Insulin has a team that pushes back, as puberty and pregnancy show

Key takeaways

• In lab tests of 357 healthy children ages 10 to 14, insulin resistance rose as puberty began, peaked midway and fell back near childhood levels by the end¹.
• Late in a normal pregnancy, the body responds to insulin about half as well as before, and the pancreas raises its insulin output by 200% to 250% to keep blood sugar normal⁴.
• Gestational diabetes affects 5% to 9% of U.S. pregnancies each year; testing usually happens at 24 to 28 weeks, and about half of those women later get type 2 diabetes⁶.
• During serious illness, stress hormones push blood sugar up on purpose, and in one major intensive-care trial, forcing it tightly down was tied to more deaths, not fewer⁸.
• In the main analysis of a 2020 trial, a year of nasal insulin did no better than a placebo for 240 people with mild cognitive impairment or Alzheimer’s, and “type 3 diabetes” remains a research idea, not a diagnosis¹³¹⁴.

In a study published in 1999, University of Minnesota researchers put 357 healthy children, ages 10 to 14, through a demanding lab test called a clamp¹. It measures how well the body responds to insulin, the hormone that helps move sugar from the blood into cells¹⁸.

The results traced an arc. Insulin resistance, a weaker response to insulin, climbed as soon as puberty began. It peaked in mid-puberty, then eased back toward childhood levels by the end¹. Girls were more resistant than boys at every stage¹.

Nothing was wrong with these children. Their bodies were doing what growing bodies do.

Pregnancy runs the same play on a bigger scale. By late pregnancy, a healthy mother’s body responds to insulin about half as well as it did before⁴⁵.

Both stories carry one lesson. Insulin never works alone. A team of other hormones pushes blood sugar the other way, and the balance shifts at predictable points in life. This guide covers how that team works, and what happens when the balance tips too far.

One hormone lowers blood sugar, and several push it up

Insulin is the body’s main sugar-lowering hormone. The hormones that raise blood sugar are often called counter-regulatory hormones, because they counter insulin. A 2018 review in the British Journal of Hospital Medicine describes what each one does⁸:

• Glucagon comes from the pancreas. Under stress, adrenaline spurs its release, and it drives the liver to make new sugar.
• Adrenaline, also called epinephrine, comes from the adrenal glands. It blocks insulin release and stirs up glucagon.
• Cortisol, another adrenal hormone, pushes the liver to make sugar and breaks down protein to supply the raw material.
• Growth hormone, from the pituitary gland at the base of the brain, blunts insulin’s effect on the body’s tissues.

Insulin has an ally, too. GLP-1, a hormone the gut releases after eating, boosts insulin release when blood sugar is up and holds glucagon back¹¹.

Our article on blood sugar numbers explains how these hormones respond within minutes when sugar drops. This article looks at slower shifts that last weeks, months or years.

Puberty makes healthy teens insulin resistant for a few years

In the Minnesota study, insulin resistance rose at the first stage of puberty and peaked at the middle stage in both girls and boys¹. By the end of puberty, it had dropped back near childhood levels¹.

A smaller study followed nine healthy, normal-weight children from before puberty into it, as reported in Pediatric Research in 2006². Their insulin sensitivity fell by about half, and their insulin output roughly doubled to make up for it². Changes in body fat didn’t explain the drop². The researchers pointed to a likely driver: the surge of growth hormone that fuels the growth spurt².

Growth hormone works as a pair with IGF-1, short for insulin-like growth factor 1. Scientists call the two the GH/IGF-1 axis³. In a later Minnesota analysis of 342 children and teens, IGF-1 rose and fell across puberty in the same pattern as insulin resistance³. The authors concluded the axis is an important contributor, though a matching pattern isn’t proof of cause³.

Body size mattered, too. Insulin resistance tracked with weight and waist size, though fat didn’t fully explain the puberty bump¹. So for most teens, this is a normal, temporary phase, but for a teen with other risk factors, it adds to the load. Our insulin resistance article lists those risk factors.

Pregnancy turns down insulin’s effect to feed the baby

In pregnancy, insulin resistance has a clear job. A 2019 review in the Journal of Diabetes Research describes it as an evolved way to limit the mother’s own use of glucose, so more sugar reaches the growing baby⁵.

The shift climbs sharply in the second half of pregnancy, and insulin sensitivity falls by 50% to 60%⁵. To keep up, the mother’s pancreas raises insulin output by 200% to 250%, according to a 2007 review in Diabetes Care⁴.

The placenta drives much of this. By about week 20, a growth hormone made by the placenta has nearly replaced the mother’s own, at roughly 10 times the usual level⁵. Researchers have also blamed other placental and maternal hormones, but the 2019 review concluded that no single hormone explains the shift⁵.

The effect ends fast. Many placental hormones break down quickly, and their effects are gone within 24 to 48 hours after delivery⁵. Women with type 1 diabetes see this in their own insulin needs, which rise about 70% on average during pregnancy and drop toward pre-pregnancy levels, or lower, within a day or two of birth⁵.

When the pancreas can’t keep up

If the pancreas can’t make enough extra insulin, blood sugar rises and gestational diabetes develops. The CDC says pregnancy hormones and weight gain both make cells respond less to insulin, and some women had insulin resistance before pregnancy⁶.

Gestational diabetes affects 5% to 9% of U.S. pregnancies each year⁶. It usually shows up around week 24, so testing typically happens between weeks 24 and 28, or earlier for people at higher risk⁶⁷. The usual first test is a sweet drink without fasting, with blood drawn an hour later; a result of 140 or higher may lead to a longer, fasting test⁷.

Most women with gestational diabetes return to normal blood sugar soon after birth⁴. But about half later develop type 2 diabetes, the CDC says⁶. Later articles in this series cover eating, activity and supplements in pregnancy.

A note on funding: the 2007 review drew on NIH grants, and the workshop that produced it also had an unrestricted educational grant from LifeScan, then a Johnson & Johnson company⁴.

Serious illness raises blood sugar on purpose

Severe infection, injury and burns switch on the body’s stress systems. Cortisol and adrenaline surge, growth hormone changes its rhythm, and inflammatory messengers called cytokines jam insulin’s signals⁸.

The result is stress hyperglycemia, a temporary rise in blood sugar during acute illness. In people without known diabetes, the 2018 review defines it as any reading above 7.8 mmol/L, about 140 mg/dL by our math⁸.

The review calls this rise protective in many cases. It sends fuel to the immune system and the brain, and glucose is the main fuel for macrophages, immune cells that swallow germs⁸. How high it goes and how long it lasts decide whether it helps or harms⁸.

That’s why hospitals don’t simply force blood sugar back to normal. The review summarizes a large intensive-care trial called NICE-SUGAR.

Among patients whose sugar was held tightly down, 27.5% died within 90 days, compared with 24.9% of those given looser control⁸. A later analysis of the same trial, as the review reports it, found low blood sugar in 6.9% of the tight-control group and 0.5% of the others⁸. By our math, that’s about 26 more deaths for every 1,000 patients.

A high reading in the hospital can still be a warning. In one study cited by the review, 60% of patients admitted with newly found high blood sugar had diabetes confirmed a year later⁸.

The same hormones explain sick-day rules

For people with diabetes, ordinary illness can tip blood sugar too high. The CDC lists illness, injury, heart attack or stroke, and some medicines, including corticosteroids, among the triggers of diabetic ketoacidosis, a dangerous buildup of acids called ketones⁹. It advises taking medicines as prescribed and asking your doctor how to adjust insulin when you’re sick⁹. Our blood sugar article lists the CDC’s sick-day checks.

Glucocorticoids, steroid medicines that work like cortisol, increase the liver’s sugar output and cause insulin resistance¹⁰. If you take one long term, ask your prescriber whether your blood sugar should be checked. Don’t stop or change a steroid on your own.

Sometimes the problem is too much insulin

Insulinoma. This is a tumor of the pancreas cells that make insulin. It’s rare, about 4 new cases per million people each year, and about 9 in 10 are not cancer¹⁰. Because the tumor keeps releasing insulin, blood sugar crashes during fasting, and some people learn to ward off spells by eating more often¹⁰. A supervised fast of up to 72 hours diagnoses more than 95% of cases, and surgery cures the great majority of the benign ones¹⁰.

Lows after gastric bypass. Some people develop low blood sugar after Roux-en-Y gastric bypass, a type of weight-loss surgery. In a Cleveland Clinic Journal of Medicine review, the average time from surgery to a documented low was about 28 months, and it can start years later¹¹. The lows usually come 1 to 3 hours after eating¹⁰¹¹.

Older reports put it at 0.1% to 0.36% of patients¹¹. In a 2015 mail survey, though, about a third of bariatric patients described symptoms that suggested lows, and 11.6% reported serious ones, such as needing someone’s help¹¹. The exact share isn’t known¹¹.

The cause isn’t fully understood. Extra release of GLP-1 and a related gut hormone, GIP, is thought to play a part¹¹. Diet changes come first: fewer fast-digesting carbs, more protein and fiber, and roughly 15 to 30 grams of carbohydrate per meal, with medicines as a next step¹¹.

Insulin also signals the ovaries and the brain

The ovaries. When the body pumps out more and more insulin, it also makes more androgens, male-type hormones, NIH’s child-health institute explains¹². High androgens can disrupt the signals that trigger ovulation¹². That’s one reason insulin resistance and polycystic ovary syndrome so often travel together. Our companion article on PCOS covers it in depth.

The brain. In 2005, Suzanne de la Monte and Jack Wands of Rhode Island Hospital and Brown Medical School reported that insulin and IGF-1 were significantly reduced in brain regions hit by Alzheimer’s disease, but not in the cerebellum, an area the disease mostly spares¹³. De la Monte said the findings raised the possibility of a “type 3 diabetes”¹³. The phrase took off, especially online. But brain tissue examined after death shows a link, not a cause.

The best test so far was a treatment trial. A team led by Suzanne Craft of Wake Forest gave adults with mild cognitive impairment or Alzheimer’s dementia 40 units of nasal insulin or a placebo every day for a year¹⁴¹⁵. In the main group of 240 people, the two arms ended up essentially tied on thinking, memory, daily function and spinal-fluid markers of Alzheimer’s¹⁴.

There’s a wrinkle. The first 49 participants used an earlier spray device that proved unreliable, and that small group showed a benefit in a secondary analysis¹⁴¹⁵. So the idea is unproven, not dead. For now, “type 3 diabetes” is a research hypothesis, not a diagnosis.

Insulin’s team at a glance

This table is our own, built from the sources in this article. It shows which way each hormone pushes and when it matters most.

Hormone	What it does to blood sugar	When it rises	What that means for you
Insulin	Lowers it by helping cells take up sugar8	After meals; output doubles in puberty and rises 200% to 250% in late pregnancy24	A healthy pancreas meets these demands; gestational diabetes means it fell short6
Glucagon	Raises it; drives the liver to make sugar8	When adrenaline prompts it during stress8	One reason illness pushes sugar up8
Adrenaline	Raises it; blocks insulin release8	Sudden stress, injury, serious illness8	Part of the pounding heart and shakiness of a low10
Cortisol	Raises it; liver makes sugar from protein8	Infection, injury, burns8	Steroid medicines act similarly; ask about sugar checks10
Growth hormone and IGF-1	Blunt insulin’s effect38	Puberty’s growth spurt23	Teen insulin resistance is usually temporary1
Placental hormones	Cut insulin sensitivity by 50% to 60%5	Second half of pregnancy; fade within 1 to 2 days of birth5	Testing at 24 to 28 weeks6
GLP-1 (gut)	Lowers it; boosts insulin, curbs glucagon11	After eating; surges after gastric bypass11	May help drive lows after meals post-surgery11

How strong is the evidence?

Ratings use our four-level evidence scale.

Claim	Rating	What the research shows
Healthy teens become temporarily insulin resistant in puberty	Strong evidence	Clamp studies in hundreds of children; levels return near baseline by the end12
Pregnancy’s insulin resistance is normal and fades within days of birth	Strong evidence	Reviews of clamp and hormone studies45
Growth hormone and IGF-1 help drive puberty’s insulin resistance	Promising but early	Matching patterns in 342 children; not proof of cause3
High blood sugar in serious illness should always be pushed to normal	Evidence says no, or unsafe	Tight control was tied to more deaths and lows in NICE-SUGAR8
Alzheimer’s disease is “type 3 diabetes”	Not enough evidence	Brain tissue findings show links, not cause13
Nasal insulin protects memory	Evidence says no, or unsafe	No benefit in a year-long trial of 240 people; a small early subgroup is unexplained1415

A body built with checks and balances

Many natural-health readers trust the body’s design, and insulin’s team is a good example of it. Puberty and pregnancy shift the balance on schedule, and serious illness diverts fuel to the immune system¹⁵⁸.

Respecting that design means two things. Don’t treat every temporary rise as a disease to fix. And notice when the design tips into illness, as in gestational diabetes or an insulin-making tumor, because those need medical care⁶¹⁰.

When to get help

• You’re pregnant. Expect gestational diabetes testing between weeks 24 and 28, or at your first visit if you’re at higher risk⁶⁷.
• You had gestational diabetes. Ask your doctor how often to have your blood sugar checked, since about half later get type 2 diabetes⁶.
• A hospital stay found high blood sugar, but you don’t have diabetes. Ask whether you need a follow-up test, since many such patients are later diagnosed⁸.
• You had gastric bypass and get shaky or confused a few hours after meals. Check your sugar with a home meter during a spell, keep a log of food and symptoms, and bring it to your care team¹¹.
• You don’t have diabetes but have repeated spells of confusion or shakiness when you skip meals. See a clinician, who may order a supervised fast¹⁰.
• You have diabetes and are sick. Follow the sick-day plan you made with your care team. The CDC lists warning signs of diabetic ketoacidosis that call for 911 or an emergency room, and our blood sugar article walks through them⁹.

Questions readers ask

The bottom line

Insulin is one member of a team. Glucagon, adrenaline, cortisol, growth hormone and placental hormones push blood sugar up, and at certain times they’re supposed to win: in puberty, in pregnancy and during serious illness.

Trouble starts when the balance tips too far. A pancreas that can’t keep up in pregnancy leads to gestational diabetes, and too much insulin can cause lows after gastric bypass or from a rare tumor. Know when to get tested, plan sick days with your care team, and treat “type 3 diabetes” as a question science hasn’t answered.

Keep exploring: PMOS new name.

Related reading

• Insulin’s patent sold for $1, and then came the fights over price and carbs
• Insulin resistance is common even without obesity, and its popular test isn’t standard
• How your body guards the roughly 4 grams of glucose in your bloodstream
• The stress response saves you in minutes, and viral cortisol fixes misread it
• PCOS is being renamed PMOS, and a study found no extra ovarian cysts

Sources

1. Moran A, Jacobs DR, Steinberger J, Hong CP, Prineas R, Luepker R, Sinaiko AR. “Insulin resistance during puberty: results from clamp studies in 357 children.” Diabetes, 1999 (University of Minnesota record). experts.umn.edu
2. “Longitudinal study of physiologic insulin resistance and metabolic changes of puberty.” Pediatric Research, 2006;60(6):759-763 (PubMed record). pubmed.ncbi.nlm.nih.gov
3. Moran A, Jacobs DR, Steinberger J, Cohen P, Hong CP, Prineas R, Sinaiko AR. “Association between the insulin resistance of puberty and the insulin-like growth factor-I/growth hormone axis.” Journal of Clinical Endocrinology & Metabolism, 2002 (University of Minnesota record). experts.umn.edu
4. Barbour LA, McCurdy CE, Hernandez TL, Kirwan JP, Catalano PM, Friedman JE. “Cellular Mechanisms for Insulin Resistance in Normal Pregnancy and Gestational Diabetes.” Diabetes Care, 2007;30(Suppl 2):S112-S119. pubmed.ncbi.nlm.nih.gov
5. Kampmann U, Knorr S, Fuglsang J, Ovesen P. “Determinants of Maternal Insulin Resistance during Pregnancy: An Updated Overview.” Journal of Diabetes Research, 2019. pmc.ncbi.nlm.nih.gov
6. Centers for Disease Control and Prevention. “Gestational Diabetes.” CDC, reviewed December 22, 2023. cdc.gov
7. National Institute of Diabetes and Digestive and Kidney Diseases. “Tests & Diagnosis for Gestational Diabetes.” NIH, reviewed May 2017. niddk.nih.gov
8. Mifsud S, Schembri EL, Gruppetta M. “Stress-induced hyperglycaemia.” British Journal of Hospital Medicine, 2018;79(11):634-639. storage.imrpress.com
9. Centers for Disease Control and Prevention. “Diabetic Ketoacidosis.” CDC, reviewed December 15, 2023. cdc.gov
10. Vinik A, Feliberti E, Perry RR. “Insulinomas.” Endotext, 2017. endotext.org
11. Millstein R, Lawler HM. “Hypoglycemia after gastric bypass: An emerging complication.” Cleveland Clinic Journal of Medicine, 2017;84(4):319-328. ccjm.org
12. Eunice Kennedy Shriver National Institute of Child Health and Human Development. “Polycystic Ovary Syndrome (PCOS)” fact sheet. NIH, accessed October 2026. nichd.nih.gov
13. Journal of Alzheimer’s Disease (IOS Press). “Researchers discover link between insulin and Alzheimer’s.” News release, March 7, 2005. j-alz.com
14. NeurologyLive. “Insulin Shows No Functional or Cognitive Effects in Alzheimer Disease.” June 30, 2020 (reporting Craft S, et al., JAMA Neurology, 2020). neurologylive.com
15. MDedge. “Still no clear answer on intranasal insulin for MCI and Alzheimer’s disease.” July 16, 2020. mdedge.com