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Perimenopause Weight Redistribution
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In one pass Many women in their forties and fifties notice that they are not eating more, yet their belly is getting bigger.
Educational content, not medical advice — consult a clinician.
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Chapter 1
Fat moves from hips to belly
Many women in their forties and fifties notice that they are not eating more, yet their belly is getting bigger. This is not a lapse of willpower. The body has entered a transition called perimenopause: the ovaries slowly retire, and estrogen swings sharply (irregular periods, hot flashes) while trending down overall, so the place where fat is stored quietly shifts from the hips and thighs to the belly.
The transition usually begins between 40 and 55, roughly 4–10 years before the final menstrual period (FMP); after 12 months without a period, you are postmenopausal.
What changes most is often not weight but where fat is stored. Weight does creep up slowly over these years, but not by much; at the same weight, though, waist circumference and waist-to-hip ratio rise clearly, and watching only body mass index () misses this layer of risk. Studies have observed that the shift of fat from under the skin of the hips and thighs into the abdomen comes before, and independently of, any change in total weight — which is how weight stays flat while the waist grows.
Sleep and mood are disrupted at the same time: hot flashes and night sweats wake you again and again, and estrogen also tugs on serotonin () and dopamine, signals that help regulate mood, so emotional eating creeps in. That is why this cannot be explained by "eating too much and moving too little". Seeing the structure is what lets you change strategy, rather than simply trying harder to eat less.
The transition usually begins between 40 and 55, roughly 4–10 years before the final menstrual period (FMP); after 12 months without a period, you are postmenopausal.
What changes most is often not weight but where fat is stored. Weight does creep up slowly over these years, but not by much; at the same weight, though, waist circumference and waist-to-hip ratio rise clearly, and watching only body mass index () misses this layer of risk. Studies have observed that the shift of fat from under the skin of the hips and thighs into the abdomen comes before, and independently of, any change in total weight — which is how weight stays flat while the waist grows.
Sleep and mood are disrupted at the same time: hot flashes and night sweats wake you again and again, and estrogen also tugs on serotonin () and dopamine, signals that help regulate mood, so emotional eating creeps in. That is why this cannot be explained by "eating too much and moving too little". Seeing the structure is what lets you change strategy, rather than simply trying harder to eat less.
Mechanism · What estrogen does at the fat cell
Saying fat moves from the hips and thighs to the abdomen is only a metaphor: fat cells do not walk. What actually gets rewritten is two things — the receiving enzyme at the fat cell's door, and the release switches inside the cell. Estrogen presses on both, and it presses harder on the hips and thighs than on the belly. The chain below rests partly on small studies of human fat tissue and partly on mechanistic reasoning.The receiving side: lipoprotein lipase (). The fat you eat travels in the blood in packaged particles. To get into a fat cell, it first has to be cut open by LPL parked on the vessel wall; only then can the cell take it in. So which depot grows faster depends largely on which depot's LPL is busier. In the reproductive years, estrogen keeps LPL activity relatively high in the fat under the skin of the hips and thighs, so more of the same meal's fat is unloaded there rather than into the belly. That is where the pear shape comes from: it is not aesthetics, it is an enzyme that is busier in one place than another.
The release side: the fat cell's accelerator and brake. Fat cells carry two kinds of adrenergic receptors with opposite effects: one is an accelerator (it tells the cell to release stored fat to be burned), the other is a brake (it tells the cell to hold on). Visceral fat has more accelerators and responds fast; the fat under the skin of the hips and thighs has more brakes and releases slowly. So hip-and-thigh fat behaves like a fixed-term deposit, and visceral fat like a checking account: money goes in fast and comes out fast. This also explains something many people find puzzling: when fat comes off, the belly often shrinks first, and the hips and thighs last.
After estrogen withdraws, the mechanism predicts that both sides reverse at once. The receiving enzyme that estrogen was keeping active in hip-and-thigh fat falls, so the same meal's fat is no longer unloaded there first. That fat still has to be stored somewhere, and it flows to the account that already takes in fast and releases fast: the abdomen. At the same time, the lock on the hip-and-thigh fixed-term deposit loosens; fat that was held there is mobilized more easily, circulates in the blood, and is taken up on the visceral side.
So you can now work out for yourself how weight stays flat while the waist grows: the totals going in and out have barely moved (the scale cannot see anything), but the delivery address has changed from the hips and thighs to the abdomen, and some of what was already stored in the hips and thighs has moved too. The scale only adds up the whole body, and a sum cannot see a move. Waist circumference measures exactly the place that received the move, so it speaks first.
One step further: since what has been rewritten is where fat is stored, not how much, simply eating less (pressing down the total) does little to target this redistribution. It takes both sides down together, including the muscle you least want to lose. What can change the allocation is giving energy another destination that is eager to take it — muscle. That is why the chapter Strength training and protein first puts strength training at the top.
Myth · Does menopause always mean weight gain?
"Once you hit menopause you will gain weight, and nothing can be done" is the most widespread line, and the one that makes people give up earliest. It bundles together two things that should be looked at separately.First, the data: women in perimenopause and early postmenopause do gain weight slowly, but not by much (studies differ on the exact yearly amount, so no single figure is given here). Much of that gain goes with age itself: men of the same age gain weight too, driven by year-by-year muscle loss plus falling activity, and it is not estrogen's doing alone. In other words, the "gain" in "menopause means gaining weight" is partly a universal feature of aging, not a verdict unique to menopause.
What truly belongs to menopause is not how much total weight goes up, but where the fat goes:
What falling estrogen genuinely drives is a change in distribution: fat shifts from under the skin of the hips and thighs (a pear shape) to the organs of the abdomen (an apple shape). This happens before, and independently of, any change in total weight: even at an unchanged weight, waist circumference and waist-to-hip ratio rise. Body mass index () only combines weight and height and cannot read where fat is stored, so this layer of risk is invisible to itSo "menopause means gaining weight" should be split into two statements: gaining with age is a general trend that can be largely offset by keeping muscle, eating enough protein and staying active; fat shifting to the organs is specific to menopause, and that is the health risk to watch
Why the distinction helps: if you believe the "you will gain anyway, effort is pointless" version, it is easy to give up early. But the evidence points the other way. Small studies suggest that women in perimenopause build muscle from strength training about as well as younger women (provided they eat enough protein and keep raising the load), and visceral fat does respond to exercise and diet. You cannot change the fall in estrogen, but you can substantially change where the body stores fat and how much muscle it keeps. It will change does not mean accept it; it means the strategy has to change.
Chapter 2
Why weight loss gets harder now
When the old approach suddenly stops working at this stage, the most common explanation is you are not disciplined enough. The more accurate explanation is that the underlying rules have been rewritten, in five places at once.
The energy baseline is sinking. Resting metabolic rate (RMR — the energy you burn lying still) is estimated to fall by about 50 kcal a day on average, from two sources: estrogen's own boost to metabolism is gone, and muscle, one of the most energy-hungry tissues in the body, is being lost year by year. By the crudest arithmetic, a year adds up to ≈ 18 000 kcal ≈ 2 kg of fat. That is a static estimate that assumes nothing else changes; in reality, as weight rises, energy use rises a little too, so the real gain is smaller than this.
The signals drift as well. The fullness signal is turned down, blood-sugar swings after meals get bigger, and sleep is chopped up by hot flashes and night sweats; and losing weight itself triggers a metabolic defense that everyone has. These five headwinds stacked together are why what used to work no longer works. What is needed is a plan aimed at each of the five, not a harsher version of the same plan.
The energy baseline is sinking. Resting metabolic rate (RMR — the energy you burn lying still) is estimated to fall by about 50 kcal a day on average, from two sources: estrogen's own boost to metabolism is gone, and muscle, one of the most energy-hungry tissues in the body, is being lost year by year. By the crudest arithmetic, a year adds up to ≈ 18 000 kcal ≈ 2 kg of fat. That is a static estimate that assumes nothing else changes; in reality, as weight rises, energy use rises a little too, so the real gain is smaller than this.
The signals drift as well. The fullness signal is turned down, blood-sugar swings after meals get bigger, and sleep is chopped up by hot flashes and night sweats; and losing weight itself triggers a metabolic defense that everyone has. These five headwinds stacked together are why what used to work no longer works. What is needed is a plan aimed at each of the five, not a harsher version of the same plan.
Mechanism · Where each of the five headwinds comes from
1. The resting-metabolism baseline is sinking.Resting metabolic rate (RMR) is the energy you burn lying still and doing nothing, and a large share of it comes from skeletal muscle: muscle is an expensive tissue, and simply maintaining it costs energy all the time. From perimenopause into postmenopause, this baseline drops for two reasons. Estrogen itself raises metabolic rate, so when it withdraws the baseline steps down a notch; and muscle is being lost year by year (sarcopenia), and muscle is exactly the part that spends the money. 50 kcal a day sounds small, but it is a notch that is there every day and does not come back by itself.
2. The fullness signal has been turned down.
Fat cells release leptin to tell the brain that stores are sufficient, and the receiver sits in the hypothalamus. Animal studies suggest that estrogen acts as an amplifier here: with the same amount of leptin, the brain hears the message more clearly. When estrogen withdraws, the volume at the receiving end is turned down, so after the same meal fullness arrives more slowly and fades faster. In humans this step has not been measured directly; it is carried over from animal research. If it holds, why you cannot stop snacking has a hormonal layer, not only a psychological one. One more point worth noticing: if the problem is at the receiver rather than the sender, then eating less cannot turn the volume back up; the signal being sent has to be made stronger, with protein and dietary fiber.
3. The same meal, bigger blood-sugar swings.
After a meal, glucose is taken up mainly by skeletal muscle, which depends on insulin moving glucose transporters from inside the muscle cell onto its surface. Animal and cell studies suggest that estrogen keeps this pathway sensitive; when it withdraws, the same amount of insulin opens the door a little more slowly, glucose stays in the blood a little longer, and the pancreas has to release extra insulin to compensate. In humans, part of the fall in insulin sensitivity after menopause also comes from age and from newly added visceral fat. Insulin is also the store fat, do not release fat signal, so a higher peak means more of that meal's energy is pushed into storage. And it reinforces itself: the new visceral fat weakens insulin sensitivity further, tightening the loop.
4. Poor sleep directly rewrites the hunger hormones.
In the Spiegel 2004 randomized crossover trial (12 healthy young men), sleeping only 4 hours a night for 2 nights (against 10 hours) lowered leptin by 18%, raised ghrelin by 28%, increased subjective hunger by 24%, and increased appetite for calorie-dense, high-carbohydrate foods by 33–45%. In other words, short sleep turns the I am full signal down and the I want to eat signal up at the same time — and it specifically asks for carbohydrates. The trial was small and short, and its volunteers were not perimenopausal women, but the direction is clear. In perimenopausal women, sleep is broken by hot flashes, night sweats and anxiety; it is structural, not something going to bed earlier can fix. Fragmented sleep also makes the next day's strength training harder to get through, so it steps on both the eating path and the exercise path at once.
5. Losing weight itself provokes a counterattack.
This one applies to everyone. The Rosenbaum 2010 review sums up the weight-loss studies: after losing about 10% of body weight, energy expenditure falls by more than having less tissue can explain (roughly an extra 200–300 kcal a day), which is called adaptive thermogenesis. Sumithran 2011 followed overweight and obese adults who lost weight on a 10-week very-low-energy diet: a year later, ghrelin was still raised, leptin was still lowered, and hunger was still stronger. This is not a willpower problem. The body treats the current weight as a water level to defend, pushing spending down on one side and appetite up on the other. Perimenopausal women face this metabolic defense with the 4 extra headwinds above stacked on top.
In practice · New rules, a new playbook
Each of the five headwinds has one lever to move first:Falling resting metabolism and muscle loss: put strength training first. Since much of the drop in metabolism comes from losing muscle, defending muscle defends the metabolic baseline. Two to three truly loaded full-body sessions a week do more than any "fat-burning workout", and they are the most underrated prescription at this stageA blunted leptin signal: push protein up to 1.6 g/kg a day, plus plenty of fiber. If the fullness signal is naturally weaker, rebuild it with food. 30–40 g of protein per meal, plus enough soluble dietary fiber, directly strengthens fullness and eases the feeling that you cannot stop snackingFalling insulin sensitivity: drink less sugar and move after meals. If blood-sugar swings after meals are bigger, cut back on liquid sugar and refined carbohydrates; a 10–15 minute walk after a meal also shaves off part of the blood-sugar peakWorse sleep: treat sleep as an intervention, not a luxury. For insomnia linked to hot flashes, cognitive behavioral therapy for insomnia () comes first, together with a cool bedroom, avoiding alcohol, and no heavy meals before bed. Sleep better, and both the hunger-hormone imbalance and your tolerance for training improveThe metabolic defense during weight loss (adaptive thermogenesis): go slowly, not hard. A gentle calorie deficit (300–500 kcal a day, losing 0.25–0.5 kg a week) combined with keeping muscle should, by the mechanism, provoke less counterattack than extreme dieting and better protect body composition
One trap to avoid: stacking extreme calorie restriction on top of perimenopause is like pressing the accelerator in a stage when muscle is already easy to lose, and the usual result is the weight came back, but body composition is worse. So the key words for this stage are not try harder to eat less but keep your muscle, eat enough protein, sleep well, go slowly. The full order of priorities, and the discussion of hormone therapy, are in the chapter Strength training and protein first.
Chapter 3
Why visceral fat is the riskier kind
Fat under the skin is mainly storage and metabolically fairly quiet; visceral fat wraps around the liver, gut and pancreas, is highly active, and is the kind most closely tied to inflammation and metabolic risk. By one leading explanation (the portal hypothesis), the free fatty acids and cytokines it releases skip dilution in the rest of the body and go straight into the portal vein that leads to the liver; it can also convert cortisone back into cortisol locally, which draws in still more visceral fat.
So in perimenopause, what deserves watching is often not the scale but the waist: while fat is shifting from under the skin to the organs, weight can stay the same while cardiovascular risk climbs.
So in perimenopause, what deserves watching is often not the scale but the waist: while fat is shifting from under the skin to the organs, weight can stay the same while cardiovascular risk climbs.
Mechanism · Why visceral fat matters more than weight
What deserves attention in perimenopause is not the number on the scale but waist circumference: health risk is decided more by the type of fat than by the total amount.How the two kinds of fat differ:
Subcutaneous fat: under the skin, mainly energy storage, metabolically fairly inactive, with a smaller contribution to cardiovascular riskVisceral fat (VAT): wrapped around the abdominal organs (liver, intestines, pancreas), highly active metabolically, and the main source of inflammatory and metabolic risk
Why visceral fat is dangerous:
A direct line to the liver: by the portal hypothesis, the free fatty acids and cytokines released by visceral fat skip dilution in the rest of the body and go straight to the liver, where they drive insulin resistance in the liver and push toward metabolic dysfunction-associated steatotic liver disease () and type 2 diabetesA source of inflammatory signals: it releases pro-inflammatory molecules such as , and resistin, producing chronic low-grade inflammation throughout the body, which in turn damages the function of the vessel lining and promotes atherosclerosisA cortisol amplifier: the Björntorp 2001 review links stress, cortisol and abdominal fat into one chain. One link is that visceral fat is rich in an enzyme called 11β-HSD1, which turns inactive cortisone back into active cortisol; local cortisol rises and draws in more visceral fat, forming a loop in which the stress axis ( axis) and visceral fat push each other up. This is a mechanistic inference; which comes first in people has not been settledTied directly to cardiovascular events: in observational studies, at the same , people with more visceral fat have a clearly higher risk of heart attack and stroke
This is one of the metabolic bases for rising cardiovascular risk after menopause:
Women of reproductive age have clearly lower rates of cardiovascular events than men of the same age, which is generally attributed to estrogen's protection of the blood vesselsIn the 5–10 years after menopause, women's cardiovascular risk rises and the gap with men gradually narrowsTwo changes stack up: estrogen's vascular protection disappears, and fat distribution shifts toward the organs
Clinical measurement: the waist says more about this than BMI:
Waist of 80 cm or more in Asian women: the warning line for excess visceral fat (IDF criteria)Waist above 88 cm in US women (NCEP-ATP III)Waist-to-hip ratio (WHR) above 0.85 (women): signals higher cardiovascular riskA BMI in the normal range (18.5–24) with a waist over the line: this is "thin outside, fat inside" (TOFI), and the risk is easily underestimated
What it means in practice: women in perimenopause should measure their waist at least every 3–6 months; it tracks the direction of metabolic risk better than the scale. Weight holding steady while the waist grows is just as much a signal to act.
In practice · Measuring the waist, and what to track
Since visceral fat matters more than total weight, the bathroom scale should not be your only dashboard. What to measure, how to measure it, and which numbers should prompt action are set out below concretely enough to follow directly.How to measure your waist accurately (it is easier to get wrong than you might think):
Timing: in the morning, before eating and after using the toilet, to reduce the effect of food and bloatingPosition: run a soft tape measure horizontally around the navel, against the skin but not pulled tightPosture: stand relaxed and read it at the end of a normal breath out; never suck your stomach in — a flattering number from a held-in stomach means nothingFrequency: once every 3–6 months is enough; it shows a trend and does not need daily checks
Numbers to take seriously (Asian women):
Waist of 80 cm or more: the warning line for excess visceral fat (this is the IDF line for Chinese and South Asian women; the US NCEP-ATP III line for women is 88 cm)Waist-to-hip ratio above 0.85: signals higher cardiovascular riskWeight unchanged but waist growing: precisely the most typical perimenopausal signal — fat moving to the organs while total weight holds. Like weight going up, it is a signal to act
Beyond the waist, track these together:
Body-composition trend: if you can, check body-fat percentage and muscle mass periodically (a scan is the most accurate; a home body-fat scale using BIA is for trends only, not absolute values)Metabolic blood tests: fasting glucose or (HbA1c, a measure of average blood sugar over the past two to three months), blood lipids and blood pressure — these show better than weight whether visceral fat is harming youStrength: rising weights lifted and repetitions completed are the most direct evidence that muscle is being kept, and more reassuring than the scale
Swap watching your weight for watching your waist, body composition, metabolic markers and strength, and you move from a single number that water can fool to the few variables that actually decide your health.
idf-2006-metabolic-syndrome-definition
Chapter 4
Strength training and protein first
The interventions that work at this stage are still the familiar ones, but the order of priority is not the same as when you were younger. Strength training comes first, because it tackles muscle loss, insulin resistance and falling resting metabolism at the same time; protein strengthens the fullness signal that has been turned down; a Mediterranean-style diet reins in sugar and alcohol; and sleep should be treated as an intervention, not a luxury.
Hormone replacement therapy can partly shift fat distribution back, but it is an individual decision to make with a doctor, and it is not a weight-loss drug. Extreme undereating, by contrast, adds another blow in a stage when muscle is already easy to lose.
Hormone replacement therapy can partly shift fat distribution back, but it is an individual decision to make with a doctor, and it is not a weight-loss drug. Extreme undereating, by contrast, adds another blow in a stage when muscle is already easy to lose.
Evidence · Ranking strength, protein, diet and sleep
The interventions that work are still the familiar ones, but at this stage the order of priority is not the same as when you were younger. Roughly ranked by strength of evidence:① Strength training: first, not third. One thing tackles three at once: muscle loss, insulin resistance and falling resting metabolism. Two to three genuinely loaded full-body sessions a week are enough, with the weight raised little by little. Small studies suggest that women in perimenopause build muscle about as well as younger women, provided they eat enough protein and keep raising the load. Note that this does not mean light-weight, high-repetition toning classes; it means training that is genuinely hard — the most underrated prescription at this stage.
② Protein up to 1.6 g per kg of body weight a day. The receiving end of the fullness signal has been turned down (see Why weight loss gets harder now), so make the signal you send stronger: 30–40 g of protein per meal, 3–4 meals a day — not the soy milk for breakfast, salad for lunch pattern that runs light early and heavy late. Eggs, fish and lean meat, whey protein, tofu and Greek yogurt all count.
③ Mediterranean-style eating, with less sugar and less alcohol. There is no need for extreme low-carb or cutting out sugar entirely; the point is the quality of food (olive oil, fish and nuts, vegetables and fruit, whole grains, legumes), and sugary drinks should be cut back. Alcohol needs its own line: there is no amount that is safe for health, and less is better; after estrogen withdraws, alcohol's harms to sleep, liver fat and hot flashes are all amplified. If you do drink, keep to no more than 1 drink a day, with several alcohol-free days.
④ Treat sleep as an intervention, not a luxury. For insomnia linked to hot flashes, cognitive behavioral therapy for insomnia () comes first: it is the first-line recommendation, and in studies it works about as well as sleeping pills without the dependence. Keep the bedroom cool (16–19°C) and the bedding breathable, and avoid alcohol, heavy meals and screens before bed. Hormone replacement therapy () has a clear effect on hot flashes and sleep, but it is an individual decision to make with your doctor (see point ⑤ below).
In practice · How to train, and why protein matters
How to structure training. One full-body session works through 8–10 main exercises (covering push, pull, lower body, hips and core), each for 6–12 repetitions and 2–4 sets. The one thing you cannot skip is progressive overload: if you cleanly finish the top of the repetition range this week, raise the weight a little next time. Muscle is called out by the signal this time is harder than last time, not by total time; an hour spent on a session whose weights never go up does limited good.Why you need enough protein even more inside a calorie deficit. The Longland 2016 randomized trial (in young men, lasting a few weeks, a proof-of-principle study) put both groups into a calorie deficit with high-intensity training; the only difference was protein. The high-protein group (about 2.4 g/kg) lost 4.8 kg of fat and gained 1.2 kg of lean mass, while the usual-protein group lost fat over the same period but gained almost no lean mass. It cannot be carried directly over to perimenopausal women, but the direction of the conclusion is this: inside a deficit, protein decides whether what comes off is fat or muscle — not that more protein is always better. For this age group, that is exactly the fork that matters most: once muscle is lost, the sinking baseline of resting metabolism sinks faster.
A side note: protein comes with a small processing fee. Digesting and absorbing it costs part of the energy it contains (the thermic effect of food is about 25–30%, higher than for carbohydrates or fat), and it is also more filling — both of which work in your favor.
Why sugary drinks are worth cutting at this stage in particular. Fructose is processed mainly in the liver; and by the portal hypothesis, visceral fat in the abdomen sends free fatty acids straight into the liver (see Why visceral fat is the riskier kind), so the liver is already being flooded while insulin sensitivity is sliding. The same sweet drink, landing on a liver under pressure from both sides, carries an amplified metabolic load. This is not sugar is poison; it is the same amount of sugar meeting a system with less spare capacity.
Clinical · Hormone therapy, and why not crash-diet
⑤ Discuss hormone replacement therapy () with your doctorHow to read the current evidence: the Women's Health Initiative (WHI) randomized trials and the reanalyses that followed show fewer fractures as a direct trial result; among women who started before 60 or within 10 years of menopause, the figures for cardiovascular disease and all-cause death lean toward benefit, but these come from subgroup and secondary analyses, not the trials' main conclusions. The risk of blood clots appears lower with low-dose transdermal estrogen (patches, gels), which comes from observational studies; breast-related risk has to be weighed individually with your doctorEffect on body shape: studies have found that hormone therapy reduces part of the redistribution of fat toward the abdominal organs and improves insulin sensitivityIt is not a weight-loss drug, but it can restore a friendlier metabolic backgroundThe decision must be individual: it has to take into account any history of breast cancer, blood clots or cardiovascular disease, and be made with a gynecologist or endocrinologist
⑥ Do not rely on extreme calorie restriction
Sumithran 2011 still found raised hunger hormones and stronger hunger a year after weight loss on a very-low-energy diet, and the Rosenbaum 2010 review sums up how energy use falls below what is expected after weight loss. Neither directly compared losing fast with losing slowly; that a gentle deficit provokes less counterattack is inferred from the mechanismPerimenopause adds the risk of muscle loss: extreme dieting worsens sarcopenia, resting metabolism drops further, and on the rebound fat returns faster than muscle, so the result is the weight came back, but body composition is worseA gentle calorie deficit (300–500 kcal a day) is recommended, together with strength training and high protein, losing 0.25–0.5 kg a week
References · 6
- Björntorp, P. (2001). Do stress reactions cause abdominal obesity and comorbidities? Obesity Reviews, 2(2), 73–86. 10.1046/j.1467-789x.2001.00027.x
- The Global BMI Mortality Collaboration. (2016). Body-mass index and all-cause mortality: Individual-participant-data meta-analysis of 239 prospective studies in four continents. The Lancet, 388(10046), 776–786. IPD from 239 prospective studies (10.6 million people); primary analyses in 3.95 million never-smokers without chronic disease who survived 5 years. All-cause mortality lowest at BMI 20.0-25.0; HR 1.13 at 18.5-20, 1.51 at 15-18.5, 1.07 at 25-27.5, 1.20 at 27.5-30, 1.45 at 30-35, 1.94 at 35-40, 2.76 at 40-60; per 5 units above 25, HR 1.39 in Europe and east Asia, 1.29 North America, 1.31 Australia/NZ; stronger in younger people and men (abstract, PMID 27423262). 10.1016/S0140-6736(16)30175-1
- Spiegel, K., Tasali, E., Penev, P., & Van Cauter, E. (2004). Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 141(11), 846–850. 10.7326/0003-4819-141-11-200412070-00008
- Rosenbaum, M., & Leibel, R. L. (2010). Adaptive thermogenesis in humans. International Journal of Obesity, 34(Suppl 1), S47–S55. Narrative review. Maintaining a 10% or greater reduction in body weight is accompanied by an approximate 20-25% decline in 24-hour energy expenditure; this fall in weight-maintenance calories is 10-15% below what is predicted from the changes in fat and lean mass, so a formerly obese person needs ~300-400 fewer calories a day than a never-obese person of the same weight and composition. Non-resting energy expenditure accounts for as much as 85-90% of the decline below predicted values, and skeletal-muscle work efficiency at low exercise levels rises by about 20%. Circulating T3 shows 'small but statistically significant decreases' - the review gives no percentage. Short-term leptin given to weight-reduced subjects, restoring pre-weight-loss leptin levels, reverses the lower energy expenditure, thyroid hormone and sympathetic activity, the higher muscle efficiency and the increased energy intake. The abstract cites an over 80% recidivism rate after weight loss (abstract, PMID 20935667; full text, PMC3673773). 10.1038/ijo.2010.184
- Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., & Proietto, J. (2011). Long-term persistence of hormonal adaptations to weight loss. The New England Journal of Medicine, 365(17), 1597–1604. 50 overweight or obese adults without diabetes on a 10-week very-low-energy diet; mean loss 13.5 kg. Measured at baseline, 10 and 62 weeks: leptin, ghrelin, PYY, GIP, GLP-1, amylin, pancreatic polypeptide, CCK, insulin and subjective appetite. At 62 weeks, leptin, PYY, CCK, insulin, ghrelin, GIP, pancreatic polypeptide and hunger still differed significantly from baseline; GLP-1 and amylin are not in that list. No thyroid hormone or energy-expenditure measure is reported in the abstract (abstract, PMID 22029981). 10.1056/NEJMoa1105816
- Longland, T. M., Oikawa, S. Y., Mitchell, C. J., Devries, M. C., & Phillips, S. M. (2016). Higher compared with lower dietary protein during an energy deficit combined with intense exercise promotes greater lean mass gain and fat mass loss: A randomized trial. American Journal of Clinical Nutrition, 103(3), 738–746. 40 young men (20 per group), 4 weeks at a ~40% energy deficit with resistance training plus high-intensity intervals 6 days a week; 2.4 vs 1.2 g protein/kg/day. Lean body mass +1.2 ± 1.0 kg vs +0.1 ± 1.0 kg; fat mass -4.8 vs -3.5 kg; exercise performance improved similarly in both groups. The authors call it a proof-of-principle trial (abstract, PMID 26817506). 10.3945/ajcn.115.119339