Soy Isoflavones

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Soy isoflavones (Genistein and Daidzein) are compounds found in a wide variety of foods, but mostly soy, that affect a wide-variety of body systems. They seem to mimic the female hormone estrogen to a degree (although slightly different).

They have been implicated in both reductions and increases of breast cancer risk, and generally are good at cardioprotection from reducing lipoprotein levels and are seen as good for bone health in the aging as well.

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Many anti-carcinogenic effects of genistein are seen in the range of 10-20mg/kg bodyweight a day. Epidemiologically, this dose is also associated with reduced lipoprotein levels.

In vitro studies on glucose and muscle cell metabolism showing a nutrient partitioning effect at 20-30uM correlate to a dietary intake of 200-300mg/kg bodyweight (assuming the 1uM circulating serum levels per 10mg/kg BW intake noted.^[1])

Edit1. Sources and Structure

1.1. Food Sources, Processing, and Preparation

Genistein can be found in a variety of foods, but is most well known for being a 'Soy' Isoflavone.^[2] Genistein has also been found in high levels in Indian Bread Root^[3] and moderately high (>400mg/kg dry weight) of most other legumes.^[3] It can also be found in foods such as kudzu, lupin, fava beans, and psoralea.^[4]

Food sources are typically as Genistin, which is a Genistein molecule bound to a sugar. It is biologically inactive, and during high-temperature heating is reduced to a smaller sized simple glycoside^[5] that can be hydrolyzed in the intestine to form the bioavailable genistein aglycone which is then absorbed.^[2] The former processing is traditional Eastern Asia processing, and soy foods made from soy flour (from hexane treatment of soybean flakes) standard in North America can either have their isoflavones lost in the hexane extract or decarboxylate their complex glycoside (6′′-O-malonyl-7-O-β-D-glucoside) into another structure (6′′-O-acetyl-7-O-β-D-glucoside) with altered pharmacokinetics.^[6] If not broken down into the simple glycoside by heat, genistein cannot be absorbed in the small intestine by the enzyme lactase phlorizin hydrolase.^[7]

Fermenting of food sources tends to break the glycoside, and release the free aglcyone (Genistein). Additionally, the free aglycone can be hydroxylated with further fermantation, which increases the anti-oxidative potential of isoflavones.^[8][6] Fermented soy sauces contain the compounds 6-hydroxygenistein, 8-hydroxygenistein, and genistein-7-tataric acid. These compounds are not in unfermented soy.^[6]

1.2. Structure

Genistein is an isoflavonoid compound, and is defined by having a hydroxy group on the 4' position of the outermost benzene ring.^[9]

Edit2. Pharmacology

2.1. Absorption and Bioavailability

The food bound glycosides Daidzin (Daidzein glycoside) and Genistin (Genistein glycoside) are enzymatically hydrolyzed in the small intestine by B-galactosidases, mostly in the jejunem.^[10][11] Some of these glycosides are not hydrolyzed in the jujenum and may reach the colon.^[12][13]

2.2. Colonic Fermentation

Daidzein can be metabolized by gut microflora (bacteria) into an estrogenic metabolite called Equol.^[14][13] In this process Daidzein is first hydrated to Dihydrodaidzein, which can then either turn into Equol or into O-Desmethylangolensin. This conversion is dependent on gut microflora and varies between individuals^[15] which is a reason for reported individual differences in estrogen status among people who consume soy.^[16] It has been noted that not all individuals may produce Equol from Daidzein^[17][14] and that only 33-50% of humans may possess this bacterial strain.^[16][12]

Persons who possess intestinal bacteria to metabolize Daidzein into Equol are classified as 'Equol Producers' and are more likely to experience estrogenic effects from soy.

Edit3. Neurology

3.1. Serotonin

One study investigating phytonutrients able to act as SSRIs noted that both genistein and daidzin were able to inhibit some degree of serotonin reuptake (11.5+/-11.6% and 5.7+/-6.7% respectively) at 50uM, but were unreliable and both much weaker than the active control of Imipramine (74.5+/-11.3% at 5uM).^[18]

Edit4. Interactions with Various forms of Cancer

4.1. Breast Cancer

Genistein is most notably in its effects against Breast Cancer. It (Soy intake) has been correlated with a reduced risk of breast cancer in numerous epidemiological studies.

Genistein appears to act as a pro-carcinogen in breast cancer lines that express Estrogen Receptor Alpha (ERa) predominately at normal doses (6-8uM), although in supra-physiological doses (more than 10uM) this effect is reversed.^{[19][20][21][22]}

4.2. Prostate Cancer

In regards to prostate cancer, genistein (via soy intake) has been implicated in epidemiological studies to be associated with a decreased risk of prostate cancer.^[23][24] This is somewhat backed up by lower rates of prostate cancer in Asian countries relative to Western countries with lower soy intakes^[25][1] paired with asian immigrants matching western rates of prostate cancer upon immigration.^[26]

In vitro results suggest that genistein can act via inhibiting nF-kB in various cells^[27] and suppression of metalloproteins associated with cancer.^[28] Other possible mechanisms of action include preventing an upregulation in 5a-reductase activity in the prostate from a high-fat diet.^[29]

These results have been applied to animal models showing genistein intervention capable of reducing prostate cancer metastasis^[30] and acting as an anti-carcinogen.^[31]

Via AMPK activation^[32], Genistein can aid in regulating a cell cycle's lifespan.^[33][34]

Edit5. Interactions with Cardiovascular Disease Risk

Consuming 60mg of Soy Protein isoflavones reduces the levels of various markers of cardiovascular disease in normal post-menopausal women^[35] although after cost-benefit analysis the recommendation to include soy protein foods is still controversial.^[36]

Edit6. Interactions with Body Fat - Obesity

Genistein appears to inhibit adipogenesis as well as induce fat cell apoptosis via AMP-Actiated protein Kinase (AMPK)^[32][37] and appears to be mediated through Reactive-Oxygen Species (ROS) release and was inhibited with treatment of an anti-oxidant.^[32][38]

Genistein can also inhibit GLUT4-mediated glucose uptake in adipocytes.^[39] Although genistein has the properties of a tyrosine-kinase protein inhibitor^[21] (of which the insulin receptor constitutes) the effects from Genistein are independent of direct receptor inhibition.^[39][40] These effects were seen best at a concentration of 20uM.

Edit7. Interactions with Glucose Metabolism - Diabetes

Numerous in vivo animal studies have linked Genistein consumption with a decreased fasting blood glucose in already diabetic animal models.^[41][42][43] The mechanism of action is hypothesized to be via acting on PI3K, an intermediate in insulin signalling cascades, and does so at concentrations of 10-50uM under conditions of normal glucose and 30uM under conditions of high glucose and was inhibited by introduction of an O-GlcNAcase inhibitor, suggesting another possible mechanism of action via decreasing O-GlcNAcylation.^[37]

Edit8. Interactions with Steroid Metabolism

8.1. Aromatase

Many actions on steroid metabolism come from Genistein's interactions with the aromatase enzyme. This is the rate-limiting enzyme that converts androsterone and testosterone to estrone and estradiol, respectively.^[44][45] Many isoflavones and flavones can interact with aromatase, in which the binding site for the androgen's D and C rings are occupied by the flavonoid's A and C rings, respectively.^[46][45] Aromatase is encoded and created by a single gene, the CYP19A1^[47] and has several promoters that are divided based on where they exist in the body.^[48][49] Currently known are I.1 through I.7, and PII promoters^[45] which are placenta (I.1) and placental minor (2a) specific, adipose specific (I.3), skin fibroblasts and preadipocytes (I.4), fetal (I.5), bone (I.6), brain (I.f) and endothelial cells (I.7).^{[50][51][52][53]} Although all these promoters vary by region, the encoded mRNA and final protein (aromatase enzyme) are structurally the same.^[54]

By aiming for the protein (aromatase), one can induce systemic wide effects. If aiming for protein transcription, one can hopefully induce more controlled effects based on promoter localization.

Genistein, directly on aromatase, can increase its activity as measured in ovarian cells and carcinoma cells.^[55][56] It can also stimulate the growth or aromatase in breast cells, and most notable estrogen-responsive breast cancer cells.^[57] It can negate the action of pharmaceutical anti-aromatases in these cells.^[58][57] In some scenarios, it has been shown to inhibit aromatase directly although it is weak in doing so; isoflavonoids in general are weaker than flavones at aromatase inhibition.^[46][59] When acting as an aromatase inhibitor, Genistein has an apparent Ki of 123+/-8uM.^[60]

Genistein, working through promoters, can suppress the adipose specific aromatase via I.3^[61] and in estrogen-non responsive breast cancers via the same promoter.^[45] At times, however, it has been shown to increase activity of this promoter in HepG2 cells and subsequently induce aromatase.^[62] It has been noted to reduce transcription in granulosa-luteal cells,^[63] and is synergistic with both Daidzein and Biochanin A in this regard.

8.2. Estrogen

Genistein, due to its structural similarity to 17b-estradiol (the most potent estrogen-like compound), is intimately involved with estrogen metabolism.

In vitro results suggest that cells with a predominance of Estrogen Receptor subtypes Alpha (ERa) accept Genistein as a pro-estrogenic compound, whereas dominance of the beta-subunit treats Genistein like an anti-estrogen.^[64] This is primarily since genistein has only 0.5-1% the relative affinity to the ERa receptor relative to 17b-estradiol^[62] but possesses a greater affinity to the ERb receptor than estradiol itself^[65] and thus changes the ratio of active ERa to ERb by selectively acting upon ERb^[66] This selectivity means that Genistein is a Selective Estrogen Receptor Modulator (SERM).

That being said, interactions between both receptors modulate a myriad of regulating factors in regards to estrogenic gene transcription, and overall estrogenic effects may not be obvious.^[19] In general, ERa is seen as proliferative and ERb suppressant of growth.^[67][68][69] They do, however, seem to collectively act as estrogen antagonists in the presence of estrogen, and agonists when there is a lack of estrogen.^[70][71]

In regards to estrogen, genistein can be seen as 'regulatory'. It seems to neither increase or decrease estrogen overall, but to normalize either excessive or deficient amounts of estrogen signalling (and effects).

8.3. Testosterone

In regards to testosterone, Genistein is able to inhibit the 3-beta hydroxysteroid dehydrogenase (3bHSD) enzyme by competing for binding with pregnenolone and by non-competitive reduction of NAD+ activation of the enzyme.^[72] It had a lesser but noticable effect on 17bHDS and these results were seen at an IC50 of 85+/-15nmol. These effects are noted in vivo as well at 40mg/kg bodyweight.^[73]

Genistein does seem to possess anti-androgenic transcription activity in male mice (by the above mechanisms), but this effect is seen in the prostate, adrenals, brain, and testis but not skeletal muscle. It seems to occur in a larger degree in the adrenals relative to testes, and causes hypertrophy of the adrenals at 40mg/kg bodyweight.^[73]

In vivo, genistein at high doses (10uM or greater) seems to impair development of rat 'masculinity' during youth.^[74][75] Using a human serum:oral intake ratio proposed here^[1] this would equate to an oral dose of 100mg/kg bodyweight or greater in youth; a dose unobtainable through a diet in moderation.

In vivo, It also seems to be pro-androgenic at 10mg/kg a day when the subject is hypogonadic, basically when there are no circulating androgens.^[1] The authors noted that this level of intake correlates to a 'soy rich diet' in man and provides about 1uM circulating levels.

Edit9. Interactions with Bone Metabolism - Osteoporosis

The anti-osteoporotic effects of Genistein are highly mediated via the ERa receptor (proliferative subset) and are drastically augmented with forms of mechanical resistance (exercise).^[76]

Edit10. Nutrient-Nutrient Interactions

10.1. Probiotics

As the bacterial conversion of Daidzein to Equol (in Equol producers) appears to be a significant aspect of the estrogenicity of soy products, it was investigated as to whether consumption of probiotics could influence this conversion. Two studies investigating Lactobacillus Acidophillus and Bifidobacterium longum found that oral administration of these probiotics does not alter Equol producing status.^[77][78]

Edit11. Safety and Toxicity

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(Common misspellings for Soy Isoflavones include genistien, genstein, genstien, genistin, genisten, daidzen, dadzen, dadzein)

(Common phrases used by users for this page include genistein testosterone, genistein supplements, daidzein in soy lecithin?, biocianine a antiaromatase, anti aromatase diabetes, alpha galactosidase daidzein)

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