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Diet and nutrition

High insulin — is it more harmful than sugar?

Sources: 14 · Article: 14 233 characters

Ewa Dąbrowska points out that insulin may worsen atherosclerosis, and that insulin levels can be high even when glucose levels are normal.

  • When cells respond poorly to insulin, the pancreas may produce more of it, while sugar remains in the blood.

What the authors write

Ewa Dąbrowska

Insulin may worsen atherosclerosis and other vascular complications.

„If fat builds up in the liver and muscles, insulin cannot effectively “open the door” for glucose—it stays in the blood. As a result, blood sugar levels rise, and the pancreas produces more and more insulin to “push” excess glucose into cells so it can be burned. Insulin may worsen atherosclerosis and other vascular complications.”Jeśli dochodzi do stłuszczenia wątroby i mięśni, insulina nie jest w stanie skutecznie „otworzyć drzwi” dla glukozy – ta pozostaje we krwi. W efekcie poziom cukru wzrasta, a trzustka produkuje coraz więcej insuliny, aby „wcisnąć” nadmiary glukozy do komórek celem jej spalenia. Insulina może nasilać miażdżycę i inne powikłania naczyniowe.
Schorzenia i świadectwa
Ewa Dąbrowska

Diabetes can persist for a long time with normal glucose levels but consistently elevated insulin levels.

„Diabetes can remain hidden for years, with normal glucose levels but consistently elevated insulin levels. Even healthy fats, such as vegetable oils, can worsen insulin resistance if consumed in excess. Natural carbohydrates, such as fruit—even sweet fruit—or potatoes, do not cause insulin resistance, as long as they are not accompanied by excess fat.”Cukrzyca może latami przebiegać skrycie – z prawidłowym poziomem glukozy, ale stale podwyższonym poziomem insuliny. Nawet zdrowe tłuszcze, np. oleje roślinne, mogą nasilać insulinooporność, jeśli są spożywane w nadmiarze. Z kolei naturalne węglowodany, takie jak owoce, nawet słodkie, czy ziemniaki, nie powodują insulinooporności – o ile nie towarzyszy im nadmiar tłuszczu.
Dieta warzywno owocowa
Bracia Rodzeń

Bracia Rodzeń link higher carbohydrate intake and increased insulin levels with weight gain and metabolic diseases.

„The more carbohydrates your food contains, the faster and more weight you will gain, and the more likely you are to develop insulin resistance and other metabolic diseases. obesity/insulin resistance, metabolic diseases (type 2 diabetes, fatty liver, high blood pressure, PCOS, numerous cancers).”Im więcej węglowodanów w Twoich pokarmach, tym szybciej i bardziej przytyjesz, zachorujesz na insulinooporność i inne choroby metaboliczne. otyłość/insulinooporność, choroby metaboliczne (cukrzyca typu 2, stłuszczenie wątroby, nadciśnienie tętnicze, PCOS, liczne nowotwory).
Bracia Rodzeń
Hubert Czerniak

In type 2 diabetes, the pancreas may produce more and more insulin to maintain normal glucose levels.

„To keep blood glucose within the normal range, the pancreas has to produce more and more insulin. After a few years, the pancreatic ß cells become exhausted and produce less and less insulin. Blood glucose levels rise, leading to a diagnosis of type 2 diabetes.”Aby utrzymać stężenie glukozy we krwi w normie, trzustka musi produkować coraz więcej insuliny. Po paru latach komórki ß trzustki ulegają wyczerpaniu i produkują coraz mniej insuliny. Stężenie glukozy we krwi ulega zwiększeniu, co prowadzi do rozpoznania cukrzycy typu 2.
Cukrzyca na widelcu. Część 1.
Hubert Czerniak

In type 2 diabetes, the pancreas may produce more and more insulin before its cells become exhausted and blood glucose levels rise.

„To keep blood glucose within the normal range, the pancreas has to produce more and more insulin. After a few years, the pancreatic ß cells become exhausted and produce less and less insulin. Blood glucose levels rise, leading to a diagnosis of type 2 diabetes.”Aby utrzymać stężenie glukozy we krwi w normie, trzustka musi produkować coraz więcej insuliny. Po paru latach komórki ß trzustki ulegają wyczerpaniu i produkują coraz mniej insuliny. Stężenie glukozy we krwi ulega zwiększeniu, co prowadzi do rozpoznania cukrzycy typu 2.
Cukrzyca na widelcu. Część 1.
Nathan S. Bryan

Nathan S. Bryan points out that high insulin combined with high glucose drives inflammation and chronic disease.

„High levels of insulin combined with elevated glucose is what drives inflammation and chronic disease. The cell becomes resistant and unresponsive to the instructions given to the cell by insulin. The disruption is because the cell has lost its ability to produce nitric oxide which is part of the signal that tells the cell to bring in glucose and use it as energy or store it as glycogen.”High levels of insulin combined with elevated glucose is what drives inflammation and chronic disease. The cell becomes resistant and unresponsive to the instructions given to the cell by insulin. The disruption is because the cell has lost its ability to produce nitric oxide which is part of the signal that tells the cell to bring in glucose and use it as energy or store it as glycogen.
Sugar, Diabetes and Nitric Oxide: Complex Biochemistry, Simple Solutions - Dr. Nathan Bryan - Molecular medicine and nitric oxide biochemistry
prof. David Ludwig

In obesity and with high insulin, blood fat and glucose levels may be normal or elevated because insulin is less effective.

„Blood levels of fat and glucose tend to be normal or elevated in people with obesity and high insulin, not lower (6, 7, 8). That’s because they’re insulin resistant, meaning that insulin isn’t doing its job of constraining blood glucose and fat levels as effectively.”Blood levels of fat and glucose tend to be normal or elevated in people with obesity and high insulin, not lower (6, 7, 8). That’s because they’re insulin resistant, meaning that insulin isn’t doing its job of constraining blood glucose and fat levels as effectively.
Ludwig Responds to Whole Health Source Article

Research from PubMed · Europe PMC

We selected 5 studies with the best, positive results. This is a selection, not a full review of all research.

Total number of studies on this topic in PubMed: 145 913.

The review indicates that excess insulin may be linked to adverse effects, but evidence of harm to the heart in humans is limited and should be interpreted with caution.

Aim of the study: The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure.

Results: Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia? · Curr Vasc Pharmacol 2020
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

The article describes how high insulin levels can maintain normal blood sugar, while being associated with an unfavorable lipid profile and a risk of cardiovascular disease.

Aim of the study: The ability of insulin to stimulate glucose disposal varies sixfold to eightfold among apparently healthy individuals. The only way that insulin-resistant persons can prevent the development of type 2 diabetes is by secreting the increased amount of insulin that is necessary to compensate for the resistance to insulin action.

Results: Although compensatory hyperinsulinemia may prevent the development of fasting hyperglycemia in insulin-resistant individuals, the price paid is the untoward physiologic effects of increased circulating insulin concentrations on tissues that retain normal insulin sensitivity. This article focused on the interplay between insulin resistance at the level of the muscle and adipose tissue and normal hepatic insulin sensitivity; this leads to the atherogenic lipoprotein profile that is characteristic of insulin-resistant individuals. It would be inappropriate to minimize the importance of differential insulin sensitivity in the genesis of the changes in lipoprotein metabolism that increase CVD risk in insulin-resistant persons.

Compensatory hyperinsulinemia and the development of an atherogenic lipoprotein profile: the price paid to maintain glucose homeostasis in insulin-resistant individuals. · Endocrinol Metab Clin North Am 2005
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

People with high insulin but normal glucose tolerance had insulin resistance similar to that of people with impaired glucose tolerance or diabetes.

Aim of the study: To evaluate the differences in insulin resistance (IR) among subjects with normal glucose tolerance (NGT), hyperinsulinemia with NGT (HINS), impaired glucose tolerance (IGT), and newly diagnosed type 2 diabetes mellitus (T2DM).

Results: The M values of NGT, HINS, IGT, and T2DM groups were 11.88 ± 2.93 mg · kg(-1) · min(-1), 6.23 ± 1.73 mg · kg(-1) · min(-1), 6.37 ± 2.12 mg · kg(-1) · min(-1), and 6.19 ± 1.89 mg · kg(-1) · min(-1), respectively. M values in HINS, IGT, and T2DM groups were lower than those in the NGT group (P = 0.005); however, the differences among the HINS, IGT, and T2DM groups were not statistically significant (P = 0.835). The independent factors influencing the M value were waistline and fasting insulin level (FINS). The simple insulin sensitivity indices, especially Matsuda and Gutt index, were significantly associated with the M value (P < 0.01). IR existed in the HINS, IGT, and T2DM groups, and IR levels were consistent in the three groups. The independent factors influencing IR were waistline and FINS.

Assessment of Insulin Resistance in Subjects with Normal Glucose Tolerance, Hyperinsulinemia with Normal Blood Glucose Tolerance, Impaired Glucose Tolerance, and Newly Diagnosed Type 2 Diabetes (Prediabetes Insulin Resistance Research). · J Diabetes Res 2016
Money for the studynot stated
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studyobservation of people

“Not stated” does not mean nobody paid — the database does not always record it.

In this small group of people with normal glucose tolerance, no clear link was found between high insulin and elevated blood pressure.

Aim of the study: A possible link between hyperinsulinemia and blood pressure was studied in non-obese subjects with normal glucose tolerance. First, the responses in plasma glucose and serum insulin to an oral glucose load (75-g oral glucose tolerance test) were compared between 42 patients with essential hypertension and 93 normotensive control subjects.

Results: of the mean), individually matched for age, sex, and body mass index. Plasma glucose and serum insulin responses to the glucose load in hypertensive subjects were identical to the respective responses in normotensive subjects, while the mean total serum cholesterol level was slightly higher (p less than 0.05) in hypertensive subjects. The respective values for systolic and diastolic blood pressures, and total serum cholesterol and triglycerides concentrations were comparable in hyperinsulinemic and normoinsulinemic subjects. These results did not suggest a close association between hyperinsulinemia and elevated blood pressure in non-obese middle-aged Japanese subjects with normal glucose tolerance.

Hyperinsulinemia and blood pressure in non-obese middle-aged subjects with normal glucose tolerance. · Tohoku J Exp Med 1991
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyobservation of people

“Not stated” does not mean nobody paid — the database does not always record it.

In a mouse study, exposure during pregnancy to high insulin with normal glucose levels was associated with transient glucose intolerance in male offspring.

Aim of the study: Fetal in-utero exposures are known to impact the long-term metabolic health of offspring. Insulin is the primary treatment to manage glucose concentrations in mothers with gestational diabetes.

Results: Both male βAkt-HIP and βTSC2KO-HIP offspring exhibited transient glucose intolerance at 6-8 weeks of age relative to the age-matched controls. Glucose homeostasis remained unaffected in female offspring of both models under NCD and HFD relative to controls. Maternal hyperinsulinemia without obesity, regardless of the presence of hypoglycemia, does not significantly impair glucose homeostasis in offspring. However, when hyperinsulinemia is accompanied by insulin resistance, it results in increased body weight in male offspring, a known risk factor for type 2 diabetes.

In-utero exposure to maternal hyperinsulinemia impacts glucose homeostasis in male offspring transiently. · J Dev Orig Health Dis 2026
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyanimal study

“Not stated” does not mean nobody paid — the database does not always record it.

Perspectives and opinion materials

The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.

Orthomolecular Medicine News Service Opinion material
„4.1 Niacin is always embedded in a low-insulin metabolic context In IOM practice, niacin is introduced only within a metabolic terrain characterized by: A low-carbohydrate or ketogenic dietary baseline Suppressed chronic hyperinsulinemia Reduced post-prandial glucose excursions Under these conditions, the biochemical drivers of niacin-associated IR signaling-namely high insulin + high glucose + impaired fatty-acid handling-are absent. 👉 Niacin amplifies the existing metabolic state. 👉 In a low-insulin terrain, NAD⁺ repletion and lipid-signaling benefits dominate.”4.1 Niacin is always embedded in a low-insulin metabolic context In IOM practice, niacin is introduced only within a metabolic terrain characterized by: A low-carbohydrate or ketogenic dietary baseline Suppressed chronic hyperinsulinemia Reduced post-prandial glucose excursions Under these conditions, the biochemical drivers of niacin-associated IR signaling-namely high insulin + high glucose + impaired fatty-acid handling-are absent. 👉 Niacin amplifies the existing metabolic state. 👉 In a low-insulin terrain, NAD⁺ repletion and lipid-signaling benefits dominate.
Niacin, NAD⁺, and Insulin Resistance
Orthomolecular Medicine News Service Opinion material
„From an IOM Systems Medicine perspective, one major problem in the modern industrialized dietary environment is that many individuals gradually lose this metabolic flexibility due to: chronic hyperinsulinemia, continuous feeding patterns, ultra-processed foods, excessive refined carbohydrate intake, physical inactivity, circadian disruption, and persistent dependence on frequent glucose intake. Over time, this may impair the body's ability to efficiently access stored fat for energy. Many individuals therefore become increasingly dependent on frequent carbohydrate intake simply to maintain perceived energy stability.”From an IOM Systems Medicine perspective, one major problem in the modern industrialized dietary environment is that many individuals gradually lose this metabolic flexibility due to: chronic hyperinsulinemia, continuous feeding patterns, ultra-processed foods, excessive refined carbohydrate intake, physical inactivity, circadian disruption, and persistent dependence on frequent glucose intake. Over time, this may impair the body's ability to efficiently access stored fat for energy. Many individuals therefore become increasingly dependent on frequent carbohydrate intake simply to maintain perceived energy stability.
What Are Humans Designed to Eat? Metabolic Flexibility, Energetic Resilience, and the Modern Food Environment
Orthomolecular Medicine News Service Opinion material
„Hyperinsulinemia has been associated epidemiologically with increased cancer progression risk, and insulin receptor/IGF signaling components are expressed across a broad spectrum of tumor types. Unlike mutation-restricted targets, insulin signaling is a systemic growth-regulatory axis affecting both tumor cells and the tumor microenvironment. Ketogenic metabolic therapy reduces circulating insulin levels - often by 30-50% or more in insulin-resistant individuals - and lowers glucose availability while increasing ketone bodies.”Hyperinsulinemia has been associated epidemiologically with increased cancer progression risk, and insulin receptor/IGF signaling components are expressed across a broad spectrum of tumor types. Unlike mutation-restricted targets, insulin signaling is a systemic growth-regulatory axis affecting both tumor cells and the tumor microenvironment. Ketogenic metabolic therapy reduces circulating insulin levels - often by 30-50% or more in insulin-resistant individuals - and lowers glucose availability while increasing ketone bodies.
Targeted Therapy at the Wrong Biological Level: A Systems Reassessment of Cancer Targeting

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