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Women & lifting
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In one pass Strength training will not give a woman a bodybuilder's bulk. Not this — Lifting weights makes women bulky — Men's blood testosterone is more than 15 times women's; with the same strength training women gain muscle at a similar relative rate, but from a much smaller base, so the result is lean and defined, not a bodybuilding-stage look.
Educational content, not medical advice — consult a clinician.
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Chapter 1
Will lifting make women bulky?
Testosterone is one of the strongest signals for muscle growth. From puberty on, men's blood testosterone is more than 15 times women's (Handelsman 2018, a review). So men start with more muscle and have a higher ceiling, and the same training adds fewer kilograms in women. Measured as a relative change, though, women respond to training just as well: in the pooled by Roberts 2020, muscle growth did not differ between men and women, and women's relative gains in upper-body strength were actually larger.
The look of the muscular women on social media comes from years of specialized training, very low body fat and sometimes hormones taken from outside the body — not from a few extra months in the gym. What strength training gives most women is more strength, more definition, and benefits for bone and metabolism.
Mechanism · How testosterone actually thickens a fiber
Testosterone is not a nutrient. It is an instruction — and the way it gets into the cell is unusual.It is a fat-soluble steroid, so it does not need to knock. It passes straight through the muscle cell's membrane, finds a protein inside called the androgen receptor, and docks on it. Think of the receptor as a lock and testosterone as the key: within the normal physiological range, more keys open more locks. Once unlocked, key and lock move together into the nucleus, sit down on the DNA, and turn up the production orders for actin and myosin — the two proteins that actually do the contracting. The newly made contractile protein is laid down in parallel layers inside the fiber, and the fiber's cross-section widens. Under a microscope, getting thicker is exactly this.
Testosterone has a second hand as well, and that one sets the ceiling. On the outside of each muscle fiber sits a layer of usually dormant repair cells called satellite cells. The micro-damage from training wakes them; they fuse into the damaged fiber and donate their own nuclei to it. Donated nuclei matter because a fiber is not run by a single nucleus. Each nucleus only supports protein building in a small patch around itself — like a cook who can only serve the few tables in front of them; to serve the whole restaurant at once, you need to hire more cooks. Testosterone drives satellite cells both to multiply and to fuse into the fiber, so the number of nuclei rises, and so does the maximum thickness that fiber can reach.
So the difference in hormonal environment lands mainly on two concrete things: how much muscle you start with, and how thick a fiber can ultimately become. It does little to change the relative response to a given block of training — which is why trials find men and women gain muscle by similar percentages. A woman who trains properly has both pathways working normally, and she does get stronger and more defined. It is just that pushing those pathways to the size of a male bodybuilder takes a number of keys her ovaries and adrenal glands cannot make.
Evidence · What two years of lifting actually does
Make the expectation concrete. A woman who strength-trains 3 times a week for 2 years adds net muscle (fat-free mass, FFM) that is measured in kilograms and summed over the whole body. Her shape moves toward lean and defined, not male bodybuilder.Spread out, that amount is smaller still: shared across two legs, two arms, the back and the shoulders, then across every month of those two years, the change in any one month is almost invisible. That is why nobody wakes up bulky. Real thickening of muscle fibers is built up over months and years, slowly enough that you cannot see it in the mirror day to day.
Look at the drug side and the gap is even clearer. What anabolic steroids and other outside androgens do is push the number of keys straight to a level neither ovaries nor testes can produce (the selective androgen receptor modulators, SARMs, marketed as working the same way target the same lock), so both pathways — turning up the production orders and supplying extra nuclei — are driven far past the physiological range. In a randomized trial Bhasin 1996 published in the NEJM, healthy men injected with testosterone at doses above the physiological range had clearly larger arm and thigh muscles and more strength even without training, and gained more still when they trained as well.
Put those two paragraphs side by side and the fear falls away on its own. You cannot copy her prescription, so you cannot copy her size; and the route you can copy is so slow that you have every chance to stop whenever you like.
Myth · When girth goes up, what actually got thicker
This is how a lot of people get scared off: a few weeks in, they measure a thigh, find it has gone up a size, conclude "I really do put on muscle easily," and stop at once.The problem is the girth measurement itself. How thick a thigh measures is the sum of at least three things: the cross-section of the muscle fibers, the layer of fat under the skin that sits over the muscle, and how much glycogen and water the muscle is holding at that moment. In a beginner's first few weeks, almost all of the extra thickness comes from the last two:
The pump: during training, blood and tissue fluid are squeezed into the working muscle and it swells for a while. This happens at the level of circulation, and it goes down within tens of minutes to a few hours after you finish.Glycogen is stored wet: with regular training, muscle raises its glycogen stores, and glycogen enters the muscle cell with water attached, so a bigger store means more water in the cell too. Both the scale and the tape measure record this, but it is not contractile protein.Swelling while sore: a heavy load or an unfamiliar movement causes micro-damage in muscle fibers, and the area draws in fluid for repair, so on sore days the muscle looks puffier. This too is temporary.
Together, these three can shift the tape measure noticeably within a few weeks, while real thickening of the fibers has barely moved over the same period.
Looking further ahead, what decides whether a leg looks thick is often not the muscle either, but the fat layer on top of it — because muscle grows slowly, while the thickness of the fat layer can change a good deal within a few months. Strength training plus enough protein usually thins the fat layer and lets the muscle hold the skin flatter, so girth may barely change or even shrink while the shape changes.
So the fear of getting thick and bulky does not hold at either end of the timescale. The extra thickness you see in the first few weeks is not muscle, and the muscle that really does arrive years later comes so slowly that changes in the fat layer will mask it.
Chapter 2
How the cycle affects training
The phase map that is often quoted looks roughly like this:
Follicular phase (days 1–14 of the cycle, estrogen rising, progesterone low): many women feel good and recover quickly.Around ovulation (about day 14): estrogen peaks. One observational study (Wojtys 2002) found anterior cruciate ligament (ACL) tears clustered in this window, so cutting and landing deserve extra care.Luteal phase (days 15–28, progesterone rising): core temperature rises by 0.3–0.5°C and heat tolerance falls, so long aerobic efforts on hot days tend to suffer; strength training is little affected.During the period: individual differences are huge. Some women train as usual; others with severe premenstrual syndrome (PMS) need to cut back.
In practice there is no need to restructure training around the cycle. Adjusting the intensity to how you feel on the day is enough.
Mechanism · What estrogen and progesterone each do
The phase map of the menstrual cycle is usually quoted from Sims 2016, the popular book *Roar*, and the Janse de Jonge 2003 review. It shows what happens when, not why. Add the why and you can work out your own case instead of memorizing a table.The estrogen side leans toward building and protection. Estrogen can dock on receptors in muscle cells and connective-tissue cells. Animal and cell studies suggest it steadies cell membranes, slows the breakdown after training, and nudges the pain threshold up a little. That is why some women find the same set feels more manageable in the second half of the follicular phase, as estrogen climbs. How large this is in people is not clear, and the group-level differences in the McNulty 2020 were small.
The same estrogen shows another face in ligaments. The fibroblasts that make collagen in a ligament also carry estrogen receptors. In cell studies, when estrogen is high they actually make collagen more slowly, so the ligament may loosen slightly. The knee, which relies first on its ligaments to hold it and only then on muscles tightening, is most exposed to this: in the fraction of a second of a sudden stop, a change of direction or a landing, the joint is allowed a little more play before the muscles lock it. Reasoning from the mechanism, this may be one reason anterior cruciate ligament (ACL) injuries cluster around ovulation. The human evidence is observational — Wojtys 2002 studied female athletes who had already been injured and used hormone levels to work out where in the cycle they were at the time — and it cannot show that estrogen caused the injuries. So the takeaway is not "do not train around ovulation" but "on those days, land and change direction more carefully, and start slowing down a little earlier."
The progesterone side moves the thermostat. Progesterone acts on the part of the hypothalamus that sets body temperature and pushes the set point up. With a higher set point, you have to get hotter before you start sweating and before blood is diverted to the skin, so the start of heat loss is delayed. For a set of squats in a cool room this hardly matters. On a long run in muggy weather, you start warmer, shed heat later, heat builds up inside faster, and performance naturally drops.
Connect these two chains and you no longer have to memorize the table: what the cycle mainly affects is not muscle itself but heat loss and connective tissue. So short, intermittent strength training with limited total heat production is little affected, while long aerobic work in the heat is affected much more. These are not two separate tips; they follow from the same mechanism.
Evidence · How well cycle-based training is supported
The idea of "loading strength in the follicular phase and endurance in the luteal phase" has become popular in recent years, especially on social media, but the evidence for it is weak:McNulty 2020, a systematic review and of 78 studies: differences in strength and endurance performance between phases were too small to matter, apart from possibly slightly lower performance in the early follicular phase. The authors rated the evidence as low quality, concluded that no general cycle-based training guidelines can be set, and recommended adjusting to each woman's own response.Blagrove 2020, a systematic review and meta-analysis: strength-related measures changed only slightly between phases, and the included studies carried a high risk of bias.Carmichael 2021, a narrative review: athletes themselves often feel worse in the early follicular and late luteal phases, but objective tests showed no clear, consistent effect of cycle phase.
So do not simply follow the prescriptions of a cycle-syncing training app. What is more useful is to log 2–3 cycles of your own training and how you feel, see your own pattern, and then fine-tune to that pattern rather than copying an influencer's template.
Chapter 3
Strength training around menopause
Strength training can hold back all three at once, and it does so through a load that is heavy enough, not through gentle activity: bone only responds to deformation that is large enough, and muscle only to loads beyond what it is already used to.
A concrete example is the LIFTMOR trial (Watson 2018). 101 postmenopausal women with low bone mass (osteopenia or osteoporosis), aged 65±5 years, did 8 months of closely supervised high-intensity resistance and impact training — squat, deadlift and overhead press, 5 sets of 5 reps at more than 85% of their one-repetition maximum (, the most they could lift once), twice a week for about 30 minutes each time. "Too heavy" is not the problem: this intensity is exactly where the data come from. Getting enough calcium and vitamin D is the other half of the job.
Mechanism · Why bone loss speeds up once estrogen falls
Bone is not a dead lump of mineral. It is taken apart and rebuilt throughout life. The cells that take it apart are osteoclasts, and the cells that build it are osteoblasts. Through adulthood the two sides run at matching speeds for a long time, which is why bone mass looks like a stable number.Estrogen has its foot on the brake in this balance, and the pedal it presses is on the take-apart side. It turns down the signal in bone that tells cells to start demolition (), and it shortens the lifespan of osteoclasts — fewer demolition workers, working shorter shifts.
At menopause estrogen drops sharply and that foot comes off the brake. The demolition signal grows stronger, osteoclasts become more numerous and live longer, and the osteoblast side does not speed up to match. So every cycle of taking apart and rebuilding leaves a small deficit, and the deficits add up, which is why falls fastest in the first years after menopause. This is not bone suddenly turning brittle; it is an account running a small overdraft every day. It also explains why those years are the window for action: the longer you wait, the larger the deficit to fill.
Once you see this chain, you also see why calcium and vitamin D alone are not enough. Calcium and vitamin D make sure the building side has materials, and that the materials can get into bone. What has actually run out of control is the speed of the take-apart side. No amount of material solves demolition that is too fast. That takes a different signal telling bone that this site is still in use and should not be taken apart. That signal is load.
Mechanism · How bone senses load
Deep inside bone lies a layer of cells sealed into the hard matrix, called osteocytes. Each lives in its own small cavity, and the cavities are linked by extremely fine channels filled with fluid. It is the least sensor-like sensor in the body, but it is bone's sensing network.When a bone is bent or pulled, the matrix deforms by a tiny amount, and that deformation pushes the fluid in the fine channels into motion. What the osteocyte actually senses is not weight but that flush of fluid beside it. If the flush is strong enough, it sends out less of the inhibitory signal that says stop building (sclerostin). Once that brake eases, the osteoblasts are let through and start adding material in the direction of the load.
Everything hangs on the words strong enough. In the pattern seen in animal loading experiments, this pathway is sensitive to the size and speed of the deformation, while extra repetitions soon stop adding anything. So ten thousand steps and one heavy lift are not the same event for an osteocyte: walking deforms bone so little that the fluid in the channels barely moves, and repeating it many more times still does not add up to much of a signal. This is exactly where "walking more is good for your bones" is most misleading.
Where, then, does the largest force on bone in everyday life come from? Not body weight — muscle. When a muscle contracts it pulls through its tendon on the point where it attaches to bone, and that pull is far larger than the force of body weight pressing down as you stand. So training muscle and training bone are two faces of the same physiology: how much weight you can pull decides how hard your bones get pulled each week.
Which is why being afraid it is too heavy gets things backward here: a weight so light it takes no effort is exactly the weight the osteocytes cannot hear.
Mechanism · Why the same training returns less
After menopause a second thing changes: from the same training session and the same protein meal, muscle builds less protein than it did when younger. This is called anabolic resistance.Taken apart, both ends have become less responsive. On the eating side, the same serving of protein produces a weaker building response in older muscle, partly because insulin sensitivity falls and partly because muscle cells respond less to amino acids, leucine in particular. The per-meal dose analyses that Morton 2018 cites show that older adults need a larger serving of good-quality protein to push protein building to about the level younger people reach. On the training side, the chain by which a muscle fiber senses mechanical tension and translates it into a building signal is also less sensitive, so light loads have a harder time making a difference.
Put the two together and the conclusion gets simpler: what this stage calls for is not gentler training but clearer training. Get a proper serving of good-quality protein at each main meal instead of scraping it together in small amounts through the day, and train with compound lifts that carry real weight rather than only small machines. Places you could get away with by training more when younger now have to be covered by training enough.
This chain also explains something else: why at this stage the waist grows while the arms and legs get thinner. Fat moves toward the abdomen while muscle quietly retreats. The number on the scale may hardly move while body composition has been swapped out — watching weight alone misses this entirely.
Evidence · How much the three chains move in trials
Each of the three mechanism chains has evidence behind it:Protecting bone: in the LIFTMOR trial (Watson 2018), 101 postmenopausal women with low bone mass (aged 65±5) trained under close supervision for 8 months, twice a week for about 30 minutes each time. Their lumbar-spine rose by 2.9% and the femoral neck held steady, while in the control group, who did a home-based low-intensity program, both sites kept falling. Only one adverse event was reported in the whole trial, a minor lower-back spasm. Note the weight of rose instead of fell: at this age, simply not losing bone is already a good result. But the trial was in women with low bone mass training under dedicated supervision; it does not mean anyone can start lifting heavy at home on their own.Keeping muscle: training clearly preserves muscle mass and strength and counters sarcopenia.Reducing visceral fat: strength training combined with aerobic exercise also lowers the visceral fat inside the abdomen, by amounts that vary between studies. Visceral fat is the layer wrapped around the abdominal organs, not the same thing as the fat under the skin. It releases signaling molecules into the blood more actively and is most closely tied to metabolic-syndrome risk, so this is about more than a smaller waist.
There are also gains in fall prevention and quality of life. Falls matter more than they seem for someone whose bone density is already slipping: bone density decides whether a fall breaks something, while strength and balance decide whether you fall at all. Strength training works on both at once, which is part of why it is worth more than calcium on its own.
The bone side is covered more fully in Osteoporosis, and the muscle side in Sarcopenia.
Chapter 4
Practical entry prescription
First, use the same program as male beginners; there is no need for a women's edition. Physiological differences change how much you gain in absolute terms, not what training should look like. What really matters is progressive overload: as your ability grows, the load goes up a little at a time. For a 12-week beginner program, see Resistance training basics.
Second, eat enough protein: about 1.6 g per kg of body weight a day. In the training trials Morton 2018 pooled, muscle gains largely leveled off around that intake; allowing for statistical uncertainty, the upper bound was 2.2 g. Training sends the get stronger instruction and protein supplies the material; if the instruction arrives without enough material, the repaired muscle fiber will be no thicker than before.
Third, be aware of your cycle without being ruled by it. On days you feel good, push a little. If you feel bad in the luteal phase or during your period, keep training but drop the intensity by 5–10%; there is no need to rewrite the plan around the cycle.
The three most common detours — only lifting light weights, scheduling by a cycle app, and waiting to lose fat before lifting — can each be traced to where they break the same chain: training supplies the signal, protein supplies the material.
Mechanism · Training sends the signal, protein the material
Training and protein do two different jobs in muscle. Look at them separately once and you no longer need to memorize the target number.Training supplies mainly the signal. When a muscle fiber is pulled by enough tension, the pathway inside the cell that starts the work is switched on, and for the next day or two the muscle turns up its rate of protein building. The signal itself contains no material.
Protein supplies the material, and a little signal as well. The protein you eat is broken down in the gut into amino acids that enter the blood; one of them, leucine, gives the start switch a push of its own, and training makes the muscle cell more sensitive to the same serving of amino acids. But protein building is not an accelerator that goes faster the harder you press: within one meal it levels off beyond a certain amount, and more of the extra amino acids are burned as fuel. So how protein is spread across meals makes some difference, but over weeks of muscle gain the day's total matters more. Protein quality matters too: protein that supplies all the essential amino acids and digests well gives more raw material for building from the same amount (Phillips 2016, a review).
So the two have to meet before anything is produced. Train without eating enough, and it is a building site that opens every day with too little material coming in: repair can only rob one wall to patch another, and the repaired fiber is no thicker than before — the most common version of working hard with no change. Eat without training, and most of the extra amino acids are burned for energy or turned into something else, because no signal told the body where to put them.
Women are more likely to get stuck on the material side, and the reason is no mystery. Total calorie intake is smaller to begin with, and common eating patterns are low in protein density (lots of salad, fruit and refined staples), so a day can easily end a long way short of the target. That gap does not show on the scale at all. It shows only as six months of training that seems to have changed nothing.
One more point: why this target does not need a separate version for women. It is set per kilogram of body weight, so a smaller person already gets a smaller absolute amount. Body-size differences are built into the number.
Myth · Three detours, and which link each one breaks
More useful than not recommended is knowing which link each one breaks.Only cardio, plus small dumbbells and high reps. This is a leftover from 1980s aerobics classes. Its problem is not the high rep count but a weight so light that you stop long before getting near failure. Muscle recruits fibers in order from small to large: under a light load only the small endurance fibers work, and the fibers that are largest and have the most growth potential are called in only when the weight is heavy enough, or when you get close to failure. Swing a small dumbbell a few hundred times while staying far from failure, and those fibers never work a single shift, so tiring and effective get mixed up into one thing. It became popular precisely because people were afraid of getting bulky, so this detour grows straight out of the fear of bulking itself.
Following an app that schedules training by cycle phase. The evidence on the menstrual cycle runs like this: cycle effects are real for some individuals but negligible across groups, so what you can use is your own training log, not a template someone else set.
Waiting to lose fat before starting to lift. This one costs the most. In a calorie deficit, the body has to break down its own tissue to make up the gap, and whether it takes fat or muscle depends on whether there is a signal saying this muscle is still in use. Strength training is that signal. With it, the gap is filled mainly from fat; without it, a substantial share of what you lose will be muscle rather than fat. And with less muscle, the energy you burn at rest each day falls a little too, which is one reason the same diet gets harder and harder to keep losing on. See Hypertrophy mechanisms.
References · 10
- Morton, R. W., et al. (2018). A systematic review, meta-analysis and meta-regression of the effect of protein supplementation on resistance training-induced gains in muscle mass and strength in healthy adults. British Journal of Sports Medicine, 52(6), 376–384. 49 RCTs, 1,863 participants, resistance training of 6 weeks or more. Protein supplementation added 2.49 kg to 1RM and 0.30 kg to fat-free mass; the effect fell with age and was larger in trained people. Break point for FFM gains at 1.62 g/kg/day (95% CI 1.03-2.20; 42 study arms, 723 participants; the biphasic model was not statistically significant, p = 0.079); given the CI, the authors say ~2.2 g/kg/day may be prudent for those maximising gains; timing, post-exercise dose and source play a minor if any role; they cite per-dose MPS break points of 0.24 (younger) and 0.40 g/kg (older). One author reports grant support from the US National Dairy Council (abstract and full text, PMC5867436). 10.1136/bjsports-2017-097608
- Schoenfeld, B. J. (2010). The mechanisms of muscle hypertrophy and their application to resistance training. Journal of Strength and Conditioning Research, 24(10), 2857-2872. 10.1519/JSC.0b013e3181e840f3
- Handelsman, D. J., Hirschberg, A. L., & Bermon, S. (2018). Circulating testosterone as the hormonal basis of sex differences in athletic performance. Endocrine Reviews, 39(5), 803-829. Before puberty there is no sex difference in circulating testosterone or athletic performance; from puberty men's circulating testosterone exceeds women's more than 15-fold at any age. A dose-response relationship links circulating testosterone to muscle mass, strength and haemoglobin in both sexes, accounting for an 8-12% ergogenic advantage in men. 10.1210/er.2018-00020
- Roberts, B. M., Nuckols, G., & Krieger, J. W. (2020). Sex differences in resistance training: a systematic review and meta-analysis. Journal of Strength and Conditioning Research, 34(5), 1448-1460. Across 10 studies hypertrophy did not differ between males and females (ES = 0.07, P = 0.31) and lower-body strength did not differ (P = 0.20); relative upper-body strength gains significantly favoured females (ES = -0.60, P = 0.002). 10.1519/JSC.0000000000003521
- Bhasin, S., Storer, T. W., Berman, N., Callegari, C., Clevenger, B., Phillips, J., Bunnell, T. J., Tricker, R., Shirazi, A., & Casaburi, R. (1996). The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. The New England Journal of Medicine, 335(1), 1-7. 43 normal men randomised to placebo or 600 mg testosterone enanthate weekly for 10 weeks, each with or without standardised weight training 3 times a week. Without exercise, testosterone increased triceps and quadriceps area and bench-press and squat strength compared with placebo; testosterone plus training gave the largest gains (fat-free mass +6.1 kg, bench press +22 kg, squat +38 kg). The abstract reports the no-exercise group's gains as muscle area and strength, not fat-free mass; mood and behaviour did not change (abstract, PMID 8637535). 10.1056/NEJM199607043350101
- Sims, S. T., & Yeager, S. (2016). ROAR: How to match your food and fitness to your unique female physiology for optimum performance, great health, and a strong, lean body for life. Rodale Books. Synthesises menstrual cycle × training response literature; the basis of cycle-aware (but not cycle-dogmatic) programming.
- McNulty, K. L., Elliott-Sale, K. J., Dolan, E., et al. (2020). The effects of menstrual cycle phase on exercise performance in eumenorrheic women: a systematic review and meta-analysis. Sports Medicine, 50(10), 1813-1827. 78 studies: exercise performance might be trivially reduced in the early follicular phase compared with all other phases (pooled ES -0.06; largest contrast early vs late follicular -0.14); large between-study variation and mostly low-quality evidence, so no general guideline can be formed and a personalised approach is recommended (abstract, PMID 32661839). 10.1007/s40279-020-01319-3
- Wojtys, E. M., Huston, L. J., Boynton, M. D., Spindler, K. P., & Lindenfeld, T. N. (2002). The effect of the menstrual cycle on anterior cruciate ligament injuries in women as determined by hormone levels. The American Journal of Sports Medicine, 30(2), 182-188. Observational: 69 female athletes studied within 24 hours of an acute ACL tear at four centres, with cycle phase checked by urinary oestrogen, progesterone and LH metabolites. More tears than expected occurred at midcycle (ovulatory phase) and fewer in the luteal phase; oral contraceptive use weakened the association (abstract, PMID 11912085). 10.1177/03635465020300020601
- Watson, S. L., Weeks, B. K., Weis, L. J., Harding, A. T., Horan, S. A., & Beck, B. R. (2018). High-intensity resistance and impact training improves bone mineral density and physical function in postmenopausal women with osteopenia and osteoporosis: The LIFTMOR randomized controlled trial. Journal of Bone and Mineral Research, 33(2), 211–220. 101 postmenopausal women (mean 65 years) with low bone mass (T-score below -1.0): 8 months of twice-weekly 30-min supervised high-intensity resistance and impact training (5 x 5 above 85% 1RM) vs home low-intensity exercise. Lumbar spine BMD +2.9% vs -1.2%, femoral neck +0.3% vs -1.9%; better function; one adverse event (minor back spasm) under close supervision (abstract, PMID 28975661). 10.1002/jbmr.3284
- Phillips, S. M. (2016). The impact of protein quality on the promotion of resistance exercise-induced changes in muscle mass. Nutrition & Metabolism, 13, 64. Per-meal 0.3-0.5 g/kg distribution + DIAAS-quality dominates over total intake alone. 10.1186/s12986-016-0124-8