islam et al. 2024).
Inflammation causes and/or contributes to MetS. In turn, MetS causes inflammation. It is a positive feedback loop. Interestingly, there seems to be sex specific pathways that differ in women and men (Ter Horst et al. 2020).
Seven ways eating too many carbs lead to metabolic syndrome
You don't need to lose weight to reduce inflammation
Weight loss by most methods reduces the risk for MetS. However, many people find losing even small amounts of weight or excess fat difficult and annoying.
Rather than task people with potentially unattainable weight loss goals, we prefer to focus on diet recommendations that reduce both MetS symptoms and its associated metainflammation even without weight loss. One extremely effective treatment for MetS is replacing carbohydrates in the diet with protein and/or fat. Fat (adipose) tissue remodeling caused by metainflammation can be reversed through lifestyle changes such as changing the amounts of fat, carbohydrate and/or protein you eat or replacing processed food with whole natural foods (Volek et al. 2021).
You can reverse MetS by eating less carbohydrates and sugar
☆ A small crossover study found that people with MetS who eat a low-carbohydrate (LC) high fat diet rapidly reversed their MetS even without weight loss. Women and men (16 people, average age 41 years) who ate a low-carbohydrate (LC) diet for 4 weeks accelerated fat oxidation while reversing MetS when compared to the same people eating a high carbohydrate diet. Nine out of the 16 people no longer met the criteria for MetS after only 4 weeks of the LC diet. All showed positive changes.
Eating a LC diet lowered triglycerides, increased HDL-C, improved LDL phenotype and decreased plasma total saturated fatty acids.
All diets were 20% protein. LC diet was 6% carb, medium carb (MC) diet was 32% carb, and HC was 57% carb. Fat content of each diet was LC=74%, MC=48%, and HC=23% energy (Hyde et al. 2019).
☆ A review found that caloric intake was not related to changes in MetS factors. However, similar to above, diets lower in carbs and higher in fat were the most relevant for improving MetS markers (Willems et al. 2021).
Interested in losing weight? Willems et al. 2021 found that increasing your protein intake was associated with reducing your body weight. For best results replace carbohydrates with protein.
Below: Drinking soda for breakfast is not the best choice. Photo of Swedish custom officer (1967) on a break by Lennart Nygren.
7 ways eating too many carbohydrates (especially sugars and processed carbohydrates) leads to metabolic syndrome
Click on each one for more details!
1) Fructose metabolism triggers metabolic changes promoting inflammation, insulin resistance (IR), cardiometabolic disorders and uric acid generation. Most fructose comes from sugar, not fruits. Table sugar is half fructose and half sucrose.
Leading sources of fructose: soda and fruit juices. Beverages listing high fructose corn syrup as an ingredient have an average of 60% fructose to 40% glucose. Beverages made with sugar have around 50% fructose and 50% glucose (Walker et al. 2014).
One medium apple contains around 11-12 g fructose. One can of Coke or Pepsi has 39-40 grams of sugar. Apples also contain fiber and vitamins.
2) High carbohydrate diets (especially processed carbohydrates) lead to development of IR over time in many people.
3) High carbohydrate consumption increases blood glucose which leads to mitochondria dysfunction and IR.
4) Excess sugar consumption stimulates leptin resistance. Leptin is a hormone that helps your body maintain weight by regulating hunger.
5) Carbohydrate consumption causes changes to the gut microbiotia.
6) Excess carbohydrate consumption promotes weight gain through overeating.
7) When you consume a high carbohydrate and low fat diet you use less calories to digest your meal. This promotes obesity.
It is likely that the ill effects of overindulgence in carbohydrates stems from a combination of these pathways.
*Hasan E. (53 year man) "I am a type 2 diabetic. I can't keep my sugar levels under control without restricting my carbs. As the carbs get lower I feel better physically and cognitively. I really try to keep to 100-110 carbs a day. My body prefers I stay under like 30 carbs a meal, I guess.
If I pig out on pizza or soda for dinner, my body feels like trash. Fatigue hits and I start having focus problems and brain fog... I don't want to end up with amputated feet, so I just keep to a lower carb lifestyle, and I usually feel much better. I need some carbs though, Keto is really too low and saps my energy."
Check out below for all the good scientific evidence!
Excess carbohydrate intake triggers metabolic syndrome
There is amble evidence that excess carbohydrate consumption, in particular excess sugar and/or processed carbohydrate consumption, is associated with the symptoms of MetS. This same overwhelming volume of evidence is not seen with excess dietary fat and/or protein intake.
Need proof? Excess carbohydrate and/or sugar consumption is correlated with:
★ MetS (Dhingra et al. 2007, Denova-Gutierrez et al. 2010, Hyde et al. 2019, Willems et al. 2021, Kuo et al. 2023)
★ Type 2 diabetes (T2D); this is especially true of consuming both sugar sweetened and artificially sweetened beverages! (Schulze et al. 2004, Montonen et al. 2007, Bhupathiraju et al. 2013, Tay et al. 2015, Imamura et al. 2016, Tay et al. 2018, Volek et al. 2021, Pavlidou et al. 2023, Della Corte et al. 2025)
★ Insulin resistance (IR); IR can lead to T2D and weight gain (Bremer et al. 2010, O'Neill 2020, Ebbeling et al. 2022, Pavlidou et al. 2023)
★ Dysfunctional lipid levels that include high triglycerides (Denova-Gutierrez et al. 2010, Tay et al. 2018, Ebbeling et al. 2022)
★ Cardiovascular disease like heart failure or strokes (Hu and Bazzano 2014, Dong et al. 2020)
★ Central adiposity or large waist circumference (Garr Barry et al. 2021)
★ Non-alcohol fatty liver disease (NAFLD). This is aggravated by fructose consumption (table sugar is half fructose and half glucose) (Ouyang et al. 2008, Umpleby et al. 2017, Lambertz et al. 2017, Jensen et al. 2018)
★ Hyperuricemia, high levels of uric acid which can cause gout or kidney stones (Thottam et al. 2017)
Keep in mind that you may react very differently to various types of carbohydrates
People react differently to different types of carbohydrates depending on their genetic makeup. Researchers looked at how 55 people with no history of Type 2 Diabetes (T2D) reacted to different standardized carbohydrate meals by measuring glucose response (how much their glucose goes up, called a spike).
The seven carbohydrate meals (50 g total carbohydrates each) were:
1) jasmine rice
2) buttermilk bread
3) shredded cooked and cooled potatoes
4) precooked and previously frozen macaroni pasta
5) canned black beans (high fiber)
6) mixed blackberries, strawberries and blueberries (high fiber)
7) grapes (low fiber)
People had different glucose spikes to the various carbs: the largest glucose responses were seen with rice 35%, bread 24% and grapes 22%. Insulin resistant (IR) people had more extreme responses to the meals. Asian people were more likely to react strongly to rice. People who were more IR, had higher fasting glucose, and had lower pancreas beta cell function reacted more strongly to potatoes. Those who were more insulin sensitive reacted more to grapes. Bread spikers had higher blood pressure (Wu et al. 2025).
What can you do?
Some people test their reactions to carbohydrates using a blood glucose meter. These are very cheap and easy to use.
Often you can tell what carbohydrates raise your blood glucose/sugar levels by seeing what foods make you feel either sluggish or really hungry soon after you eat them.
Blue Box of Science: Want to know the details? Here are the references and hard science.
1) Fructose metabolism leads to metabolic changes that increase metainflammation, IR and visceral adiposity (Basciano et al. 2005, Stanhope and Havel 2009, DiNicolantonio et al. 2015). Table sugar, sucrose, is composed of half fructose and half glucose, so diets high in refined carbohydrates and added sugars contain approximately 50% fructose.
Glucose can be used directly by cells or by the liver, but most dietary fructose is processed by the liver in a procedure initiated by fructokinase (Teff et al. 2009, Zhang et al. 2017). Unlike the enzymes that initiate glucose processing, fructokinase is not regulated by hepatic energy status as measured by ATP (Adelman et al. 1967). Due to this, fructose consumption leads to unchecked increases in de novo lipogenesis (DNL), triglycerides, carbohydrate oxidation, and liver fat even without weight gain (Schwarz et al. 2015).
In addition, rapid fructose metabolism depletes liver ATP and intracellular inorganic phosphate (Pi) levels (Van den Berghe et al. 1977, Abdelmalek et al. 2012), ultimately causing a buildup of uric acid and adenosine monophosphate deaminase (AMPD). Both uric acid and AMPD adversely regulate energy sensor AMP kinase (AMPK). AMPK inhibits fatty liver and has anti-inflammatory effects in cells such as leukocytes (Smith et al. 2016, Zhang et al. 2017). Thus, restricting AMPK may promote fatty liver and inflammation.
Fructose metabolism interacts with purine degradation pathways to further increase uric acid generation (Thottam et al. 2017). Interestingly, urate also promotes fructokinase which generates a positive feedback loop ultimately resulting in even higher uric acid levels (Lanaspa et al. 2012, Jensen et al. 2018). Uric acid increases metabolic and oxidative stress partly by inducing mitochondrial oxidative stress (Xie et al. 2021).
Healthy mitochondria are one of the main generators of reactive oxygenated species (ROS) and other free radicals (Bhatti et al. 2017, Choi et al. 2024). Stressed mitochondria release even more free radicals due to electron transport chain dysfunction. As the mitochondria deteriorate ATP production decreases and free radical production increases.
Increased ROS damages the mitochondria further promoting a positive feedback cycle (Bhatti et al. 2017). In turn, mitochondrial oxidative stress promotes IR, hypertension and cardiac dysfunctions (Dikalov and Zoltan Ungvari 2013). Stressed mitochondria contribute to NAFLD pathology as well by generating ROS that trigger inflammation, damage hepatocytes, and contribute to IR (Bhatti et al. 2017).
Willem van Aelst, Fruit Still Life with a Snail, c1649 oil on canvas.
2) Excessive carbohydrate consumption may lead to insulin resistance (IR) over time. Highly refined carbohydrate consumption is a risk factor for MetS, weight gain, fatty liver and IR (Bray and Popkin 2014, Lopez-Alarcon et al. 2014).
Refined carbohydrates and sugars enter the blood stream quickly as simple sugars (mainly glucose and fructose). High blood glucose triggers insulin release by the pancreas to balance blood glucose (Qaid and Adelrahman 2016). Insulin; a hypoglycemic, anabolic and storage hormone; stimulates cellular glucose transport protein, GLUT4, to rise to the cell’s membrane surface and take up glucose. To maximize glucose storage, insulin promotes lipoprotein lipase (LPL), a fat storage enzyme, and suppresses hormone sensitive lipase (HSL), an enzyme that breaks down triglycerides. Insulin also suppresses liver glucose production, gluconeogenesis (Edgerton et al. 2017).
Insulin concentrations are higher on a high carbohydrate diet than a low carbohydrate diet (Hernandez et al. 2010). Chronic hyperinsulinemia may promote metainflammation and obesity . Over time, cells become less sensitive to the chronically high insulin levels and more insulin has to be produced to balance blood glucose. This process may be initiated or accelerated by chronic inflammation (Wensveen et al. 2015, Kumar et al. 2018). Chronically elevated insulin concentrations promote cellular IR and obesity. Cellular IR prompts increased insulin release and the cycle accelerates.
3) High carbohydrate diets increase blood glucose after a meal (postprandial) when compared to lower carbohydrate diets (Feinman et al. 2015). High blood glucose concentrations influence mitochondrial dynamics, promoting overproduction of ROS and insulin resistance (IR) (Patti and Corvera 2010, Zheng et al. 2015, Fung and Berger 2016, Wang and Wei 2017).
IR, in turn, is linked to several mitochondria abnormalities including systemic inflammation (Fung and Berger 2016). IR reduces insulin-stimulated mitochondrial activity due to stunted mitochondrial plasticity (Szendroedi et la. 2012). A reduction in mitochondria plasticity means that mitochondria are unable to effectively switch fuels from fatty acids to glucose in skeletal muscle. IR also significantly decreases the copy number of mitochondrial DNA (mtDNAn). A reduction in mtDNAn precedes diabetes development and predicts IR (Zheng et al. 2015).
4) Fructose and sucrose intake may promote obesity and leptin resistance through several mechanisms including alterations in central and peripheral metabolism and/or leptin receptor signaling (Vasselli et al. 2013). Leptin is an adipocyte hormone that helps balance food intake with energy expenditure in the hypothalamus. Higher concentrations of leptin decrease appetite, switch food preferences from fatty acids to carbohydrates, and promote thermogenesis through UCP3 activation in muscle tissue. Chronic fructose consumption caused leptin resistance and increased susceptibility to overeating and weight gain in rats (Shapiro et al. 2008).
Diets containing excessive fructose affects regulatory pathways for energy homeostasis even without weight gain (Vasselli et al. 2013). Weight maintaining diets high in fructose prime rats to overeat when they are later put on an obesogenic diet (Shapiro et al. 2008, Vasselli et al. 2013). High fructose diets quickly induce leptin resistance (Shapiro et al. 2008). Fructose-induced leptin resistance may initiate a chain reaction contributing to the rapid weight gain of animals later exposed to a more palatable high caloric diet. (Vasselli et al. 2013). Interestingly, high fat diets seem to protect against fructose-initiated leptin resistance (Haring and Harris 2011). This may explain the conflicting studies on this topic.
Humans are more complicated. For one thing, it is harder to measure leptin resistance in humans since there is no overreaching definition of this disorder. Overall, when people overeat carbohydrates, fructose, sucrose, and saturated fat while neglecting protein, they can become leptin resistant (Mendoza-Herrera et al. 2021). Low calorie diets and weight loss can reverse leptin resistance.
Evaristo Baschenis - Boy with a Basket of Bread c1655-65 oil on canvas.
5) There is evidence that lower carbohydrate diets shift gut microbiota composition (Rondanelli et al. 2021). Gut microbiota composition may be associated with body weight. Several exploratory studies report that prebiotics and probiotics improve insulin sensitivity, inflammatory markers, postprandial incretins, and glucose tolerance. This is an emerging field and more research is needed (see discussion Mora-Flores et al. 2023).
6) High carbohydrate diets may promote overeating. Parvaresh Rizi et al. (2018) noted that obese men who consumed a high carbohydrate meal had a less favorable postprandial satiety and appetite hormonal response compared to when they consumed either a high fat or a high protein meal. In addition, Ebbeling et al. 2018 reported higher ghrelin and leptin concentrations in people consuming a 60% carbohydrate, 20% fat diet compared to those consuming a 20% carbohydrate, 60% fat diet. Ghrelin is a circulating orexigenic hormone that increases hunger in the short term. Leptin, produced by fat cells, is an endocrine adiposity factors that inhibits appetite while interacting with insulin. However, obese people develop leptin resistance which results in higher amounts of circulating leptin.
7) People who eat high amounts of carbohydrates burn less calories. Low fat, high carbohydrate diets decreased resting energy expenditure (REE) and total energy expenditure (TEE) compared to high fat, low carbohydrate diets (Ebbeling et al. 2012, Ebbeling et al. 2018). Ebbeling et al. (2018) reported a linear trend of an additional 52 kcal/d used for every 10% decrease of carbohydrate to total energy intake. In the same study, people who had high levels of insulin secretion burned even more calories with a high fat diet compared to a high carbohydrate diet.
Similarly, high glycemic load diets had a lower REE than high glycemic load diets (Pereira et al. 2004, Ebbeling et al. 2012). This means that people would use more energy on a lower carbohydrate diet compared to a higher carbohydrate diet. A lower carbohydrate diet is more likely to increase weight loss during dieting and increase energy expenditure during weight maintenance (Ebbeling et al. 2018).
Consuming excess energy can increase mitochondria oxidative stress. From 0.4-4% of the oxygen used by mitochondria is incompletely consumed and results in primary ROS (Murphy 2009). Electrons escaping during electron transfer in the ETC produce ROS. This is more likely to occur in mitochondria when there is a large proton gradient build-up. Large proton gradients occur when energy consumption (NADH production) is excessive or when there is a functional impairment of one of the electron transport complexes (Murphy 2009, Bhatti et al. 2017).
cardiometabolic disorders: a cluster of related risk factors such as high blood pressure, fat around the middle, high triglycerides, weird blood fats and high fasting blood sugar.
*Names and some minor identifying details in all stories in this website are changed to protect people's privacy
I'm not your doctor so this is not medical information. I'm just a person who would like to see you happy and healthy. If you have any questions or concerns about starting an exercise regiment, diet program, or supplements please consult a professional.
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