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Immune Aging & Inflammaging
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In one pass An aging immune system is not weaker across the board; it is out of balance.
Educational content, not medical advice — consult a clinician.
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Chapter 1
Aging immunity: off balance, not weaker
An aging immune system is not weaker across the board; it is out of balance. It grows blunt where it should respond, and smolders for years where it should not burn at all.
The blunting starts in the thymus, the organ that trains new T cells. From puberty on it shrinks year by year and is replaced by fat, so fewer and fewer new T cells can recognize pathogens the body has never met. Old antigens it has seen before are still guarded by memory cells; to a brand-new virus or vaccine, the body responds more slowly and more weakly. The smoldering side is chronic low-grade inflammation that rises slowly with age.
So turning immunity as high as possible was the wrong direction from the start; what really helps are things that tune it — vaccines, exercise, enough protein. One more thing to remember: infections in older people can move fast and look atypical. If an infection is spreading quickly, or there is shortness of breath or a change in consciousness, go to the emergency department right away.
The blunting starts in the thymus, the organ that trains new T cells. From puberty on it shrinks year by year and is replaced by fat, so fewer and fewer new T cells can recognize pathogens the body has never met. Old antigens it has seen before are still guarded by memory cells; to a brand-new virus or vaccine, the body responds more slowly and more weakly. The smoldering side is chronic low-grade inflammation that rises slowly with age.
So turning immunity as high as possible was the wrong direction from the start; what really helps are things that tune it — vaccines, exercise, enough protein. One more thing to remember: infections in older people can move fast and look atypical. If an infection is spreading quickly, or there is shortness of breath or a change in consciousness, go to the emergency department right away.
Mechanism · Why a shrinking thymus means fewer recruits
The age-related change in the immune system is, strictly speaking, not an overall weakening but a structural reorganization plus a failure of regulation: some functions really do slow down, while others become overactive. That combination is what researchers call immunosenescence.The core hardware change is shrinking of the thymus, known as thymic involution (reviewed by Thomas 2020). The thymus is where recruits are trained: naïve T cells, which have not yet met any antigen, mature there and learn to recognize new antigens they have never seen. From puberty on the thymus degenerates year by year and is replaced by fat tissue, so from midlife it turns out fewer and fewer new naïve T cells.
The consequences are concrete. Old antigens met over a lifetime — childhood measles, flu strains that circulate every year — are still guarded by memory cells. But against a brand-new pathogen or vaccine antigen there are not enough recruits, and the range of antigens T cells can recognize (called T-cell receptor diversity, or TCR diversity) shrinks, so first recognition is slow and blunted.
Mechanism · What blunting plus smoldering looks like
This explains three things common in older adults:Slower clearance of new infections: the same viral infection runs a longer course with more complications.Blunted vaccine responses: the same vaccine dose produces fewer antibodies that last a shorter time. That is exactly why there are high-dose vaccines, and vaccines with an adjuvant (an ingredient that strengthens the response), designed for older adults.Weaker immune surveillance: abnormal cells are cleared less efficiently.
But notice the word dysregulated. Immune aging is not simply a loss of firepower. It comes with a rise in chronic low-grade inflammation (the inflammaging described in the chapter Low-grade inflammation with age) and a drift toward autoimmunity: the aging immune system is blunt where it should respond, yet smolders for years where it should not burn.
This point is the key to the whole story. If the problem is dysregulation and imbalance, then turning immunity as high as possible is the wrong direction from the start — and that is the mechanistic reason immune boosters do not hold up, as later chapters show. The general mechanism of chronic low-grade inflammation is covered in another story (see Chronic low-grade inflammation); chronic stress speeds this process up through immune disruption (see Chronic Stress); and it also shares some roots with brain aging (see Cognitive Aging & Cognitive Reserve).
Chapter 2
Low-grade inflammation with age
What rises slowly with age is not the red, swollen, hot, painful fire of acute inflammation. It is a low-grade smolder throughout the body with no infection behind it: inflammatory signals such as interleukin-6 (), C-reactive protein () and tumor necrosis factor () run slightly high year after year.
In 2000, Franceschi gave it a name: inflammaging. It is the same machinery as chronic inflammation in general, with a few extra drivers that only become prominent with age. The most central is senescent cells — cells that have stopped dividing but do not die — which keep releasing pro-inflammatory signals into their surroundings.
Know the limits of this chain: senescent cells pushing up inflammation, and inflammation in turn driving disease, has strong evidence in animals and cell experiments; in people it is so far mostly association plus mechanistic reasoning. So what you can act on rests on lifestyle evidence that already holds up, not on anti-aging drugs that are still in trials.
In 2000, Franceschi gave it a name: inflammaging. It is the same machinery as chronic inflammation in general, with a few extra drivers that only become prominent with age. The most central is senescent cells — cells that have stopped dividing but do not die — which keep releasing pro-inflammatory signals into their surroundings.
Know the limits of this chain: senescent cells pushing up inflammation, and inflammation in turn driving disease, has strong evidence in animals and cell experiments; in people it is so far mostly association plus mechanistic reasoning. So what you can act on rests on lifestyle evidence that already holds up, not on anti-aging drugs that are still in trials.
Background · Where the name inflammaging comes from
In 2000, the Italian immunologist Claudio Franceschi named the other half of immune aging: inflammaging, the chronic, infection-free, body-wide low-grade inflammation that rises slowly with age (Franceschi 2000). He proposed it from an evolutionary angle: the same inflammatory response that exists to fight infection is switched on again and again over a long life, and in later years it leaves behind a background hum that stays high.How does it relate to chronic inflammation in general (see Chronic low-grade inflammation)? That story covers the general mechanism: a master switch called pushes up , which in turn pushes up made by the liver; visceral fat, ultra-processed food and short sleep are all drivers. Inflammaging is the same machinery seen through the lens of aging: the same low-grade inflammation, but with several extra drivers that only become prominent with age. This story does not repeat the general mechanism; it adds only the part that is specific to aging.
Mechanism · The inflammation drivers unique to aging
First, the limits of the evidence: the drivers below are clear in mice and in cell experiments; in people, most of what we have is association — the older people are, the more of these markers they carry, and the higher their inflammation — plus mechanistic reasoning.What senescent cells secrete is the most central driver (reviewed by Birch and Gil 2020). Cells that stop dividing but do not die switch to releasing a whole suite of pro-inflammatory signals, called the senescence-associated secretory phenotype (SASP), rich in , IL-1β, and protein-cutting enzymes that break tissue down. The older we get, the more senescent cells build up in tissues, and like countless tiny sprinklers they push the whole-body inflammatory baseline up little by little.
Several more stack on top:
Debris from damaged cells: DNA and mitochondrial pieces released by damaged cells are read by the immune system as danger signals, repeatedly switching on the master switch even without infection.A looser gut barrier: with age, the gut barrier may become less tight, so bacterial endotoxins such as lipopolysaccharide (LPS) leak into the blood more easily. This is the same route as the metabolic endotoxemia described for chronic inflammation in general (see Chronic low-grade inflammation).Fat moving to the belly: even when body weight does not change, fat is redistributed around the organs after midlife, and visceral fat is itself an inflammation factory.
Inflammaging ties aging to a whole run of diseases of later life (see the chapter How it feeds many age-related diseases), but it is slow and adjustable, not a verdict. The causal chain from senescent cells to inflammation to disease has not been directly shown in people. That is why the practical advice later rests on lifestyle evidence that already holds up, not on still-experimental anti-aging drugs designed to clear senescent cells.
Chapter 3
How it feeds many age-related diseases
Low-grade inflammation is not the label of any single disease of old age. It is more like one amplifier shared by several disease pathways: the same smolder can push atherosclerosis forward and can also take muscle apart.
A review by Furman 2019 connects this root to cardiovascular disease, metabolic disease, neurodegenerative disease and frailty in old age. The heart has the most direct human evidence: in a large randomized trial (CANTOS), an antibody that specifically blocks the inflammatory signal IL-1β reduced cardiovascular events somewhat without lowering blood lipids, supporting inflammation itself as one causal link.
Seeing this changes the strategy: rather than fighting diseases one at a time, turn down the switch they share. It does not mean every disease of aging is caused by inflammation; it means lifestyle habits that lower inflammation overall tend to pay off in several places for one effort.
A review by Furman 2019 connects this root to cardiovascular disease, metabolic disease, neurodegenerative disease and frailty in old age. The heart has the most direct human evidence: in a large randomized trial (CANTOS), an antibody that specifically blocks the inflammatory signal IL-1β reduced cardiovascular events somewhat without lowering blood lipids, supporting inflammation itself as one causal link.
Seeing this changes the strategy: rather than fighting diseases one at a time, turn down the switch they share. It does not mean every disease of aging is caused by inflammation; it means lifestyle habits that lower inflammation overall tend to pay off in several places for one effort.
Evidence · Which diseases low-grade inflammation touches
Singling out inflammaging is not about memorizing one more term. Its weight lies here: a whole set of diseases of old age that look unrelated may share the same root of low-grade inflammation (Furman 2019).The evidence for where this root lands is mostly association plus mechanism, not one cause and one effect:
Cardiovascular disease: inflammation drives atherosclerosis. A review by Libby 2017 laid out the experimental and clinical evidence that the inflammatory signal IL-1β takes part in this process both locally in the vessel wall and throughout the body, and noted that treatments interfering with IL-1 can improve cardiovascular outcomes — the basis on which the CANTOS trial was built. This is the part of the root closest to causal evidence (see Chronic low-grade inflammation).Type 2 diabetes and metabolic syndrome: inflammation in fat tissue pushes the body step by step toward insulin resistance.Neurodegeneration and cognitive decline: inflammation in the nervous system is one of the mechanisms involved in Alzheimer's disease and similar conditions (see Cognitive Aging & Cognitive Reserve).Frailty and sarcopenia: this landing point deserves a closer look, because inflammation and muscle loss push each other along.
Mechanism · How inflammation and muscle loss feed each other
Inflammaging and sarcopenia — the loss of muscle mass and strength that comes with age — reinforce each other (Cruz-Jentoft 2019). Chronic inflammation, especially and that stay high year after year, speeds up muscle breakdown and holds back muscle building, and is one of the drivers of muscle loss in old age. Yet muscle is itself an important anti-inflammatory organ: when it contracts, it releases anti-inflammatory signals (explained in the chapter Vaccines, exercise and protein help more).So a loop forms: inflammation rises and muscle shrinks; with less muscle, the capacity to damp inflammation falls too, and inflammation climbs higher. Once muscle loss is joined by less activity, visceral fat builds up again and pushes inflammation up another notch. This is exactly why keeping your muscle ranks so high in the health of older adults (see Sarcopenia).
How to read this shared root correctly: it does not say every disease of aging is caused by inflammation; age, genes and the pathology of each organ all have causes of their own. It says low-grade inflammation is a common amplifier on many disease pathways, so lifestyle habits that lower inflammation overall — exercise, losing visceral fat, sleeping well, not smoking — tend to pay off in several places for one effort. It is also why the interventions that really work are not some pill aimed at immunity, but improvements to overall metabolism and lifestyle.
Chapter 4
Why immune boosters don't work
The trouble with an aging immune system is dysregulation, not a shortage. Turning the firepower up further leads to autoimmunity and chronic smoldering, not a better system.
Vitamin C fizzy tablets, zinc lozenges and echinacea sell a state that does not exist: immunity where higher is better. Fear of getting sick is a real feeling, but no supplement can upgrade this finely tuned regulation. The three best-studied ones all land between no effect and a weak one in Cochrane systematic reviews: taking vitamin C all year does not prevent colds, zinc may shorten a cold a little but with low certainty, and echinacea offers at most a weak benefit of doubtful clinical importance.
When you are genuinely short of a nutrient, bringing it back to normal makes sense; that is a different thing from boosting immunity in someone who is not short.
Vitamin C fizzy tablets, zinc lozenges and echinacea sell a state that does not exist: immunity where higher is better. Fear of getting sick is a real feeling, but no supplement can upgrade this finely tuned regulation. The three best-studied ones all land between no effect and a weak one in Cochrane systematic reviews: taking vitamin C all year does not prevent colds, zinc may shorten a cold a little but with low certainty, and echinacea offers at most a weak benefit of doubtful clinical importance.
When you are genuinely short of a nutrient, bringing it back to normal makes sense; that is a different thing from boosting immunity in someone who is not short.
Myth · Can a supplement turn immunity up?
Boost your immunity is one of the supplement industry's longest-running selling points. Fear of getting sick and the wish for an extra layer of protection are real feelings, but the very idea of an immune booster does not hold up at the level of mechanism.The chapters Aging immunity: off balance, not weaker and Low-grade inflammation with age made it clear: the trouble with an aging immune system is dysregulation — blunt where it should respond, smoldering where it should not — not a shortage. The ways an overactive immune system fails are real and serious: one is autoimmune disease, where the immune system attacks the body's own tissues; the other is chronic inflammation, smoldering for years and damaging the body.
So the goal of pushing immunity as high as possible contradicts itself. What you want is well tuned and balanced, not turned up. No supplement can upgrade this finely regulated system to a better state.
Evidence · How much vitamin C, zinc and echinacea do
Vitamin C (Hemilä and Chalker 2013, a Cochrane systematic review): in the general population, taking it all year does not reduce how many colds people catch. Taking it regularly makes colds in adults a little shorter, by about 8%; starting it once symptoms appear has essentially no effect. It is not an immune booster; at most it is a marginal effect.Zinc (Nault 2024, a Cochrane systematic review): for prevention it does little or nothing. Taken once a cold has started, zinc may shorten it by about two days, but the certainty of that evidence is low; and minor side effects such as a bad taste in the mouth and an upset stomach are also more common. That is hardly raising immunity.
Echinacea (Karsch-Völk 2014, a Cochrane systematic review): pooling 24 trials and 4,631 people, it concluded that for prevention there is at most a possible weak benefit of doubtful clinical importance, and for treatment no reliable effect.
The shared message of these reviews: even the most thoroughly studied immune supplements land between no effect and a weak one, and not one delivers on the promise to boost your immunity so you do not get sick.
In practice · Filling a gap is not turning it up
Genuine nutrient deficiency does damage immune function, and in that case bringing it back to normal makes sense:Zinc: some older adults, vegetarians and people with absorption problems may be short of zinc; filling the gap can improve immune function.Vitamin D: for people who are deficient, correcting it may give a small, marginal help against respiratory infections; for people who already have enough, taking more gives no extra benefit (see Vitamin D).
The crucial difference: this is filling a gap and returning to normal, which is a completely different thing from someone who is not deficient taking supplements to push immunity above normal. The latter has no evidence behind it and points in the wrong direction.
Immune boosters sell something that does not exist: an immune state where higher is better. Move the money and attention you would spend on them to the few high-leverage things in the chapter Vaccines, exercise and protein help more — above all vaccines — and the return is far greater. This page is not a diagnosis; if you have repeated infections or signs of an immune problem, have a doctor evaluate you.
Chapter 5
Vaccines, exercise and protein help more
A shrinking thymus makes the body slow to recognize a new antigen the first time. A vaccine does not turn immunity up; it builds the memory in advance and routes around this weakness in the hardware.
Against immune aging, the single move with the highest return is not a supplement but vaccination. The second is exercise: the that contracting muscle releases is anti-inflammatory, and it is not the same thing as the IL-6 that visceral fat releases year after year. The third is eating enough protein: antibodies and immune cells use it as raw material, and older people need more of it than younger ones. Sleeping enough, not smoking and keeping your waistline in check turn overall inflammation down a little further.
Repeated, severe or unusual infections are not slightly weaker immunity and need a doctor to look for the cause; an infection that spreads quickly, shortness of breath or a change in consciousness is an emergency.
Against immune aging, the single move with the highest return is not a supplement but vaccination. The second is exercise: the that contracting muscle releases is anti-inflammatory, and it is not the same thing as the IL-6 that visceral fat releases year after year. The third is eating enough protein: antibodies and immune cells use it as raw material, and older people need more of it than younger ones. Sleeping enough, not smoking and keeping your waistline in check turn overall inflammation down a little further.
Repeated, severe or unusual infections are not slightly weaker immunity and need a doctor to look for the cause; an infection that spreads quickly, shortness of breath or a change in consciousness is an emergency.
In practice · Why vaccines come first
If the problem in immune aging is dysregulation plus inflammaging, then what really helps is not turning immunity up, but giving it a hand where it is weakest — recognizing new antigens — and then lowering that low-grade inflammation overall.Tier one, with the biggest leverage: vaccines (the US CDC's 2025 adult immunization schedule). Since a shrinking thymus leaves older adults slow to respond to new antigens and slow to clear a first infection, building the memory in advance with a vaccine routes neatly around that weakness. It is borrowed strength, not a boost.
Under the CDC's adult schedule, the core vaccines recommended for older adults are as follows (for specifics, follow local guidance and your doctor):
Influenza: at 65 and over, high-dose, adjuvanted or recombinant versions are preferred; they are designed for the blunted response.Pneumococcal (conjugate vaccine, PCV): recommended for everyone aged 50 and over.Shingles (recombinant adjuvanted vaccine, RZV): at 50 and over, two doses.Respiratory syncytial virus (RSV): recommended for everyone aged 75 and over, and for people aged 60-74 with risk factors.COVID-19: follow current guidance; older adults usually need boosters.
These are backed by and large-scale data, and they are hard interventions that directly reduce the severe illness and hospital stays most common in older adults.
In practice · Exercise, protein and daily habits
Tier two: exercise, because muscle is an anti-inflammatory organ (Pedersen and Febbraio 2008). Contracting muscle releases a class of signaling molecules called myokines. The that muscle releases during exercise is completely different from the chronic IL-6 that visceral fat releases year after year: it holds down and promotes anti-inflammatory signals such as IL-10 and the IL-1 receptor antagonist (IL-1ra). That is anti-inflammatory in the real sense, not a marketing word. Long-term regular exercise lowers the baseline of low-grade inflammation while preserving muscle, breaking the vicious circle between inflammaging and sarcopenia (see Sarcopenia; see Exercise as medicine). Aerobic exercise plus strength training — strength training especially, for keeping muscle — is double insurance against inflammation and frailty in older age.Tier three: enough protein, because immune cells need raw material too (Bauer 2013). Antibodies and immune cells are built from protein; older adults need more protein than younger ones, and the PROT-AGE expert group recommends about 1.0-1.2 g/kg a day for healthy older adults, paired with exercise so the body can put it to use. Too little protein means losing muscle and running short of immune raw material — a loss on both fronts (see Protein & Amino Acids; see Sarcopenia).
Tier four: a few basic lifestyle habits that lower inflammaging, each with benefits of its own:
Sleep: chronically short or broken sleep raises IL-6 and TNF-α; sleeping 7-9 hours a night by itself turns down both the inflammation switch and the metabolic one.Not smoking, drinking less: smoking is a strong source of inflammation; after quitting, inflammatory markers gradually come down.Keeping visceral fat in check: visceral fat is an inflammation factory; a smaller waist (you do not need to become thin) reflects falling inflammation more directly than a lower weight does (see Chronic low-grade inflammation).The overall eating pattern: a Mediterranean-style diet (plenty of vegetables, fruit and whole grains, plus fish, olive oil, nuts, legumes and enough protein, with little ultra-processed food) is associated with lower inflammation. What works is the whole pattern, not one anti-inflammatory superfood.
Red flag · Infections not to blame on age
Within the range of normal immune aging, and open to improvement: an occasional cold, recovering a little more slowly than when you were young, wanting to protect yourself ahead of time. Doing vaccines, exercise, protein, sleep and not smoking well is enough.Situations that need a doctor's evaluation: repeated, severe or unusual infections — for example several bouts of pneumonia in one year, shingles that keeps coming back, or opportunistic infections (infections caused by microbes that do not usually cause disease). That is not slightly weaker immunity; underlying immune deficiency, blood disorders, diabetes and other causes need to be ruled out. How to schedule vaccines for an older person also varies (existing illnesses, medications, allergy history), so leave it to a doctor to tailor to guidelines.
Red flags — seek care promptly, and do not write them off as old-age immunity: unexplained persistent fever together with weight loss, night sweats or swollen lymph nodes, which need checking for blood cancers and similar conditions; repeated opportunistic infections (thrush in the mouth, shingles that keeps recurring, unusual pathogens), which need checking for immune deficiency; and any rapidly progressing infection (spreading cellulitis, shortness of breath, a change in consciousness), which needs the emergency department.
Immune aging is not immunity got weaker, so boost it hard; it is immune dysregulation plus rising low-grade inflammation. The things with real leverage — vaccines (borrowed strength that routes around the weakness), exercise (muscle's anti-inflammatory effect), enough protein, sleep, not smoking, keeping visceral fat in check — are none of them immune-boosting supplements. Once you know the mechanism, you need not panic about declining immunity, and you will not pay for a higher-is-better state that does not exist. This page is popular science and does not replace a doctor's individual assessment.
References · 12
- Thomas, R., Wang, W., & Su, D.-M. (2020). Contributions of age-related thymic involution to immunosenescence and inflammaging. Immunity & Ageing, 17, 2. Reviews how thymic involution reduces naïve T-cell output and TCR diversity, blunting responses to novel antigens and vaccines in older adults. 10.1186/s12979-020-0173-8
- Franceschi, C., Bonafè, M., Valensin, S., Olivieri, F., De Luca, M., Ottaviani, E., & De Benedictis, G. (2000). Inflamm-aging: an evolutionary perspective on immunosenescence. Annals of the New York Academy of Sciences, 908, 244-254. Coined 'inflammaging' — the chronic, low-grade, sterile pro-inflammatory state that rises with age and underlies age-related disease. 10.1111/j.1749-6632.2000.tb06651.x
- Birch, J., & Gil, J. (2020). Senescence and the SASP: many therapeutic avenues. Genes & Development, 34(23-24), 1565-1576. Reviews the senescence-associated secretory phenotype (IL-6, IL-1β, TNF-α) as a driver of inflammaging and a senotherapy target. 10.1101/gad.343129.120
- Furman, D., Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., et al. (2019). Chronic inflammation in the etiology of disease across the life span. Nature Medicine, 25(12), 1822-1832. 10.1038/s41591-019-0675-0
- Cruz-Jentoft, A. J., & Sayer, A. A. (2019). Sarcopenia. The Lancet, 393(10191), 2636-2646. 10.1016/S0140-6736(19)31138-9
- Libby, P. (2017). Interleukin-1 beta as a target for atherosclerosis therapy: biological basis of CANTOS and beyond. Journal of the American College of Cardiology, 70(18), 2278-2289. 10.1016/j.jacc.2017.09.028
- Hemilä, H., & Chalker, E. (2013). Vitamin C for preventing and treating the common cold. Cochrane Database of Systematic Reviews, (1), CD000980. Regular vitamin C does not reduce cold incidence in the general population; it modestly shortens duration (~8% in adults), with no benefit when started at symptom onset. 10.1002/14651858.CD000980.pub4
- Nault, D., Machingo, T. A., Shipper, A. G., et al. (2024). Zinc for prevention and treatment of the common cold. Cochrane Database of Systematic Reviews, (5), CD014914. Zinc may reduce cold duration by ~2 days but with low-certainty evidence; insufficient to recommend zinc for preventing or treating colds. 34 RCTs, 8,526 participants. Prevention: little or no effect on getting a cold (RR 0.93, 0.85-1.01; low certainty). Treatment: may shorten colds (MD -2.37 days, -4.21 to -0.53; I2 = 97%; 8 studies; low certainty). Non-serious adverse events probably increase with treatment (RR 1.34, 1.15-1.55; moderate certainty); no treatment study reported serious adverse events (abstract, PMID 38719213). 10.1002/14651858.CD014914.pub2
- Karsch-Völk, M., Barrett, B., Kiefer, D., Bauer, R., Ardjomand-Woelkart, K., & Linde, K. (2014). Echinacea for preventing and treating the common cold. Cochrane Database of Systematic Reviews, (2), CD000530. 24 trials / 4,631 participants: at most a possible weak prevention benefit of questionable clinical relevance; no reliable treatment effect. 10.1002/14651858.CD000530.pub3
- Advisory Committee on Immunization Practices. (2025). Recommended Adult Immunization Schedule for Ages 19 Years or Older, United States, 2025. Centers for Disease Control and Prevention / MMWR. High-dose/adjuvanted/recombinant influenza preferred at 65+; pneumococcal at 50+; RZV shingles at 50+; RSV at 75+ (60-74 with risk factors); COVID-19 boosters for older adults. www.cdc.gov/vaccines/hcp/imz-schedules/adult-age.html
- Pedersen, B. K., & Febbraio, M. A. (2008). Muscle as an endocrine organ: focus on muscle-derived interleukin-6. Physiological Reviews, 88(4), 1379-1406. Establishes contraction-induced myokine IL-6 as anti-inflammatory (suppresses TNF-α, induces IL-10/IL-1ra), distinct from chronic adipose IL-6. 10.1152/physrev.90100.2007
- Bauer, J., Biolo, G., Cederholm, T., Cesari, M., Cruz-Jentoft, A. J., Morley, J. E., et al. (2013). Evidence-based recommendations for optimal dietary protein intake in older people: PROT-AGE Study Group. JAMDA, 14(8), 542-559. 10.1016/j.jamda.2013.05.021