Abdominal weight gain after 40: understanding the mechanisms to take action

Contrary to popular belief, basal metabolic rate (the amount of energy burned at rest) remains relatively stable between the ages of 20 and 60, given equivalent muscle mass. It is not, therefore, a case of the engine spontaneously "slowing down". What changes is what keeps the engine running: body composition, physical activity levels and hormones. During perimenopause, these three factors shift simultaneously, and their combined effects can explain weight gain without any change in lifestyle habits.

In this process, two fundamental changes are at play: the decline in muscle mass and the reduction in physical activity levels.

Muscle mass decreases

From the two years preceding the last menstrual period, fat mass increases and lean mass decreases at a rate that accelerates during perimenopause. Muscle tissue is the body's primary energy consumer at rest: less muscle mechanically means fewer calories burned at a cellular level, even without any actual slowing of the metabolism itself. This is why regular strength training exercises are so important for metabolic health during this period.

Physical activity levels tend to decline

Data show that energy expenditure from physical activity decreases during the perimenopause years. Yet this is precisely the lever that allows the body to compensate for the progressive loss of muscle mass and maintain a sufficient level of daily energy expenditure.

Added to this is the disappearance of an often overlooked effect: during the luteal phase, progesterone slightly increases energy expenditure. Studies estimate this increase at between 2 and 10% depending on the woman, with significant variability from one woman to another [1]. This is far from a negligible factor. Indeed, as cycles become irregular and then stop altogether, this additional expenditure gradually fades away, without anything in your diet or habits having changed.

Before perimenopause, women tend to store fat peripherally: in the hips, thighs and buttocks. This type of storage, known as "gynoid", is protected by oestrogens. As they decline, the distribution changes dramatically: fat migrates towards the abdomen.

Abdominal (or visceral) fat is not simply a passive storage tissue. It is a metabolically active tissue that secretes pro-inflammatory molecules, disrupts insulin sensitivity and increases cardiovascular and metabolic risks. Excess visceral fat is associated with increased risks of type 2 diabetes, cardiovascular disease and metabolic syndrome, independently of the total weight shown on the scales. It is waist circumference (not weight alone) that is the most relevant indicator for assessing these risks: above 80 cm in women, they increase significantly. This fat is fundamentally different from the subcutaneous fat one may have had in previous years.

Why this redistribution? Oestradiol (the principal form of oestrogen) appears to play a role in regulating thermogenesis, that is, the body's capacity to burn fat in the form of heat. Some data suggest that brown adipose tissue, involved in this thermogenesis, may be less active after the menopause than before [2]. These findings remain preliminary and the actual role of this tissue in overall weight gain is still debated, but they form part of a coherent picture of reduced fat oxidation.

What is better documented is the effect of oestradiol on fat distribution itself. Its decline promotes a redistribution of fat more concentrated around the abdomen, independently of total weight [3].

At the cellular level, research conducted primarily on animal and cellular models suggests that oestradiol influences AMPK signalling, a protein that regulates energy metabolism [4]. When oestrogen levels fall, certain pathways that promote fat oxidation appear to be less well activated, whilst lipogenesis increases. These mechanisms still need to be confirmed at scale in humans, but they offer coherent biological leads to explain the observed changes.

The perimenopause is accompanied by a progressive insulin resistance, driven by hormonal changes and shifts in body composition. This mechanism contributes significantly to our understanding of abdominal weight gain [5].

Here is what happens in practice:

The decline in oestrogens disrupts the insulin response at several levels. Initially, the pancreas often compensates by producing more insulin (compensatory hyperinsulinaemia), but this response gradually deteriorates. The muscles become less sensitive to insulin, reducing their ability to absorb glucose. The liver is also affected, increasing its production of triglycerides and glucose. The digestion of carbohydrates is generally less well regulated, resulting in greater blood sugar fluctuations after meals.

The result: an excess of glucose that tends to be converted into fat, blood sugar that is harder to regulate, and storage directed primarily towards the abdomen. Visceral fat is precisely the type of deposit favoured in a context of insulin resistance.

Another mechanism that is often poorly understood in weight gain: low-grade chronic inflammation.

When oestrogen levels drop, their anti-inflammatory effects disappear along with them. Studies have shown that the fall in oestradiol is accompanied by a rise in pro-inflammatory markers, particularly IL-6 and TNF-α, two cytokines that are especially well documented in this context [6]. This chronic inflammation is not visible, it does not cause pain, but it fuels insulin resistance and promotes the storage of visceral fat. And visceral fat itself produces inflammatory molecules, creating a self-perpetuating cycle.

The gut microbiome also plays a role in this equation. Studies have highlighted that after the menopause, high visceral adiposity is associated with a more pro-inflammatory microbial profile, with an increased presence of bacteria expressing LPS (lipopolysaccharides) that amplify systemic inflammation. Furthermore, data suggest that the transition to the menopause is accompanied by a tendency towards reduced intestinal microbial diversity, although these findings still need to be confirmed on a larger scale [7]. Digestion and nutrient absorption are also affected, which reinforces the risks of metabolic disruption. Ultra-processed foods high in refined sugars contribute directly to this impoverishment of the microbiome.

Abdominal weight gain during this period of life is not the result of a single cause. It is a convergence of several disruptions.

Cortisol becomes dysregulated

It is not so much that cortisol increases in a linear fashion with age; what changes during the transition to menopause is mainly its circadian rhythm and the way the body responds to stress: higher cortisol levels over 24 hours have been observed in the late menopausal transition, with a circadian rhythm whose amplitude tends to flatten and variability to increase — two characteristics with unfavourable metabolic effects [8]. Cortisol, particularly when chronically elevated, promotes abdominal fat storage and worsens insulin resistance.

Sleep deteriorates

Between 40 and 56% of women report sleep disturbances during the menopause [9]. Poor-quality sleep reduces glucose tolerance, increases sympathetic nervous system activity, and disrupts the hormones that regulate appetite, including leptin. Lack of sleep directly worsens the metabolic disruptions already under way.

Sarcopaenia sets in

Muscle mass decreases as oestrogen levels fall. Less muscle means a lower basal metabolic rate, reduced insulin sensitivity, and a greater tendency to store fat. Sarcopaenia and metabolic syndrome feed into each other.

The thyroid can be affected

During this phase, women face an increased risk of thyroid dysfunction (in particular hypothyroidism), which further slows metabolism, raises cholesterol and disrupts glucose regulation [10]. A medical check-up including a TSH test is recommended in cases of unexplained weight gain, persistent fatigue, or digestive issues.

Understanding the mechanisms behind abdominal weight gain is useful. Acting on the right levers is even better. Here are the points that enjoy the greatest scientific consensus.

Exercise and physical activity: essential allies

Exercise is one of the few levers capable of acting on several mechanisms at once: it improves insulin sensitivity, promotes fat oxidation, supports muscle mass and can partly compensate for the loss of oestrogen's beneficial effects. It is also the most effective approach for lasting reduction of abdominal fat, provided the right types of exercise are chosen.

High-intensity interval training (HIIT) programmes are more effective than moderate continuous training for reducing visceral fat mass. Strength training exercises are essential for preserving and rebuilding lean mass and, with it, resting energy expenditure. The ideal approach combines both: cardio exercise to promote fat oxidation and strength training to support muscle over the long term.

In terms of duration, 45 minutes of activity three times a week (brisk walking, jogging, cycling at variable intensity) is already enough to produce measurable improvements in body composition, waist circumference, blood sugar levels and lipid profile.

Diet: glycaemic stability and combating inflammation

Key principles to remember:

• Prioritise protein-rich foods at every meal to preserve muscle mass and reduce insulin resistance.
• Rely on fibre (vegetables, legumes, whole grains) to stabilise blood sugar levels, support digestion and nourish the microbiome.
• Reduce ultra-processed foods, which are high in fast-release sugars and pro-inflammatory fatty acids.
• Favour quality fats (omega-3, olive oil) that support the regulation of inflammation.
• Avoid excess added sugars and alcohol, which directly contribute to visceral fat storage.

The microbiome: an underestimated lever

One study showed that premenopausal women have higher plasma GLP-1 levels than postmenopausal women — a difference the authors attribute in part to the effect of oestradiol on the secretion of this hormone by intestinal cells [11]. Data on microbial diversity remain more mixed across studies. That said, a balanced microbiome plays a central role in digestion, nutrient absorption and the regulation of inflammation. Supporting the microbiome with prebiotics and probiotics may help improve gut integrity, optimise digestion and promote metabolic balance.

Among the available approaches, targeted nutrition can provide complementary support — particularly to cover the specific nutritional needs of this period and to address two factors directly linked to abdominal weight gain: energy metabolism and blood sugar regulation. As a complement to a balanced diet and appropriate medical follow-up, certain nutrients help fill the gaps that everyday foods alone do not always fully cover during this time.

Péri Essentials is Jolly Mama's multivitamin complex, specifically formulated for women before, during and after the menopause.

It contains 17 essential nutrients in highly bioavailable forms, including:

• B vitamins (B1, B2, B3, B5, B6, B12) and vitamin C, which contribute to normal energy metabolism and the reduction of tiredness and fatigue — particularly helpful when the metabolic slowdown makes itself felt in daily life.
• Chromium, which helps maintain normal blood glucose levels — a relevant support given the physiological insulin resistance that develops during perimenopause.
• Bacopa Bacognize®, a patented extract supporting cognitive function, concentration and memory, which are often put to the test during this period of transition.
• Vitamin B6, which contributes to the regulation of hormonal activity.

Just 2 capsules per day. Vegan. Made in France.