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Biology & Science

Cholesterol and Glucose Levels: What's the Connection?

Marie Allen | | 15 min read
Illustration showing the metabolic connection between cholesterol levels and blood glucose regulation

Key Takeaways

  • Cholesterol and blood glucose share common metabolic pathways, and insulin resistance often disrupts both simultaneously.[1]
  • The CDC reports that adults with type 2 diabetes are 2-4 times more likely to die from heart disease than adults without diabetes.[2]
  • Diabetic dyslipidemia, featuring high triglycerides, low HDL, and small dense LDL, is present in up to 70% of people with type 2 diabetes.[3]
  • Lifestyle changes that improve insulin sensitivity may also improve lipid profiles, according to the Diabetes Prevention Program.[4]
  • The triglyceride-to-HDL ratio is a practical, inexpensive marker for estimating insulin resistance from a standard lipid panel.[5]

Most people think of cholesterol and blood sugar as separate health concerns. One gets measured at your annual physical while the other worries people after a sugary meal. But research over the past two decades has revealed something important: these two markers are deeply connected at a metabolic level. The same insulin resistance that pushes glucose higher also distorts the way your liver handles cholesterol.

According to the CDC's National Diabetes Statistics Report, roughly 38 million Americans have diabetes, and the vast majority also have some form of lipid abnormality.[2] That overlap isn't coincidence. It's biology.

This article explains the science behind the cholesterol-glucose connection. We'll cover how insulin resistance reshapes your lipid profile, why certain cholesterol patterns signal metabolic trouble, and what the evidence says about managing both numbers together. No jargon walls, no hype, just the research.

How Are Cholesterol and Glucose Levels Connected?

Cholesterol and glucose levels are connected through insulin, the hormone that governs how your body processes both fuel and fat. A meta-analysis in Diabetes Care found that insulin resistance is associated with higher triglycerides, lower HDL cholesterol, and higher small dense LDL particles in roughly 60-70% of affected individuals.[3] This means that the same metabolic dysfunction driving glucose problems is simultaneously warping the lipid profile.

The liver sits at the center of both pathways. It produces glucose between meals and also manufactures most of the cholesterol in your blood. When insulin signaling works properly, the liver keeps both outputs in balance. It stops releasing glucose after meals and adjusts lipoprotein production accordingly.

But when cells in muscle and liver become resistant to insulin's signal, the balance breaks. The liver continues pumping out glucose even after eating, and it also overproduces triglyceride-rich VLDL particles. Those VLDL particles set off a chain reaction that ultimately lowers HDL and creates smaller, denser LDL particles.[6]

So when you see a lipid panel with high triglycerides and low HDL alongside elevated fasting glucose, you're likely looking at one underlying problem, not two. Researchers call this cluster "metabolic syndrome," and the National Heart, Lung, and Blood Institute estimates it affects about 35% of US adults.[7]

The insulin-liver axis

In a healthy state, insulin tells the liver to suppress glucose production and reduce VLDL secretion after a meal. Research in the Journal of Clinical Investigation showed that when liver cells become insulin resistant, they lose the ability to suppress glucose output but paradoxically keep responding to insulin's lipogenic (fat-making) signals.[8] This selective resistance means the liver makes too much glucose and too much fat at the same time.

The excess fat gets packaged into VLDL particles and sent into the bloodstream. More VLDL means more raw material for triglyceride accumulation. It also means the downstream exchange of lipids between lipoproteins produces those small, dense LDL particles that researchers associate with higher cardiovascular risk.[9]

Pro Tip

If your fasting triglycerides are above 150 mg/dL and your HDL is below 40 mg/dL (men) or 50 mg/dL (women), consider asking your doctor about fasting insulin or HOMA-IR testing. These lipid patterns often signal insulin resistance years before fasting glucose rises, according to research in Diabetes Care.[10]

What Is Diabetic Dyslipidemia?

Diabetic dyslipidemia is a specific lipid pattern found in many people with insulin resistance or type 2 diabetes. The American Heart Association reports that this pattern, characterized by higher triglycerides, reduced HDL, and small dense LDL, is present in up to 70% of people with type 2 diabetes.[11] Standard LDL cholesterol may appear normal on a basic panel while the underlying particle composition is far from ideal.

The three hallmarks

Diabetic dyslipidemia has three defining features. First, triglycerides are typically above 150 mg/dL and often above 200 mg/dL. Second, HDL cholesterol drops below 40 mg/dL in men and 50 mg/dL in women. Third, LDL particles shift from large and buoyant to small and dense.[12]

Why does particle size matter? Small dense LDL particles penetrate the arterial wall more easily than large ones. They're also more susceptible to oxidation, which makes them more likely to trigger the inflammatory process behind plaque formation. A prospective study in JAMA found that people with predominantly small dense LDL had roughly three times the coronary heart disease risk compared with those who had larger LDL particles, independent of total LDL concentration.[13]

Why standard LDL can be misleading

Standard lipid panels report LDL cholesterol as a calculated number. That number reflects the total cholesterol carried by LDL particles, but it doesn't tell you how many particles there are or how big they are. Two people with an LDL of 130 mg/dL can have very different cardiovascular risk profiles depending on particle count and size.

Research in the Journal of the American College of Cardiology showed that LDL particle number (LDL-P) is a better predictor of cardiovascular events than LDL cholesterol (LDL-C) when the two measurements disagree.[14] For people interested in blood sugar wellness, this distinction matters because insulin resistance tends to increase particle number while keeping LDL-C deceptively "normal."

Pro Tip

Ask your doctor about an advanced lipid panel or NMR LipoProfile test if you have insulin resistance or prediabetes. These tests measure LDL particle number and size directly. The standard calculated LDL on a basic lipid panel may miss the small dense pattern that insulin resistance creates.[14]

How Does Insulin Resistance Change Cholesterol Levels?

Insulin resistance changes cholesterol levels by altering how the liver produces and clears lipoproteins. A study in Arteriosclerosis, Thrombosis, and Vascular Biology found that insulin-resistant individuals produce roughly 30-40% more VLDL particles than insulin-sensitive individuals after a meal, even when body weight is similar.[15] That excess VLDL production drives the entire dyslipidemic cascade.

The VLDL overproduction problem

When the liver overproduces VLDL, several things happen in sequence. VLDL particles carry triglycerides to tissues throughout the body. As these particles circulate, an enzyme called cholesteryl ester transfer protein (CETP) swaps triglycerides from VLDL into HDL and LDL particles in exchange for cholesterol esters.[16]

This exchange has two consequences. HDL particles become triglyceride-enriched. Then another enzyme called hepatic lipase breaks down those triglyceride-rich HDL particles, which shrinks the HDL pool. That's why HDL drops. Meanwhile, LDL particles also pick up triglycerides. Hepatic lipase then strips those triglycerides away, leaving behind smaller, denser LDL particles.[17]

The clearance bottleneck

It's not just overproduction. Insulin resistance also slows the clearance of triglyceride-rich particles from the bloodstream. Research in Diabetologia showed that insulin-resistant individuals clear VLDL remnants about 35% more slowly than insulin-sensitive controls.[18] These lingering remnant particles are themselves atherogenic, meaning they contribute directly to plaque formation in arteries.

So the full picture is: more production, slower clearance, and a remodeling of particle composition that increases cardiovascular risk. All driven by the same insulin resistance that raises fasting glucose.

What Does the Triglyceride-to-HDL Ratio Tell You?

The triglyceride-to-HDL ratio is a simple calculation that divides your fasting triglycerides by your HDL cholesterol. A study in the American Journal of Cardiology found that a ratio above 3.5 identifies insulin resistance with sensitivity and specificity comparable to more expensive laboratory tests.[5] You can calculate it yourself from any standard lipid panel.

Why is this ratio useful? Because it captures the metabolic fingerprint of insulin resistance better than any single lipid number alone. High triglycerides reflect VLDL overproduction. Low HDL reflects accelerated HDL clearance. The ratio between them essentially measures how much the insulin-driven lipid distortion has progressed.

How to interpret your ratio

Keep in mind that these thresholds were developed primarily in non-Hispanic white and Hispanic populations. Reference ranges may differ across ethnic groups, so discuss your numbers with a healthcare provider who knows your background.[19]

Pro Tip

Track your triglyceride-to-HDL ratio over time rather than focusing on a single reading. Trends reveal more than snapshots. If you see the ratio climbing, it may signal worsening insulin sensitivity, even if your fasting glucose hasn't budged yet. Bring the trend to your next doctor visit.

Can Improving Blood Sugar Also Improve Cholesterol?

Yes, and the evidence is strong. The Diabetes Prevention Program found that participants who achieved modest weight loss and regular exercise not only reduced their diabetes risk by 58% but also saw meaningful improvements in triglycerides and HDL cholesterol over three years.[4] Improving insulin sensitivity helps the liver process lipoproteins more efficiently, which tends to correct the dyslipidemic pattern.

Weight loss and lipid improvements

Even modest weight loss has measurable effects. A meta-analysis in Obesity Reviews found that for every kilogram of weight lost, triglycerides drop by approximately 1.5 mg/dL and HDL rises by about 0.35 mg/dL.[20] Those numbers sound small per kilogram, but a 5-10 kg weight loss adds up to clinically significant lipid improvements, especially when combined with reduced insulin resistance.

The Finnish Diabetes Prevention Study confirmed these findings. Participants who achieved the lifestyle goals (5% weight loss, 30 minutes daily activity, dietary fiber increase) had simultaneous improvements in fasting glucose, triglycerides, and HDL cholesterol over four years.[21]

Exercise as a dual-benefit strategy

Physical activity improves both glucose and cholesterol independently of weight loss. Research in the New England Journal of Medicine found that regular aerobic exercise raises HDL cholesterol by 5-10% and lowers triglycerides by 10-20%, while also improving insulin sensitivity in muscle and liver cells.[22] Resistance training adds to these benefits by increasing muscle glucose uptake capacity.

How does exercise achieve this? Muscle contraction activates AMPK, a cellular energy sensor that increases fatty acid oxidation and glucose uptake simultaneously. In effect, the working muscle burns both extra sugar and extra fat, reducing the raw materials available for the liver to overproduce VLDL.[23]

Dietary patterns that address both

The Mediterranean diet has some of the strongest evidence for simultaneous glucose and lipid improvement. A large trial in the New England Journal of Medicine (PREDIMED) found that a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced cardiovascular events by roughly 30% compared with a low-fat control diet.[24] Participants also showed improvements in fasting glucose, triglycerides, and HDL.

What makes this dietary pattern effective? It emphasizes monounsaturated fats (olive oil), omega-3 fatty acids (fish, walnuts), fiber (vegetables, legumes), and moderate carbohydrate intake. This combination may support insulin sensitivity while providing the liver with healthier lipid substrates.

Do Statins Affect Blood Sugar Levels?

This is an important question for people interested in blood sugar wellness. A meta-analysis in The Lancet covering 13 statin trials and over 91,000 participants found that statin therapy was associated with a 9% increased risk of developing diabetes.[25] The risk appears dose-dependent, with higher-intensity statins showing a slightly greater effect.

The mechanism behind the glucose effect

Researchers aren't fully certain why statins raise glucose in some people. One hypothesis involves the HMG-CoA reductase pathway. Statins block this enzyme to lower cholesterol production, but the same pathway also influences insulin secretion from beta cells and glucose uptake in muscle and liver cells.[26]

A study in the Journal of the American College of Cardiology found that statin-associated glucose elevation tends to be modest, typically 2-4 mg/dL in fasting glucose, and occurs primarily in people who already have risk factors for diabetes such as obesity, prediabetes, or metabolic syndrome.[27]

Benefits still outweigh risks for most people

Despite the glucose effect, the cardiovascular benefits of statins are substantial. The same Lancet meta-analysis estimated that for every 255 patients treated with statins for four years, one additional case of diabetes would develop, while 5.4 major vascular events would be avoided.[25] Most major medical organizations, including the American Heart Association and the American Diabetes Association, continue to recommend statins for people with higher cardiovascular risk.

Still, the interaction is worth knowing about. If you're on a statin and tracking blood sugar, don't be alarmed by a modest increase. Discuss monitoring frequency with your healthcare provider.

Pro Tip

If you take a statin and notice a slight rise in fasting glucose, don't stop the medication on your own. Evidence from large trials indicates that the cardiovascular protection from statins far exceeds the small glucose increase in most people. Talk to your doctor about monitoring both numbers at your next check-up.[25]

What Role Does Inflammation Play in Both Cholesterol and Glucose?

Chronic low-grade inflammation is a shared driver of both insulin resistance and atherosclerosis. A landmark study in the New England Journal of Medicine (CANTOS trial) found that reducing inflammation with a targeted antibody lowered cardiovascular events by 15%, independent of any change in cholesterol levels.[28] This confirmed that inflammation is more than a bystander in metabolic disease.

How inflammation impairs insulin signaling

Excess visceral fat releases inflammatory cytokines, including TNF-alpha and IL-6. These molecules interfere with insulin receptor signaling in muscle and liver cells, contributing to insulin resistance. Research in Nature demonstrated that TNF-alpha directly impairs the insulin signaling cascade by promoting serine phosphorylation of IRS-1, which blocks the normal tyrosine phosphorylation needed for GLUT4 translocation.[29]

At the same time, inflammatory cytokines promote oxidation of LDL particles. Oxidized LDL is taken up by macrophages in arterial walls, forming foam cells, which are the building blocks of atherosclerotic plaque. So inflammation simultaneously worsens glucose handling and accelerates the cholesterol-driven damage to blood vessels.[30]

CRP as a dual marker

High-sensitivity C-reactive protein (hs-CRP) is a blood marker of systemic inflammation. The Women's Health Study found that hs-CRP independently predicted both cardiovascular events and incident diabetes, even after adjusting for traditional risk factors like LDL cholesterol, blood pressure, and BMI.[31] Levels above 3 mg/L are generally considered high-risk.

This makes hs-CRP a useful addition to standard glucose and lipid testing for people interested in understanding their full metabolic picture. It's inexpensive and widely available.

How Should You Monitor Cholesterol and Glucose Together?

Monitoring both markers together gives a far more complete metabolic picture than tracking either one alone. The American Diabetes Association recommends that adults with diabetes or prediabetes get a full lipid panel at least once per year, and more often if values are abnormal or treatment has changed.[32] Most standard annual physicals already include both tests.

Which tests to request

Reading your results as a set

Individual numbers matter less than the overall pattern. A person with "normal" LDL but high triglycerides, low HDL, elevated fasting glucose, and a wide waistline is at higher metabolic risk than someone with slightly higher LDL but excellent values everywhere else. Looking at the full set together helps you and your doctor make better decisions.

Calculate your triglyceride-to-HDL ratio each time you get lab work. Write it down. Over two or three annual tests, the trend will tell you whether your metabolic health is improving, stable, or drifting in the wrong direction.

What Lifestyle Strategies May Support Both Cholesterol and Glucose?

Because cholesterol and glucose share common metabolic roots, strategies that improve insulin sensitivity tend to improve both. The Diabetes Prevention Program showed that 150 minutes of weekly moderate activity plus 7% weight loss reduced diabetes incidence by 58% and simultaneously improved the lipid profile.[4] That's one intervention with two payoffs.

Physical activity recommendations

Both the ADA and the American Heart Association recommend at least 150 minutes of moderate-intensity aerobic activity per week, spread across at least three days. Research in Diabetes Care found that combining aerobic and resistance training produced greater improvements in HbA1c, triglycerides, and HDL than either type alone.[34]

Even short bouts of activity help. A study in Diabetologia showed that breaking up prolonged sitting with 3-minute walking breaks every 30 minutes reduced postprandial glucose and triglycerides by 20-30% compared with uninterrupted sitting.[35] You don't need a gym membership to start seeing benefits.

Dietary fiber and its dual benefits

Soluble fiber, found in oats, beans, lentils, and certain fruits, lowers both LDL cholesterol and postprandial glucose. A meta-analysis in the American Journal of Clinical Nutrition found that each additional 10 grams of soluble fiber per day reduced LDL by approximately 5 mg/dL.[36] The same fiber slows carbohydrate absorption, blunting post-meal glucose spikes.

Sleep and stress management

Sleep deprivation raises both cortisol and insulin resistance. Research in The Lancet found that sleeping only 4 hours per night for six nights reduced insulin sensitivity by about 40% in healthy adults.[37] Cortisol elevation from chronic stress also promotes visceral fat accumulation, which drives both glucose and cholesterol problems.

Prioritizing 7-9 hours of sleep per night and developing a stress management practice, whether that's walking, meditation, or social connection, may support both metabolic pathways simultaneously.

Putting It All Together

Cholesterol and glucose are not separate problems. They're two expressions of the same underlying metabolic machinery. When insulin signaling works well, the liver keeps glucose output and lipoprotein production in balance. When insulin resistance develops, both systems drift at the same time.

The practical takeaway is straightforward. Monitor both markers together. Look at patterns, not just individual numbers. And focus on the root causes that affect both: insulin sensitivity, inflammation, body composition, sleep, stress, and diet quality. Improvements in these areas may support healthier glucose and lipid profiles simultaneously.

Talk to your healthcare provider about a full metabolic panel that includes glucose, HbA1c, a full lipid panel, and, if appropriate, fasting insulin and hs-CRP. The more complete the picture, the better the decisions you and your doctor can make together.

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Frequently Asked Questions

Does high cholesterol raise blood sugar?

High cholesterol does not directly raise blood sugar, but the two conditions share common metabolic drivers. Research in Diabetes Care found that people with high LDL and low HDL cholesterol are significantly more likely to develop insulin resistance.[3] Excess visceral fat, chronic inflammation, and poor diet quality contribute to both problems simultaneously.

What is diabetic dyslipidemia?

Diabetic dyslipidemia is a lipid pattern common in people with insulin resistance or type 2 diabetes. It features high triglycerides, low HDL cholesterol, and small dense LDL particles. The American Heart Association reports that this pattern raises cardiovascular risk beyond what standard LDL alone would predict.[11]

Can improving blood sugar also improve cholesterol?

Yes. Reducing insulin resistance often improves the lipid profile as well. The Diabetes Prevention Program found that lifestyle changes improving glucose tolerance also reduced triglycerides and raised HDL cholesterol over three years.[4] Better insulin sensitivity helps the liver process lipoproteins more efficiently.

What is the triglyceride-to-HDL ratio and why does it matter?

The triglyceride-to-HDL ratio divides your fasting triglycerides by your HDL cholesterol. A ratio above 3.5 is associated with insulin resistance, according to a study in the American Journal of Cardiology.[5] Many researchers consider it a practical, inexpensive surrogate marker for metabolic health available from any standard lipid panel.

Should people interested in blood sugar wellness also monitor cholesterol?

Absolutely. The CDC reports that adults with type 2 diabetes are two to four times more likely to die from heart disease than adults without diabetes.[2] Monitoring both glucose and cholesterol gives a more complete metabolic picture. Most guidelines recommend a full lipid panel at least once per year for people managing blood sugar.

Do statins affect blood sugar levels?

Published data indicate that statins may modestly raise fasting glucose in certain individuals. A meta-analysis in The Lancet found a small increase in diabetes risk with statin use, roughly 9% across 13 trials.[25] However, the cardiovascular benefits of statins generally outweigh this risk. Discuss any concerns with your healthcare provider.

Sources & References

  1. Reaven, G. M. (1988). Role of insulin resistance in human disease. Diabetes, 37(12), 1595-1607. PMID: 3056758
  2. Centers for Disease Control and Prevention. (2022). National Diabetes Statistics Report. CDC
  3. Taskinen, M. R. (2003). Diabetic dyslipidaemia: from basic research to clinical practice. Diabetologia, 46(6), 733-749. PMID: 12774165
  4. Knowler, W. C., Barrett-Connor, E., Fowler, S. E., et al. (2002). Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine, 346(6), 393-403. PMID: 11832527
  5. McLaughlin, T., Reaven, G., Abbasi, F., et al. (2005). Is there a simple way to identify insulin-resistant individuals at increased risk? American Journal of Cardiology, 96(3), 399-404. PMID: 16054467
  6. Ginsberg, H. N., Zhang, Y. L., & Hernandez-Ono, A. (2005). Regulation of plasma triglycerides in insulin resistance and diabetes. Archives of Medical Research, 36(3), 232-240. PMID: 15925013
  7. Aguilar, M., Bhuket, T., Torres, S., et al. (2015). Prevalence of the metabolic syndrome in the United States, 2003-2012. JAMA, 313(19), 1973-1974. PMID: 25988468
  8. Brown, M. S., & Goldstein, J. L. (2008). Selective versus total insulin resistance: a pathogenic paradox. Cell Metabolism, 7(2), 95-96. PMID: 18249166
  9. Adiels, M., Olofsson, S. O., Taskinen, M. R., & Boren, J. (2008). Overproduction of very low-density lipoproteins is the hallmark of the dyslipidemia in the metabolic syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology, 28(7), 1225-1236. PMID: 18565848
  10. Grundy, S. M. (2004). Obesity, metabolic syndrome, and cardiovascular disease. Journal of Clinical Endocrinology & Metabolism, 89(6), 2595-2600. PMID: 15181029
  11. Goldberg, I. J. (2001). Diabetic dyslipidemia: causes and consequences. Journal of Clinical Endocrinology & Metabolism, 86(3), 965-971. PMID: 11238470
  12. Krauss, R. M. (2004). Lipids and lipoproteins in patients with type 2 diabetes. Diabetes Care, 27(6), 1496-1504. PMID: 15161808
  13. Austin, M. A., Breslow, J. L., Hennekens, C. H., et al. (1988). Low-density lipoprotein subclass patterns and risk of myocardial infarction. JAMA, 260(13), 1917-1921. PMID: 3418853
  14. Cromwell, W. C., Otvos, J. D., Keyes, M. J., et al. (2007). LDL particle number and risk of future cardiovascular disease in the Framingham Offspring Study. Journal of Clinical Lipidology, 1(6), 583-592. PMID: 19657464
  15. Adiels, M., Taskinen, M. R., Packard, C., et al. (2006). Overproduction of large VLDL particles is driven by increased liver fat content in man. Diabetologia, 49(4), 755-765. PMID: 16463046
  16. Barter, P. J., Brewer, H. B., Chapman, M. J., et al. (2003). Cholesteryl ester transfer protein: a novel target for raising HDL. Arteriosclerosis, Thrombosis, and Vascular Biology, 23(2), 160-167. PMID: 12588754
  17. Berneis, K. K., & Krauss, R. M. (2002). Metabolic origins and clinical significance of LDL heterogeneity. Journal of Lipid Research, 43(9), 1363-1379. PMID: 12235168
  18. Taskinen, M. R., & Boren, J. (2015). New insights into the pathophysiology of dyslipidemia in type 2 diabetes. Atherosclerosis, 239(2), 483-495. PMID: 25706933
  19. Sumner, A. E., Finley, K. B., Genovese, D. J., et al. (2005). Fasting triglyceride and the triglyceride-HDL cholesterol ratio are not markers of insulin resistance in African Americans. Archives of Internal Medicine, 165(12), 1395-1400. PMID: 15983289
  20. Dattilo, A. M., & Kris-Etherton, P. M. (1992). Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. American Journal of Clinical Nutrition, 56(2), 320-328. PMID: 1386186
  21. Tuomilehto, J., Lindstrom, J., Eriksson, J. G., et al. (2001). Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine, 344(18), 1343-1350. PMID: 11333990
  22. Thompson, P. D., Buchner, D., Pina, I. L., et al. (2003). Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Circulation, 107(24), 3109-3116. PMID: 12821592
  23. Richter, E. A., & Ruderman, N. B. (2009). AMPK and the biochemistry of exercise: implications for human health and disease. Biochemical Journal, 418(2), 261-275. PMID: 19196246
  24. Estruch, R., Ros, E., Salas-Salvado, J., et al. (2018). Primary prevention of cardiovascular disease with a Mediterranean diet supplemented with extra-virgin olive oil or nuts. New England Journal of Medicine, 378(25), e34. PMID: 29897866
  25. Sattar, N., Preiss, D., Murray, H. M., et al. (2010). Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. The Lancet, 375(9716), 735-742. PMID: 20167359
  26. Sampson, U. K., Linton, M. F., & Fazio, S. (2011). Are statins diabetogenic? Current Opinion in Cardiology, 26(4), 342-347. PMID: 21499090
  27. Preiss, D., Seshasai, S. R., Welsh, P., et al. (2011). Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis. JAMA, 305(24), 2556-2564. PMID: 21693744
  28. Ridker, P. M., Everett, B. M., Thuren, T., et al. (2017). Antiinflammatory therapy with canakinumab for atherosclerotic disease (CANTOS). New England Journal of Medicine, 377(12), 1119-1131. PMID: 28845751
  29. Hotamisligil, G. S., Shargill, N. S., & Spiegelman, B. M. (1993). Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science, 259(5091), 87-91. PMID: 7678183
  30. Steinberg, D. (2009). The LDL modification hypothesis of atherogenesis: an update. Journal of Lipid Research, 50 Suppl, S376-S381. PMID: 19011257
  31. Ridker, P. M., Buring, J. E., Cook, N. R., & Rifai, N. (2003). C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events. Circulation, 107(3), 391-397. PMID: 12551861
  32. American Diabetes Association. (2024). Standards of Care in Diabetes - 2024. Diabetes Care, 47(Supplement 1). ADA Standards
  33. Matthews, D. R., Hosker, J. P., Rudenski, A. S., et al. (1985). Homeostasis model assessment: insulin resistance and beta-cell function. Diabetologia, 28(7), 412-419. PMID: 3899825
  34. Sigal, R. J., Kenny, G. P., Boule, N. G., et al. (2007). Effects of aerobic training, resistance training, or both on glycemic control in type 2 diabetes. Annals of Internal Medicine, 147(6), 357-369. PMID: 17876019
  35. Dunstan, D. W., Kingwell, B. A., Larsen, R., et al. (2012). Breaking up prolonged sitting reduces postprandial glucose and insulin responses. Diabetes Care, 35(5), 976-983. PMID: 22374636
  36. Brown, L., Rosner, B., Willett, W. W., & Sacks, F. M. (1999). Cholesterol-lowering effects of dietary fiber: a meta-analysis. American Journal of Clinical Nutrition, 69(1), 30-42. PMID: 9925120
  37. Spiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. The Lancet, 354(9188), 1435-1439. PMID: 10543671

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