If you’ve found yourself thinking,

“I haven’t changed anything — why is my weight going up?”
“Why does my body feel so different?”
“Why does nothing work like it used to?”

I want you to know something clearly from the start:

You are not imagining it.
And this is not a willpower problem.

Weight regulation is not simply about eating less and moving more. It is the result of a deeply intelligent, highly protective biological system — one that evolved to keep you alive during times of famine, not during a modern life filled with constant food availability, chronic stress, disrupted sleep, and hormonal transition.

To understand why weight often becomes harder to manage during perimenopause, we first need to understand how body weight is regulated in the first place.

Body Weight Is Actively Regulated — Not Accidental

Body weight is regulated in much the same way as body temperature or blood glucose. It does not drift randomly. Instead, the brain actively defends body weight within a preferred range — sometimes referred to as a weight-defended point. In reality, this is not a fixed number but a range that can shift over time.

From an evolutionary perspective, this makes perfect sense. For most of human history, food scarcity posed a greater threat than food abundance. Humans who could efficiently store energy — and defend those stores when food disappeared — were more likely to survive and reproduce.

As a result, the body evolved very strong mechanisms to prevent weight loss. The systems preventing weight gain are comparatively weaker. When body fat falls below what the brain perceives as safe, powerful biological mechanisms activate to restore it. That is not weakness. It is survival physiology doing exactly what it was designed to do.

Where Your Energy Actually Goes

One of the most misunderstood aspects of weight is how the body uses energy each day.

A large proportion of daily energy expenditure comes from resting metabolic rate (around 70%) — the energy required simply to keep you alive and functioning. Your brain, heart, lungs, immune system, hormone production, and cellular repair processes are constantly active, even when you are at rest.

Exercise is incredibly valuable for metabolic health, muscle preservation, insulin sensitivity, bone density, and long-term disease prevention. But from a purely energy perspective, structured exercise represents only one component of total daily energy expenditure.

This helps explain why “just move more” often fails as a standalone weight strategy. Weight regulation is driven primarily by baseline metabolism and neuroendocrine signalling — not by effort alone.

The Limits of “Calories In, Calories Out”

The calorie equation is not wrong — but it is incomplete. It treats the body like a passive container. In reality, the body is adaptive.

When calorie intake drops, the brain does not simply accept the deficit. It responds protectively. Hunger increases. Thoughts about food become more persistent. Energy expenditure falls. Spontaneous movement decreases, often without conscious awareness. The body becomes more metabolically efficient.

This coordinated response is often described as adaptive thermogenesis. Importantly, these changes can persist long after weight loss has occurred, strongly promoting weight regain.

From the brain’s perspective, weight loss may look like famine. The response is protection.

The Brain as the Control Centre

At the centre of this system sits the hypothalamus — a small but powerful region of the brain that acts as a regulatory hub.

I often describe it as air-traffic control. It integrates signals from fat tissue, the gut, the pancreas, stress pathways, sleep rhythms, and the immune system. Based on these signals, it adjusts two primary levers: hunger and energy expenditure.

When energy stores fall, hunger rises and metabolism falls. When energy stores are perceived as adequate, appetite eases and energy use can increase.

These changes are largely automatic and unconscious. They are not moral failings. They are regulatory responses.

Leptin: The Long-Term Energy Messenger

Leptin is a hormone produced by fat cells. Its job is to inform the brain about the size of stored energy reserves.

When fat mass increases, leptin tends to rise. When fat mass decreases, leptin falls — often quickly. A drop in leptin acts as a powerful alarm signal. The brain responds by increasing hunger and reducing energy expenditure, thereby defending fat stores.

This system evolved to prevent starvation, and it is extremely effective.

However, in many people with long-standing weight gain, leptin levels are high but the brain does not respond appropriately. This is often described as leptin resistance.

Imagine your fuel tank is full, but the dashboard gauge reads empty. You would keep searching for fuel. That is what the brain does when it does not properly “hear” the leptin signal. Hunger increases and energy conservation persists, even when fat stores are abundant.

This signalling disruption can occur through reduced leptin transport into the brain, impaired intracellular signalling, and chronic low-grade inflammation within appetite-regulating centres.

Inflammation and Insulin Resistance

Low-grade inflammation acts like static in the communication lines between the body and brain. It interferes with leptin signalling and appetite regulation. This inflammation can be driven by visceral fat, chronic stress, sleep disruption, repeated glucose spikes, and ultra-processed dietary patterns.

Insulin resistance often develops alongside this inflammatory environment. Insulin’s role is to move glucose from the bloodstream into cells. Over time, cells can become less responsive to insulin’s signal, prompting the body to produce more (insulin resistance). Persistently elevated insulin encourages fat storage and further disrupts metabolic signalling.

Insulin and leptin resistance frequently reinforce one another, creating a loop in which hunger signals remain elevated and fat storage becomes easier.

The Gut–Brain Axis

The gut is far more than a digestive tube. It is a powerful signalling organ.

After a meal, gut hormones communicate satiety to the brain. In many weight-gain states, these satiety signals may be quieter, while hunger signals remain louder. This can make meals feel less satisfying and cravings more persistent.

The gut microbiome also influences energy extraction, inflammatory tone, immune signalling, and appetite pathways. Changes in microbial diversity and gut barrier integrity (often termed leaky gut) can subtly shift the metabolic environment toward inflammation and energy storage.

This area of science is evolving rapidly, but it reinforces an important point: weight regulation is not simply about calories — it is about signalling.

Stress, Sleep, and Cortisol

Chronic stress activates the body’s stress response system and increases cortisol signalling. Cortisol is essential for survival, but when elevated chronically, it can increase appetite, worsen insulin resistance, and promote abdominal fat storage.

Sleep disruption compounds this effect. Poor sleep alters appetite hormones, reduces insulin sensitivity, increases cravings, and disrupts circadian regulation of metabolism.

Many women describe this stage of life as exhausting — and biologically, that exhaustion matters.

Why Repeated Dieting Often Backfires

Repeated calorie restriction can amplify protective brain responses. Each significant drop in energy intake lowers leptin levels, triggering increased hunger and reduced metabolic rate.

Over time, weight cycling can strengthen the brain’s defence of body weight. Regain is not a lack of discipline. It is a predictable physiological response from a brain designed to protect against famine.

Why Perimenopause Changes the Equation

Now layer all of this onto perimenopause.

Perimenopause is not only a reproductive transition. It is a metabolic one.

Many women describe sudden abdominal weight gain, reduced response to strategies that once worked, increased hunger, greater sensitivity to stress, and sleep disruption. These experiences reflect measurable physiological change.

While gradual midlife weight gain can occur with aging alone, menopause changes where fat is stored. As estrogen declines, fat distribution shifts toward the abdomen, with increased visceral fat accumulation. This change in body shape can occur even without dramatic changes on the scale- 'The Meno-belly'.

Estrogen as a Metabolic Regulator

Estrogen plays a central role in metabolic health. It supports insulin sensitivity, influences fat distribution, promotes fuel use in muscle, and helps regulate inflammatory balance.

During perimenopause, estrogen often fluctuates before gradually declining. As levels fall, fat oxidation tends to decrease (reduced ability to burn fat for fuel), abdominal fat storage becomes more likely, and insulin sensitivity can worsen.

I often describe estrogen as a metabolic traffic controller. When it is present and stable, fuel flows more readily into cells for use. As it declines, that regulation shifts, and storage becomes more likely.

Muscle, Metabolism, and Resting Energy Needs

Many women say, “My metabolism has slowed.” Often, that reflects a real physiological shift.

Muscle mass naturally declines with age, and this process can accelerate during the menopausal transition. Muscle is metabolically active tissue that supports resting energy expenditure and insulin sensitivity. As lean mass decreases (you lose muscle), baseline energy needs fall (lower metabolism).

This creates a mismatch: your body may require fewer calories than it once did, but appetite signals and life demands do not automatically adjust.

Insulin Sensitivity and Inflammation in Midlife

Estrogen decline is associated with reduced insulin sensitivity. Blood glucose may rise more after meals, insulin levels may increase, and fat burning may be more easily suppressed. Increased visceral fat further drives inflammatory signalling. Estrogen loss also leads to increased inflammation in the body (think achy joints).

Inflammation, insulin resistance, and abdominal fat reinforce one another. This is one reason weight regulation can feel more “stubborn” during perimenopause.

The Added Layer of Stress

Midlife often coincides with significant life demands — career pressure, caregiving, teenagers, aging parents, and reduced recovery time. Hormonal fluctuations can also heighten stress sensitivity and disturb sleep.

Elevated cortisol during this period further promotes abdominal fat storage and worsens insulin resistance. When multiple biological and environmental pressures converge, weight regulation becomes more vulnerable.

Bringing It All Together

Perimenopausal weight gain is rarely caused by one single factor.

It reflects the combined effects of hormonal shifts, changes in fat distribution, loss of muscle mass, reduced resting metabolic rate, declining insulin sensitivity, increased inflammation, gut microbiome changes, chronic stress, and sleep disruption.

Your body is not broken.
It is adapting to a new hormonal environment using ancient survival pathways.

Understanding this shifts weight away from morality and into physiology. And once we understand physiology, we can respond with clarity, compassion, and confidence rather than blame. 

If you need more support with weight management book a consultation and we can go through this together and support your body to a healthier metabolism. Let's find your biggest levers- we can test for chronic inflammation, we can look at insulin resistance, we can investigate gut microbiome, support stress, increased muscle mass and look at supportive herbs, supplements and medications where appropriate to make a personalised plan for you that supports sustainable weight loss.

Written by: Dr Taisia Cech

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