rewrite this title Early-Life Stress May Leave Lasting Effects on Metabolic Health in Women

• Researchers examined early-life conditions that quietly shape long-term health — Early-life adversity was measured using a validated composite score that captured experiences from before birth through childhood. This included factors such as low birth weight, maternal smoking around birth, physical or sexual abuse, neglect, family instability, and maternal mental illness, alongside protective factors like breastfeeding and access to medical care.

Each adverse exposure lowered the score, while each supportive exposure raised it, creating an overall picture of how nurturing or stressful the early developmental environment was. This approach reflects real life, where many people experience combinations of stress and support rather than extreme trauma alone.

• The study focused on insulin signaling in the brain, not just blood sugar — Instead of measuring insulin only in the bloodstream, the researchers examined how insulin works inside the brain. They used a genetic score called the insulin receptor expression-based polygenic risk score (ePRS-IR), which is based on a co-expression network of 263 genes associated with the insulin receptor in key brain regions.

These regions include the prefrontal cortex and striatum in the mesocorticolimbic system, which are areas involved in decision-making, reward, impulse control, eating behavior, and energy balance. A higher ePRS-IR score reflects greater genetic predisposition for activity in this brain insulin signaling network.

• Early adversity and brain insulin signaling interacted to raise metabolic risk — The researchers found that early-life adversity alone was linked to higher visceral fat and greater metabolic risk in adulthood. However, the strongest effects appeared in participants whose brains showed higher insulin receptor network activity.

Among these individuals, greater childhood adversity was associated with more visceral fat stored deep in the abdomen and a higher likelihood of meeting criteria for metabolic syndrome, a cluster of risk factors that includes impaired blood sugar control, abnormal lipids, inflammation, and high blood pressure.

• Visceral fat acts as an early warning signal of stress-driven metabolic disruption — It reflects central regulation of energy storage rather than surface-level weight gain. Unlike subcutaneous fat, visceral fat responds strongly to stress hormones, inflammatory signaling, and neuroendocrine inputs. Its expansion indicates that the brain is shifting energy allocation toward defensive storage patterns linked to long-term metabolic risk.

• Women showed a much stronger vulnerability than men — When the data were analyzed separately by gender, the interaction between early adversity and brain insulin signaling was consistently stronger in women. Women with both higher ePRS-IR scores and greater childhood adversity had significantly higher visceral fat and a much higher risk of metabolic syndrome.

These patterns were not statistically significant in men or in women with lower brain insulin signaling scores. This points to a gender-specific biological sensitivity in how early stress reshapes metabolism.

• Metabolic disruption appeared before clinical disease — The differences observed in the study were based on MRI-measured visceral fat and an expanded definition of metabolic syndrome that included inflammation markers. Many of the individuals identified as higher risk had not yet met the standard clinical thresholds for diabetes or cardiovascular disease.

This suggests that the biological effects of early adversity and altered brain insulin signaling may appear well before someone is formally diagnosed with a metabolic disorder.

• Early adversity alters long-term stress regulation — Earlier evidence shows that early-life stress affects the developmental calibration of stress-response systems, including the hypothalamic-pituitary-adrenal (HPA) axis, which controls cortisol release.

“These associations may be explained by high cortisol levels/Hypothalamic-Pituitary-Adrenal axis programming induced by early adverse experiences, which can trigger a pro-inflammatory state that promotes hedonic food consumption, fat tissue inflammation, and the subsequent development of metabolic disorders,” the authors wrote.4

• One of the clearest behavioral effects involves changes in food motivation — Processes linking early-life adversity to adult metabolic alterations center on behavioral shifts.

“For example, exposure to prenatal adversity culminating in poor fetal growth has been associated with impulsivity and hedonic food intake later in life. Intrauterine growth restriction combined with rapid early growth increases the risk of impulsivity in childhood,” the researchers explained.

“Adolescents born with low birth weight have increased activation of brain regions involved in impulsive control and decision-making in response to palatable food images.”5

• Brain insulin signaling directly regulates impulsivity and food reward — Insulin acts as a neuromodulator in the prefrontal cortex and striatum. The researchers cited animal studies wherein increased impulsivity and preference for palatable food were reversed when insulin signaling in the striatum was restored.

• Stress hormones are designed for brief activation, not constant demand — Hormones such as norepinephrine and epinephrine are released through activation of the sympathetic nervous system. Their primary function is to increase alertness, mobilize energy, and prepare the body for action.

These responses are adaptive in short bursts, but they are also metabolically demanding. Both hormones act on mitochondria, altering how cells generate and use energy in response to stress signals. Problems arise when this system remains chronically activated.

Research published in Cell Metabolism has shown that sustained sympathetic nervous system activity, particularly in the context of excess energy intake, promotes insulin resistance and metabolic dysfunction. Under these conditions, stress signaling disrupts normal metabolic regulation even when insulin is still being produced.6

• Cortisol further amplifies these effects — Elevated cortisol promotes glucose release from the liver and increases the circulation of free fatty acids from fat tissue.7 Over time, this hormonal environment makes it harder for insulin to regulate blood sugar efficiently, encouraging both fat accumulation and rising glucose levels. These effects place additional strain on mitochondrial function, reducing energy efficiency and increasing oxidative byproducts.

• Modern stressors keep stress hormones chronically elevated — Disrupted sleep, persistent mental strain, and dietary excess can keep these hormonal systems activated well beyond their intended role. When combined with highly processed foods, including vegetable oils that impair mitochondrial metabolism, stress signaling, and metabolic dysfunction reinforce each other over time.

1. Cut linoleic acid (LA) from your diet to repair your mitochondria — The most damaging modern dietary toxin is not sugar but excess LA, the polyunsaturated fat found in seed oils. These oils integrate into cell membranes, disrupt energy metabolism, and drive chronic inflammation. If you regularly eat restaurant meals or ultraprocessed snacks, your intake is likely far above healthy levels.

Replace seed oils such as soybean, corn, sunflower, safflower, and canola with stable saturated fats like tallow, ghee, or grass fed butter. Aim for less than 5 grams of LA per day, with an ideal target under 2 grams.

To help track your intake, I recommend you download my Mercola Health app once it becomes available. Its Seed Oil Sleuth feature monitors LA consumption down to a tenth of a gram, so you can stay in charge of your metabolism.

2. Rebuild energy production with healthy carbohydrates — Your metabolism depends on a steady supply of glucose to support efficient mitochondrial function. Diets that rely heavily on carb restriction or prolonged fasting suppress thyroid function and lower metabolic rate, slowing the very processes needed for metabolic recovery.

I recommend consuming 250 grams of carbohydrates per day from whole-food sources such as fruit and root vegetables. If your gut is sensitive, start with whole fruits and white rice, which are easy to digest. As your digestion improves, add starches later. This steady fuel supply turns your mitochondria back on and keeps your metabolism resilient.

3. Reduce exposure to everyday metabolic stressors — Metabolic stress doesn’t just stem from diet. Environmental stress from plastics, personal care products, and electromagnetic fields (EMFs) also interferes with your body’s ability to convert fuel into energy, worsening insulin resistance over time.

Reducing this load starts with small, practical steps. Choose glass or stainless steel containers, avoid heating food in plastic, and keep your phone away from your body while sleeping.

4. Move, breathe, and sleep consistently — Daily movement plays a direct role in restoring energy balance. Incorporate regular walking, ideally around 60 minutes per day into your routine. Adding resistance training two to three times per week builds muscle tissue, which serves as a reservoir for glucose and helps buffer metabolic stress.

Rest is equally important. Deep, consistent sleep supports mitochondrial adenosine triphosphate (ATP) production, lowers cortisol levels, and helps align hormonal rhythms. Breathing patterns also matter. Slow nasal breathing allows carbon dioxide levels to rise gently, calming the nervous system and improving oxygen delivery to tissues. This supports the cellular processes that underlie metabolic recovery.

5. Get daily sunlight exposure — Sunlight stimulates melatonin production inside your mitochondria, where it acts as a powerful antioxidant. This improves insulin sensitivity, protects against oxidative damage, and helps your cells maintain steady energy output — a key part of healthy metabolic function.

Make sunlight exposure a part of everyday life — spend time outdoors walking, biking, or sitting in natural light whenever possible. If your diet has been high in vegetable oils, give it at least six months of lowering those fats before extending midday sun exposure, as LA increases your vulnerability to sunburn. Learn more in “Beyond Vitamin D Production — How Sensible Sun Exposure Supports Overall Health.”

1. Use breathing to restore cellular equilibrium — Slow nasal breathing increases carbon dioxide levels, which improves oxygen delivery to your cells and helps mitochondria work more efficiently. Techniques like progressive muscle relaxation, autogenic training, or even mindful crying all release emotional tension stored in your body.

These methods teach your system to downshift from energy-draining stress responses into energy-restoring repair states. In essence, you’re teaching your mitochondria when it’s safe to recharge.

2. Embrace your creativity — Practices such as gratitude journaling, laughter, creative hobbies, and positive visualization shift the body away from a sustained stress response and toward healing. When attention is directed toward safety, pleasure, and creativity, the brain generates mitochondrial-friendly signals that promote calm and stability.

Creative activities like painting, playing an instrument, or writing engage neural pathways that support oxygen flow and energy metabolism, reducing hormonal surges that drain metabolic reserves.

3. Boost your emotional state with optimism and laughter — A more positive mental outlook shifts brain chemistry in ways that ease stress, while laughter triggers endorphin release and helps calm the nervous system. Whether that comes from reframing negative thoughts or simply watching something that makes you laugh, these emotional resets lower stress and support recovery.

4. Try the Emotional Freedom Techniques (EFT) — EFT is a form of psychological acupressure based on the energy meridians used in acupuncture that quickly restores inner balance and healing. In the video below, EFT practitioner Julie Schiffman demonstrates how to tap for stress relief.