Uridine - Scientific Review On Usage, Dosage, Side Effects - Examine

16/12/2017 Uridine - Scientic Review on Usage, Dosage, Side Effects | Examine.
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SUPPLEMENTS NUTRITION STORE
Uridine
Uridine is a nucleotide base found in high levels in beer which is used for increasing synthesis of cellular membranes
and for other neurological properties. It appears to have potentially cognitive enhancing properties, and is synergistic
with sh oil (/supplements/ sh-oil/).
This page features 107 unique references to scienti c papers.
History (/history/uridine/)
THINGS TO KNOW HOW TO TAKE HUMAN EFFECT MATRIX SCIENTIFIC RESEARCH CITATIONS
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Things to Know
Also Known As
UDP, UMP
Is a Form Of
Pseudovitamin
Nootropic
Goes Well With

Fish Oil (/supplements/ sh-oil/) (Speci cally DHA, for cognition)
Choline (/supplements/choline/) or other cholinergics (Cognition)
https://examine.com/supplements/uridine/ 1/15
16/12/2017 Uridine - Scientic Review on Usage, Dosage, Side Effects | Examine.com
Caution Notice
()
Examine.com Medical Disclaimer (/disclaimer)
How to Take
Recommended dosage, active amounts, other details
Supplementation of uridine seems to be in the 500-1,000mg range, with the lone human study using the higher end of this range. It is
recommended to take uridine with food out of prudency, but this has not been noted to be an absolute requirement.
Human E ect Matrix
The Human E ect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what e ects uridine
has on your body, and how strong these e ects are.
GRADE LEVEL OF EVIDENCE
Robust research conducted with repeated double-blind clinical trials
Multiple studies where at least two are double-blind and placebo controlled
Single double-blind study or multiple cohort studies
Uncontrolled or observational studies only
LEVEL OF OUTCOME MAGNITUDE OF EFFECT CONSISTENCY OF RESEARCH RESULTS NOTES

EVIDENCE
? ? ?
Depression -
Depressive symptoms in bipolar disorder have been noted to be
(/topics/depression/ See study
Minor reduced
) (/rubric/e ects/view/19733c094dc52172473bcc57e6ccd88b/821f28d3c7fa09e434c519e4de576207/all/)
()
-
Symptoms of
Depressive symptoms of bipolar disorder are fairly strongly
Bipolar Disorder
reduced with uridine supplementation, but currently only open
(/topics/symptoms-
label studies are in existence
of-bipolar-disorder/) See study
Minor
(/rubric/e ects/view/19733c094dc52172473bcc57e6ccd88b/e1bd4ea065704afee067dbf9bcb1e0cd/all/)
Studies Excluded from Consideration

Highly confounded with other nootropic compounds[1]
Scienti c Research
Table of Contents:
1 Sources and Structure
1.1 Sources
1.2 Structure and Properties
1.3 Dietary Interactions
1.4 NucleoMaxX (Mitocnol)
2 Pharmacology
2.1 Bioavailability and Absorption
2.2 Endogenous Regulation
3 Neurology (Mechanisms)
3.1 Kinetics
3.2 Phospholipids
3.3 P2 receptors
3.4 Synapses
3.5 Neurite Outgrowth
3.6 Catecholamines
3.7 Cognition and Learning
3.8 Alzheimer's Disease
3.9 Bipolar Disorder
4 Cardiovascular Health
4.1 Cardiac Tissue

()
5 Fat Mass and Obesity
5.1 Lipodystrophy
6 Interactions with Cancer
6.1 Pancreatic
7 Interactions with Aesthetics
7.1 Hair
8 Nutrient-Nutrient Interactions
8.1 Choline
8.2 Docosahexaenoic Acid
1 Sources and Structure
1.1. Sources
Uridine per se has been noted in the following foods:
Beer, usually said to be 0.05mg/mL (210.6+/-27.2umol/L)[2] although greater concentrations (91-161mg/L) have been noted when using
more samples from di erent breweries[3]
Breast milk[4][5] and many infant formulations[6]
Beer seems to be a great source of uridine, relatively speaking
Whereas a signi cant DNA and RNA content (possibly indicative of some Uridine content) has been noted in (all values dry weight
unless speci ed):[7]
Liver (Pig and Beef) at 2.12-2.3% for beef and 3.1-3.5% for pig (RNA) and 1.7-2% for beef and 1.4-1.8% for pig (DNA); all dry weight
Pancreas, the largest source of RNA at 6.4-7.8% (pig) and 7.4-10.2% (beef)
Lymph Nodes, the largest source of DNA at 6.7-7.0% (pig) and 6.7-11.5% (beef)
Fish at 0.17-0.47% (RNA) and 0.03-0.1% (DNA), with Herring having the highest RNA at 1.53%
Baker's Yeast (6.62% RNA, 0.6% DNA)
Mushrooms; Boletus at 1.9-2.4% RNA, Champignon at 2.05% RNA, and Chestnut at 2.1% RNA all with minute (0.06-0.1%) DNA
Broccoli at 2.06% RNA and 0.51% DNA
()
Oats at 0.3% RNA with no detectable DNA
Chinese Cabbage, Spinach, and Cauli ower with similar levels at 1.5% RNA and 0.2-0.3% DNA
Parsley at 0.81% RNA and 0.27% DNA
Organ meats and, surprisingly, Cruciferous vegetables appear to generally have a high RNA and DHA content which
insinuates they have a Uridine content
Ingestion of beer at 10mL/kg can increase serum Uridine levels 1.8-fold, which is similar levels at supplemental intake of the same
uridine dosage (0.05mg/kg); alcohol (/supplements/alcohol/) content does not in uence absorption and urinary levels of Uridine
increased by similar degrees.[2] Uridine in beer does not appear to be causative of the increases seen in Uric Acid after beer
consumption,[2] and inhibiting Uric Acid synthesis with Allopurinol does not appear to in uence the serum levels of Uridine achieved
via beer.[8][9]
1.2. Structure and Properties
It has been noted that uridine, in aqueous solution and subject to UV radiation, readily degrades and forms into photohydrates.[10]
May not be stable in solution subject to UV radiation
1.3. Dietary Interactions

During periods of undernutrition (from 1600kcal to 400kcal of only sugar; similar to a juice fast), plasma uridine can decrease up to
36% by three days after fasting and is reduced by 13% (nonsigni cant) after one day.[11] These results mimick previous results
obtained in rabbits during starvation.[12]
1.4. NucleoMaxX (Mitocnol)

Mitocnol is a patented blend of Uridine derived from Cane Sugar with a high (17%) Nucleoside content, with 6g out of 36g satchels
consisting of nucleosides. These satchels contain 0.58g Uridine (1.61%) and 5.4g (15%) 2,3,5-tri-O-acetyluridine (TAU), a structure
similar to Uridine; when considering the weight of both molecules, each satchel contains about 1.7x10-2mol Uridine.[13]
Simply a source of Uridine and TAU, the latter of which is a better absorbed form of Uridine (a pro-drug)
2 Pharmacology
()
2.1. Bioavailability and Absorption
Uridine is absorbed from the intestinal tract via either facilitated di usion or speci c Uridine transporters.[14]
Due to limits on absorption, the maximum tolerated dose (with doses higher than this inducing diarrhea) is either 12-15g/m2 (20-25g
for an average sized male) acutely which elevates serum levels up to 60-80uM or 5g/m2 (8.5g for an average sized male) thrice a day
every 6 hours, which maintains serum concentrations of 50uM; this confers a bioavailability of 5.8-9.9%.[15]
Practical limits on absorption exist for Uridine since high doses may induce diarrhea, but these limits appear to be much
higher than standard supplemental dosages
Mitocnol is a cane sugar extract with a high (17%) content of nucleosides, and a pharmacokinetic study on one 'satchet' of the brand
NucleoMaxX (36g) with 200mL orange juice noted that serum uridine levels were elevated from 5.4-5.8uM at baseline to
152+/-29.2uM (Cmax) after 80 minutes (Tmax), with high interindividual variability of Cmax values from 116-212uM.[16] This study also
noted a half-life of 2 hours initially and a terminal half-life of 11.4 hours, with serum concentrations after 8 and 24 hours declining to
19.3+/-4.7uM and 7.5+/-1.6uM, respectively.[16] This study was later replicated in a proper pharmacokinetic study,[13] and replicated
similarly high values for Cmax (150.9uM) at 80 minutes (Tmax) but noted a half-life of 3.4h and an AUC of 620.8+/-140.5uM; both
studies noted higher concentrations of uridine in women that was due to di erences in body mass, which disappeared upon factoring
that into the equation.[13] When Mitocnol was compared against isolated Uridine when the two were controlled for Uridine content, it
noted 4-fold enhanced absorption[13] and the concentrations reached with Mitocnol exceed those with isolated Uridine.
The increased bioavailability of Mitocnol may simply be due to the high Triacetyluridine (TAU) content, as TAU has 7-fold greater
bioavailability than an equimolar amount of Uridine[17] secondary to its lipophilicity and passive di usion, as claimed by the patents
on it.[18] It is degraded into Uridine by intestinal and plasma esterases,[18] but is resistant to Uridine phosphorylase.[19]
Mitocnol appears to be useful for situations when one wants a high serum Uridine concentrations without
gastrointestinal side-e ects, due to enhanced bioavailability
2.2. Endogenous Regulation

Serum levels of Uridine under resting conditions uctuate in the 3-8uM range.[20][13]
Erythrocytes contain the enzyme UDP-Glucose, which is involved in the P450 system; if needed, this enzyme can be lysed to provide
free Uridine and Glucose to the body when Uridine levels are depleted.[20]
3 Neurology (Mechanisms)
3.1. Kinetics
Uridine is known to be bypass the blood brain barrier[21][22] and is taken up by one of two transporters, one class being known as
equilibrative[23] (SLC29 family; speci cally the transporters ENT1, ENT2, and ENT3) which are low a nity (100800M range[24]) and
sodium independent and concentrative[25] (SLC28 family consisting of ENT4 as well as CNT1, 2, and 3) which are sodium dependent
active transporters with higher a nity (1-50M[24]).[26][27]
3.2. Phospholipids
Uridine is a substrate in phosphatidylcholine (/supplements/phosphatidylcholine/) (PC) synthesis via the Kennedy cycle (also known as
the CDP-choline pathway, phosphatidylethanolamine also made via this pathway).[28][29][30]
In this pathway, choline kinase (CK) catalyzes choline (/supplements/choline/) into phosphocholine consuming an ATP molecule in the
()
process[31][32] and has a micrmolar a nity in doing so (thus, much cellular choline is readily converted into phosphocholine[30]), and
although this is not the only possible way to create phosphocholine (sphingomyelin degradation also confers phosphocholine[33]) it is
the most prominent one and the rst committed step of PC synthesis via the Kennedy cycle[30] and concentrations of phosphocholine
are readily in uenced by increasing choline intake.[34]
Elsewhere, Phosphocholine cytidylyltransferase (CCT) converts cytidine triphosphate (CTP) into CDP-choline (/supplements/cdp-choline/)
plus pyrophosphate (using the previously created phosphocholine as the source of choline). This stage is the slowest in the Kennedy
cycle and rate-limiting, thus its activity determines overall PC synthesis.[35][36][37] Usually in cellular cultures, there is an abundance of
phosphocholine and a lack of CDP-choline[30] and the rate-limit at this step is thought to be determined by availability of CTP.[38] This
enzyme is also negatively regulated by brain phospholipids,[39][40] which seems to be one of the main mechanisms behind
phospholipid homeostasis and prevent excessive phospholipid synthesis.[41]
Finally, Choline phosphotransferase (CPT, not to be confused with carnitine palmitoyltransferase which shares the CPT acronym)
transfers the phosphocholine from CDP-choline to diacylglycerol (DAG).[42][43] There is also an enzyme called cholineethanolamine
phosphotransferase (CEPT) which has dual speci city for CDP-choline and CDP-ethanolamine[44][45] (and one speci c for CDP-
ethanolamine[46]), the donation of phosphocholine towards DAG is what nally creates phospholipids such as phosphatidylcholine
(the other enzymes that use CDP-ethanolamine instead create phosphatidylethanolamine). This enzyme is not stimulated by
incubation with uridine,[47] but is stimulated by nerve growth factor (NGF).[48]
Uridine and Cytidine are synthesized into phospholipids via the Kennedy cycle, and in the above cycle there is a rate-
limit just before the CCT enzyme. The thing that determines the rate is the provision of cytidine for the enzyme to act
upon
Uridine is used as a substrate from which CDP-Choline is synthesized from (albeit before the rate-limiting step) vicariously through
cytidine.[47] Provision of cytidine (synthesized from uridine) is the rate-limit in the above pathway, and providing extra cytidine to cells
or brain slices under adequate choline concentrations accelerates CDP-Choline synthesis.[38][49][50] Uridine is demonstrated to have
the same property[47] via converting into cytidine through initial conversion to uridine triphosphate (UTP) and then CTP[47][51] and this
has been con rmed in a living model.[52]
While uridine produced UTP at 5M, it stimulated CDP-Choline synthesis maximally at 50M in vitro;[47] the production of CDP-Choline
from uridine has been con rmed in vivo from orally administered uridine.[53]
Adding uridine or cytidine to cellular cultures will increase cellular levels of cytidine and overcome the rate limit, which
results in production of phospholipids
When looking at interventions, one study in otherwise healthy males given 500mg Uridine once daily for a week reported an increase
in total brain phosphomonoesters (6.32%) mostly due to an increase in total brain phosphoethanolamine (7.17%), as the increase in
phosphatidylcholine in the uridine group failed to be statistically signi cant.[54] This increase in phosphoethanolamine has been noted
elsewhere with CDP-choline, and is not necessarily met with an increase in phosphatidylethanolamine.[55][56]
In regards to phosphatidylcholine, it has been hypothesized[54] that the lack of increase is due to rapid accumulation of PC into
phospholipid membranes; this was due to previous studies noting a decrease in PC concentrations with uridine or uridine prodrugs.
[57][55]
Oral intake of uridine does appear to increase brain phospholipid precursors in otherwise healthy persons, and seems
to favor phosphatidylethanolamine. Although an increase in phosphatidylcholine cannot be ruled out, it has not been
reliably detected in humans
3.3. P2 receptors
P2 receptors are a meta-class of receptors that respond to extracellular purines and pyrimidines (such as ATP[58]), and mediate what
is known as purinergic neurotransmission.[58] This class of receptors are structurally similar to adenosine receptors (insofar that they
are classically referred to as such) and are divided into a P2Y and P2X class (which di er as P2Y receptors are GPRCs while P2X are
ligand-gated ion channels).[59][58][60][61]
Uridine is known to be an agonist of P2 receptors, particularly the P2Y subclass,[62] of which
()
consist eight known human P2Y receptors (1,2,4,6, and 11-14) with the missing numbers being non-mammalian[63] with
phosphorylated uridine having a nity mostly for the P2Y2 receptor[64] and to a lesser extent P2Y4,[65] P2Y6,[66][67] and P2Y14.[68]
The nervous system is also known to express seven P2X receptors, although seemingly uninvovled with uridine.[69][70]
Uridine has its own set of receptors that it can act upon, the P2 receptors, where it seems to most in uence activity of
P2Y2, P2Y4, P2Y6, and P2Y14. When uridine is not acting as a substrate for phospholipid synthesis, it is likely acting as a
novel neurotransmitter via purinergic receptors
The P2Y2 receptor has structural motifs that promote interactions with integrins and growth factor receptors[71][72] and activation of
this receptor is known to activate NGF/TrkA signalling[73] and be generally neuroprotective.[74]
3.4. Synapses
Uridine is thought to bene t synaptic functions due to increasing levels of brain phosphatidylcholine, which is a component of
dendrite membranes. This is thought to then confer bene t to populations su ering from a loss of synaptic function or regulation
such as Alzheimer's Disease,[75][76] where loss of synaptic function is thought to be downstream of the typical amyloid-beta
aggregates exerting toxic e ects on neruonal synapses and dendritic spines.[77]
Via providing phoshpatidylcholine, Uridine supposedly helps to create membranes and dendrites which may aid
synaptic function
Studies assessing synaptic construction in response to Uridine supplementation tend to measure dendritic spines, due to
complications in quantifying synaptic function per se but dendritic spines being the most reliable biomarker as 90% of dendrites form
synapses.[78][79][80][81]
Feeding animals a combination of Uridine, choline (/supplements/choline/), and omega-3 fatty acids (from sh oil (/supplements/ sh-
oil/)) appears to increase synaptic formation and function[82][83] and has shown improvement in a cohort of persons (n=221) with mild
Alzheimer's Disease.[84]
3.5. Neurite Outgrowth

Purines and pyrimidines have been known to induce cellular di erentiation in neurons[85] and uridine is thought to induce neuronal
di erentiation and outgrowth due to activating NGF signalling via its receptor TrkA (well known to increase neuronal growth[86][87])
secondary to acting on its own receptor, P2Y2.[73] Ablating the P2Y2 receptor prevents proper NGF signalling via TrkA,[74] and the two
receptors appear to interact with each other to function as they coimmunoprecipitate.[74]
In this sense P2Y2 agonists augment NGF signalling via increasing neuronal sensitivity to NGF[74] and NGF-induced neuronal growth,
[88] and this has been noted with the P2Y2 agonist uridine (triphosphate).[74]
Activation of the P2Y2 receptor appears to promote the actions of NGF via its own receptor (TrkA), which ultimately
appears that agonists of the P2Y2 receptor augment NGF-induced neuronal growth
6 weeks, but not 1 week, of feeding 330mg/kg (1mmol/kg) Uridine to aged rats increases levels of Neuro lament-70 (+82%) and
Neuro lament-M (+121%),[89] two cytoskeletal proteins involved in neurite outgrowth and used as biomarkers[90] that have previously
been induced in vitro with NGF di erentiated PC12 neuronal cells in response to Uridine, where neurite outgrowth was noted.[62]
Interestingly, the in vitro study noted that Uridine may act via a P2Y receptor to induce neurite growth.[62]
3.6. Catecholamines
A elderly rat diet forti ed with 2.5% Disodium Uridine (500mg/kg, or 330mg/kg Uridine and a human equivalent of around 50mg/kg)
failed to in uence resting levels of dopamine in neuronal slices from the rats, but enhanced the K+ invoked dopamine release, with 1
and 6 weeks of supplementation increasing average dopamine levels by 11.6-20.5% with no di erence in the transient decrease after
action potential, and no in uence on DOPAC or HVA concentrations.[89]
()
Uridine supplementation appears to enhance dopamine output from activated neurons without signi cantly a ecting
basal levels of dopamine
3.7. Cognition and Learning

One study using a brand name called Cognitex (50mg Uridine-5'-Monophosphate, but otherwise highly confounded with 600mg
Alpha-GPC (/supplements/alpha-gpc/), 100mg Phosphatidylserin (/supplements/phosphatidylserine/), 50mg Pregnenolone, 20mg
Vinpocetine (/supplements/vinpocetine/) and others) that 3 capsules daily for 12 weeks in an open-label study noted improvements in
spatial short term memory, recognition, recall, attention, and executive functions which increased further after 10 more weeks of
supplementation.[1]
3.8. Alzheimer's Disease

Uridine is thought to aid Alzheimer's Disease due to helping with synaptic connections, which appear to be reduced in the state of
Alzheimer's.[75][76]
Due to proliferating synapses, uridine supplementation is thought to be therapeutic for Alzheimer's disease
One study noting signi cant improvements in Alzheimer's pathology in rats with accelerated -amyloid production (and thus are
predisposed to Alzheimer's), but was too confounded with other nutrients to assess the e ects of Uridine.[91]
The evidence currently for uridine is lacklustre and not suited to assess the e cacy of uridine
3.9. Bipolar Disorder

6 weeks supplementation of Uridine in an open-label trial of bipolar disorder in children noted that 500mg twice daily (1,000mg total)
was associated with signi cantly less depressive symptoms relative to baseline (from an average score of 65.6 on the CDRS-R to 27.2
with e cacy within a week); manic symptoms were not assessed.[92]
Triacetyluridine (TAU) has been used in treatment of bipolar disorder in adults at 18g daily over 6 weeks, where a signi cant
improvement in depressive symptoms was noted.[93]
4 Cardiovascular Health
4.1. Cardiac Tissue

Uridine is able to exert an acute cardioprotective e ect against myocardial ischemia when preloaded which is abolished by blocking
potassium channels on the mitochondria (with 5-hydroxydecanoate);[94] it appears that uridine preloading preserves levels of energy
metabolites (ATP, creatine (/supplements/creatine/) phosphate, and uridine) and subsequently reduced lipid peroxidation.[94]
5 Fat Mass and Obesity
5.1. Lipodystrophy
()
Lipodystrophy is a localized loss of fat mass, and usually seen alongside HIV therapy using Nucleoside reverse transcriptase inhibitors
(NRTIs).[95]
In a multicenter study, Uridine was associated with an increase of limb fat (seen as an endpoint marker of normalizing lipodystrophy)
after 24 weeks but was no longer present at 48 weeks; it was well tolerated and did not negatively in uence virological response.[96]
These lacklustre results were replicated in a double-blind trial, where Uridine supplementation via NucleoMaxX (brand name product)
bene cially in uenced mitochondrial RNA yet negatively in uenced mitochondrial DNA without in uencing limb fat; this was met with
an increase in systemic in ammation (asssessed by IL-6 and CRP)[97] yet another trial suggests signi cant improvements with a similar
Uridine protocol on fat mass.[98]
Mixed results on interventions assessing Lipodystrophy in persons being given standard HIV therapy
6 Interactions with Cancer
6.1. Pancreatic
Activation of the P2Y2 receptor by uridine triphosphate appears to induce proliferation of the pancreatic cancer cell line PANC-1,
which was replicated by a selective agonist of the receptor and was mediated via PKC-dependent activation of Akt.[99]
7 Interactions with Aesthetics
7.1. Hair
During the early anagen phase of hair growth, there is a marked increase in uridine accumulation into dermal papillae cells and hair
germ cells relative to the dormant phase (telogen) in vitro,[100] which seems to extend to other nucleotides (such as thymidine[101] and
cytidine[102]); it is thought that this is indicative of an increased RNA and DNA synthesis rate during spontaneous growth of hair cells.
[100]
No studies have currently assessed whether provision of uridine is at all rate-limiting in this context, so the role of supplementing
exogenous uridine to act as a substrate for DNA synthesis is not certain.
Uridine is accumulated into hair cells during the growth phase (anagen), but it is not ascertained if uridine acting as a
substrate for DNA/RNA synthesis as mentioned above is at all relevant to supplementation of uridine
It has been noted that P2Y1 and P2Y2 receptors (the latter of which is a target of uridine) are expressed in hair cells undergoing
anagen, with the P2Y2 receptors expressed in the living cells at the edge of the cortex/medulla and the P2Y1 receptors in the root
sheath and bulb;[103] P2X5 receptors were detected in the inner and outer root sheaths and medulla while P2X7 receptors were noted
to not be present.[103] The P2Y2 receptors were detected early on, as they were no longer present in the di erentiated hair cuticle, and
due to the roles of uridine as an agonist of this receptor causing proliferation in keratinocytes[104][105][106] it was hypothesized that
uridine may stimulate hair cell di erentiation.[103]
()
It is theoretically possible, but not yet demonstrated, that uridine can act via the P2Y2 receptor to stimulate hair cell
di erentiation at the beginning of the growth (anagen) phase
8 Nutrient-Nutrient Interactions
8.1. Choline
Choline (/supplements/choline/) and Uridine are both seen as dietary in uences on neuronal function, as oral choline can increase
brain phosphocholine levels in rats[34] and humans where a 3-6% in choline levels in serum result in an increase of 10-22%
phosphocholine in the brain.[107] Uridine administration increases CDP-choline levels in the brain.[53]
8.2. Docosahexaenoic Acid

DHA, one of the two sh oil (/supplements/ sh-oil/) fatty acids, can increase brain levels of phosphatidylcholine up to 30% higher than
control at 300mg/kg feed intake when it is paired with 0.5% Uridine.[83]
Scienti c Support & Reference Citations
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Goes Well With

Choline (/supplements/choline/) or other cholinergics (Cognition)

Human E ect Matrix

GRADE LEVEL OF EVIDENCE

Robust research conducted with repeated double-blind clinical trials

Single double-blind study or multiple cohort studies

Uncontrolled or observational studies only

LEVEL OF OUTCOME MAGNITUDE OF EFFECT CONSISTENCY OF RESEARCH RESULTS NOTES

Studies Excluded from Consideration

1.2 Structure and Properties

1.3 Dietary Interactions

1.4 NucleoMaxX (Mitocnol)

2.1 Bioavailability and Absorption

2.2 Endogenous Regulation

3.5 Neurite Outgrowth

3.7 Cognition and Learning

3.8 Alzheimer's Disease

3.9 Bipolar Disorder

4.1 Cardiac Tissue

6 Interactions with Cancer

7 Interactions with Aesthetics

8.2 Docosahexaenoic Acid

1 Sources and Structure

Breast milk[4][5] and many infant formulations[6]

Beer seems to be a great source of uridine, relatively speaking

Baker's Yeast (6.62% RNA, 0.6% DNA)

Broccoli at 2.06% RNA and 0.51% DNA

Parsley at 0.81% RNA and 0.27% DNA

1.2. Structure and Properties

May not be stable in solution subject to UV radiation

1.3. Dietary Interactions

1.4. NucleoMaxX (Mitocnol)

2.2. Endogenous Regulation

3.5. Neurite Outgrowth

3.7. Cognition and Learning

3.8. Alzheimer's Disease

3.9. Bipolar Disorder

4.1. Cardiac Tissue

5 Fat Mass and Obesity

6 Interactions with Cancer

7 Interactions with Aesthetics

8.2. Docosahexaenoic Acid

Scienti c Support & Reference Citations

Fish Oil (/supplements/ sh-oil/)

Garcinia cambogia (/supplements/garcinia-cambogia/)

Whey Protein (/supplements/whey-protein/)

Detoxes: an unde ned scam (/nutrition/detoxes-an-unde ned-scam/)

Top 10 Nutrition Myths (/nutrition/10-awful-myths-perpetuated-by-the-media/)

How can I increase testosterone naturally? (/nutrition/how-can-i-increase-testosterone-naturally/)

Is diet soda bad for you? (/nutrition/is-diet-soda-bad-for-you/)

Are eggs healthy? (/nutrition/are-eggs-healthy/)

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