| Ingredient
Polyphenols are the broad chemical family. Flavonoids are one major subgroup within that family.
| Category | Polyphenols | Flavonoids |
| ----------------------- | ------------------------------------------------------------------------------ | --------------------------------------------------------------------------- |
| Scope | Broad umbrella term | Subclass of polyphenols |
| Main structural feature | One or more phenolic rings | Typically a 15-carbon C6–C3–C6 structure |
| Includes | Flavonoids, phenolic acids, stilbenes, lignans, tannins and related compounds | Flavonols, flavones, flavanones, flavan-3-ols, anthocyanins and isoflavones |
| Examples | Curcumin, resveratrol, caffeic acid, chlorogenic acid, ellagic acid, quercetin | Quercetin, kaempferol, apigenin, luteolin, EGCG, cyanidin, genistein |
| Relationship | All flavonoids are polyphenols | Not all polyphenols are flavonoids
|
Common Flavonoids and Their Potential Effects in Cancer and Alzheimer’s Disease
Flavonoids are a major subclass of polyphenols found in fruits, vegetables,
tea, cocoa, herbs, and legumes. Major subclasses include flavonols, flavones,
flavanones, flavan-3-ols, anthocyanidins, and isoflavones.
| Flavonoid |
Subclass |
Common Sources |
Basic Potential Effect Against Cancer |
Basic Potential Effect in Alzheimer’s Disease (AD) |
| Quercetin |
Flavonol |
Onions, apples, capers, berries, kale |
May induce apoptosis and cell-cycle arrest and inhibit proliferation,
angiogenesis, invasion, PI3K/Akt, MAPK, STAT3, and NF-κB signalling.
|
May reduce oxidative stress, neuroinflammation, amyloid-β toxicity,
tau phosphorylation, and mitochondrial dysfunction.
|
| Kaempferol |
Flavonol |
Kale, spinach, broccoli, beans, tea |
May promote apoptosis and inhibit proliferation, angiogenesis,
epithelial–mesenchymal transition, PI3K/Akt, and inflammatory signalling.
|
May reduce oxidative stress, microglial activation, amyloid toxicity,
neuroinflammation, and neuronal apoptosis.
|
| Myricetin |
Flavonol |
Berries, grapes, tea, walnuts |
May inhibit proliferation, migration, angiogenesis, and inflammatory
signalling and promote apoptosis and cell-cycle arrest.
|
May inhibit amyloid-β aggregation, reduce oxidative injury, and
support mitochondrial and neuronal function.
|
| Fisetin |
Flavonol |
Strawberries, apples, persimmons, onions |
May induce apoptosis and inhibit proliferation, invasion, NF-κB,
PI3K/Akt/mTOR, and epithelial–mesenchymal transition.
|
May support synaptic function and reduce oxidative stress,
neuroinflammation, senescent-cell burden, and memory impairment.
|
| Isorhamnetin |
Flavonol |
Sea buckthorn, onions, pears, almonds |
May inhibit proliferation, migration, angiogenesis, and PI3K/Akt and
NF-κB signalling while promoting apoptosis.
|
May reduce oxidative stress, neuroinflammation, microglial activation,
and amyloid-associated neuronal damage.
|
| Rutin |
Flavonol glycoside |
Buckwheat, apples, citrus fruit, asparagus |
May inhibit oxidative damage, inflammation, proliferation,
angiogenesis, and tumour-cell migration.
|
May reduce oxidative stress, neuroinflammation, amyloid toxicity,
cholinergic dysfunction, and neuronal apoptosis.
|
| Apigenin |
Flavone |
Parsley, celery, chamomile, oregano |
May induce apoptosis and cell-cycle arrest and inhibit NF-κB, STAT3,
PI3K/Akt, angiogenesis, invasion, and metastasis.
|
May suppress microglial activation, inflammatory cytokines,
oxidative stress, amyloid toxicity, and tau-related abnormalities.
|
| Luteolin |
Flavone |
Celery, parsley, peppers, thyme |
May inhibit proliferation, angiogenesis, metastasis, NF-κB, STAT3,
MAPK, and PI3K/Akt signalling and promote apoptosis.
|
May reduce neuroinflammation, microglial activation, amyloid
accumulation, tau phosphorylation, and oxidative damage.
|
| Baicalein |
Flavone |
Chinese skullcap root |
May induce apoptosis, autophagy, and cell-cycle arrest and inhibit
proliferation, angiogenesis, invasion, and PI3K/Akt signalling.
|
May inhibit amyloid aggregation and reduce neuroinflammation,
ferroptosis, oxidative stress, and neuronal injury.
|
| Baicalin |
Flavone glycoside |
Chinese skullcap root |
May suppress proliferation, inflammation, angiogenesis, migration,
and NF-κB and PI3K/Akt signalling.
|
May reduce amyloid deposition, tau phosphorylation,
neuroinflammation, oxidative stress, and neuronal apoptosis.
|
| Chrysin |
Flavone |
Propolis, honey, passionflower |
May induce apoptosis and inhibit proliferation, angiogenesis,
invasion, NF-κB, STAT3, and PI3K/Akt signalling.
|
May reduce oxidative stress, neuroinflammation, amyloid toxicity,
acetylcholinesterase activity, and memory impairment.
|
| Hispidulin |
Flavone |
Artemisia, sage and other medicinal herbs |
May inhibit proliferation, migration, angiogenesis, and STAT3 and
PI3K/Akt/mTOR signalling and promote apoptosis.
|
May reduce neuroinflammation, oxidative stress, neuronal excitotoxicity,
and cognitive dysfunction in experimental models.
|
| Naringenin |
Flavanone |
Grapefruit, oranges, tomatoes |
May inhibit proliferation, migration, angiogenesis, NF-κB, and
PI3K/Akt signalling and promote apoptosis and cell-cycle arrest.
|
May reduce oxidative stress, neuroinflammation, amyloid accumulation,
acetylcholinesterase activity, and mitochondrial dysfunction.
|
| Naringin |
Flavanone glycoside |
Grapefruit and other citrus fruits |
May suppress proliferation, inflammation, invasion, and angiogenesis
and promote apoptosis.
|
May reduce amyloid toxicity, neuroinflammation, oxidative stress,
cholinergic dysfunction, and neuronal apoptosis.
|
| Hesperetin |
Flavanone |
Oranges, lemons and other citrus fruits |
May inhibit proliferation, migration, angiogenesis, and inflammatory
signalling and induce apoptosis and cell-cycle arrest.
|
May protect mitochondria and reduce oxidative stress,
neuroinflammation, amyloid toxicity, and cognitive impairment.
|
| Hesperidin |
Flavanone glycoside |
Orange and lemon peel and pulp |
May inhibit inflammation, proliferation, angiogenesis, and metastasis
and promote apoptosis in experimental cancer models.
|
May reduce oxidative stress, neuroinflammation, amyloid deposition,
tau phosphorylation, and cholinergic dysfunction.
|
| Eriodictyol |
Flavanone |
Citrus fruits, yerba santa, peppermint |
May suppress proliferation, migration, oxidative stress, and
inflammatory signalling and promote apoptosis.
|
May activate Nrf2-mediated antioxidant defence and reduce
neuroinflammation, oxidative injury, and amyloid toxicity.
|
| Epigallocatechin gallate (EGCG) |
Flavan-3-ol |
Green tea |
May inhibit proliferation, angiogenesis, invasion, EGFR, DNMT,
NF-κB, and PI3K/Akt signalling and promote apoptosis.
|
May inhibit or redirect amyloid-β aggregation, reduce tau
phosphorylation and neuroinflammation, and support neuronal survival.
|
| Epigallocatechin (EGC) |
Flavan-3-ol |
Green tea and white tea |
May reduce oxidative stress and inflammatory signalling and inhibit
proliferation and tumour-cell survival.
|
May reduce oxidative damage, neuroinflammation, amyloid toxicity,
and neuronal injury.
|
| Epicatechin gallate (ECG) |
Flavan-3-ol |
Green tea |
May inhibit proliferation, inflammatory signalling, angiogenesis,
and tumour-cell invasion.
|
May inhibit amyloid aggregation and reduce oxidative stress,
neuroinflammation, and synaptic injury.
|
| Epicatechin |
Flavan-3-ol |
Cocoa, dark chocolate, tea, apples |
May reduce inflammation and oxidative injury and inhibit proliferation,
angiogenesis, and metastatic signalling.
|
May improve cerebral blood flow and synaptic plasticity and reduce
oxidative stress, neuroinflammation, and cognitive decline.
|
| Catechin |
Flavan-3-ol |
Tea, cocoa, grapes, apples |
May inhibit proliferation, oxidative DNA damage, angiogenesis,
inflammation, and tumour-cell migration.
|
May inhibit amyloid aggregation and reduce oxidative stress,
neuroinflammation, mitochondrial injury, and neuronal apoptosis.
|
| Procyanidins |
Flavan-3-ol oligomers |
Grape seed, cocoa, apples, cranberries |
May inhibit proliferation, angiogenesis, invasion, MMP activity,
and inflammatory signalling and promote apoptosis.
|
May reduce amyloid aggregation, oxidative stress, neuroinflammation,
synaptic damage, and cognitive impairment.
|
| Cyanidin |
Anthocyanidin |
Berries, cherries, red cabbage, black rice |
May inhibit proliferation, inflammation, angiogenesis, invasion,
and metastatic signalling and promote apoptosis.
|
May reduce oxidative stress, neuroinflammation, amyloid toxicity,
and synaptic dysfunction.
|
| Cyanidin-3-glucoside |
Anthocyanin |
Blackberries, blueberries, cherries, black rice |
May suppress proliferation, inflammation, angiogenesis, and
metastatic signalling and promote apoptosis.
|
May support memory and synaptic function and reduce amyloid toxicity,
neuroinflammation, and oxidative damage.
|
| Delphinidin |
Anthocyanidin |
Blueberries, blackcurrants, purple grapes |
May inhibit proliferation, angiogenesis, invasion, EGFR, and
inflammatory signalling and promote apoptosis.
|
May reduce oxidative stress, microglial activation,
neuroinflammation, and amyloid-associated neuronal injury.
|
| Malvidin |
Anthocyanidin |
Blueberries, grapes, red wine |
May inhibit proliferation, inflammation, invasion, and oxidative
damage and promote apoptosis.
|
May reduce oxidative stress, neuroinflammation, amyloid toxicity,
and cognitive dysfunction.
|
| Pelargonidin |
Anthocyanidin |
Strawberries, raspberries, red radish |
May inhibit proliferation and inflammatory signalling and promote
apoptosis in experimental cancer models.
|
May reduce oxidative stress, neuroinflammation, amyloid-associated
damage, and neuronal apoptosis.
|
| Genistein |
Isoflavone |
Soybeans, tofu, tempeh |
May inhibit tyrosine kinases, proliferation, angiogenesis, and
hormone-dependent signalling and promote apoptosis.
|
May reduce oxidative stress and neuroinflammation and support
mitochondrial and estrogen-receptor-mediated neuronal protection.
|
| Daidzein |
Isoflavone |
Soybeans and other legumes |
May modulate estrogen receptors, inhibit proliferation and migration,
and promote apoptosis in some hormone-responsive cancers.
|
May provide estrogen-receptor-mediated neuroprotection and reduce
oxidative stress, inflammation, and cognitive dysfunction.
|
| Glycitein |
Isoflavone |
Soybeans and soy products |
May modulate estrogen-receptor signalling and inhibit oxidative
stress and proliferation; evidence is less extensive than for genistein.
|
May provide antioxidant and estrogen-receptor-mediated neuronal
protection, but AD-specific evidence remains limited.
|
| Equol |
Isoflavonoid metabolite |
Gut-microbial metabolite of daidzein |
May modulate estrogen receptors and inhibit proliferation,
inflammation, and oxidative stress; effects can depend on cancer type.
|
May support neuronal antioxidant defence, mitochondrial function,
cerebral circulation, and estrogen-receptor-mediated neuroprotection.
|
Major Flavonoid Subclasses
- Flavonols: quercetin, kaempferol, myricetin and fisetin
- Flavones: apigenin, luteolin, baicalein and chrysin
- Flavanones: naringenin, hesperetin and eriodictyol
- Flavan-3-ols: catechin, epicatechin and EGCG
- Anthocyanidins: cyanidin, delphinidin, malvidin and pelargonidin
- Isoflavones: genistein, daidzein and glycitein
Frequently Modulated Cancer Targets and Pathways
NF-κB, STAT3, PI3K/Akt/mTOR, MAPK/ERK, Wnt/β-catenin, EGFR, p53,
BCL-2, BAX, caspases, cyclins, CDKs, VEGF, HIF-1α, MMP-2, MMP-9,
Nrf2/HO-1, AMPK, autophagy, angiogenesis, epithelial–mesenchymal
transition, invasion, and metastasis.
Frequently Modulated Alzheimer’s Disease Targets and Pathways
Amyloid-β aggregation, APP processing, BACE1, tau phosphorylation,
GSK-3β, acetylcholinesterase, microglial activation, NF-κB, NLRP3,
Nrf2/HO-1, SIRT1, AMPK, CREB/BDNF, mitochondrial function, autophagy,
synaptic plasticity, oxidative stress, and inflammatory cytokines.
Evidence note: Most reported anticancer and
Alzheimer’s-related effects are derived from cell-culture and animal studies.
Human efficacy has not been established for most individual flavonoids.
Absorption, metabolism, gut-microbial conversion, dose, formulation, and
blood–brain-barrier penetration can substantially affect biological activity.
Flavonoids should not be considered substitutes for established cancer or
Alzheimer’s disease treatments.
|