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There are over 2000 enzymes in your Body that maybe dormant including Gene simply because your not getting the right amount of Zinc!!!!

Ingredients: Rosemary, Chlorella, Sage to Power Zinc Function!!!!

Cilantro and Chlorella can Remove 80% of Heavy Metals from the Body within 42 Days


There are many heavy metals that people are exposed to regularly without realizing it. Mercurycadmium, and aluminum, among others, are able to imbed themselves into our central nervous systems and bones, bio-accumulating for years until we start to suffer acute health problems from heavy metal poisoning. Fortunately, there is a simple one-two-combination that helps to chelate heavy metals so that they are no longer circulating in the body cilantro and chlorella.

Chelating agents are those that bind to heavy metal toxin ions, and then are removed from the body through our regular excretory channels. Pharmaceuticals like 2,3-Dimercaprol have long been the mainstay of chelation therapy for lead or arsenic poisoning, but they have serious side effects. The simple, and proper dose of cilantro (Chinese parsley) and chlorella; however is a powerful chelator for numerous heavy metals.

Dr. George Georgiou says:

“Many health practitioners use synthetic chelating agents such as DMPS, DMSA, EDTA and others to mobilize and eliminate heavy metals from the body. There are advantages and disadvantages to using these. One advantage is the power of their mobilizing activity—they are quick to mobilize and eliminate certain metals in the body, but this may place a huge burden on the body’s detoxification systems.”

Cilantro is best used in conjunction with chlorella because it, mobilizes more toxins then it can carry out of the body, it may flood the connective tissue (where the nerves reside) with metals, that were previously stored in safer hiding places.” This can cause retoxificaiton if another binding agent isn’t used to help rid the body of the heavy metals that are ‘found’ in their hiding places throughout the body.

People who have eaten large salads daily full of cilantro have experienced this effect – moodiness, terrible acne, joint pain and more. While they were mobilizing heavy metals, they weren’t all excreted from the body fast enough, which meant they were detoxing and toxifying themselves the same time!

Read: 6 Foods for Natural Heavy Metal Chelation

Simply by adding chlorella – an intestinal absorbing agent, the retoxificaiton of the system is prohibited. Clinical studies completed recently proved that heavy metal chelation [using cilantro and chlorella] can naturally remove an average of 87% of lead, 91% of mercury, and 74% of aluminum from the body within 42 days.

The properties of chlorella lend themselves nicely to aiding cilantro for detoxifying the body:

  • Chlorella is antiviral.
  • It binds to dioxins and other environmental toxins.
  • It repairs the body’s detoxification functions.
  • Improves glutathione – the bodies ‘master’ antioxidant.
  • Binds to heavy metals exceptionally well.
  • Alpha and gamma lineolic acids in chlorella help increase the intake of fish oil and other important fatty acids.
  • Methyl-coblolamine repairs the nervous system and damaged neurons which often suffer from heavy metal poisoning.
  • Chlorella contains the most easily absorbed form of B12 and B6.
  • Chlorella is high in amino acids, and thus ideal for vegetarians.
  • Chlorella is able to open cell walls, which is necessary for detox processes.
  • Chlorella restores healthy gut flora.
  • Chlorella is still being studied for its detoxifying effects, since science cannot fully understand how it has developed over millions of years to be so effective in ridding the body of unwanted substances.

The Therapeutic Potential of Rosemary (Rosmarinus officinalis) Diterpenes for Alzheimer’s Disease


Rosemary (Rosmarinus officinalis L.) is one of the most economically important species of the family Lamiaceae. Native to the Mediterranean region, the plant is now widely distributed all over the world mainly due to its culinary, medicinal, and commercial uses including in the fragrance and food industries. Among the most important group of compounds isolated from the plant are the abietane-type phenolic diterpenes that account for most of the antioxidant and many pharmacological activities of the plant. Rosemary diterpenes have also been shown in recent years to inhibit neuronal cell death induced by a variety of agents both in vitro and in vivo. The therapeutic potential of these compounds for Alzheimer’s disease (AD) is reviewed in this communication by giving special attention to the chemistry of the compounds along with the various pharmacological targets of the disease. The multifunctional nature of the compounds from the general antioxidant-mediated neuronal protection to other specific mechanisms including brain inflammation and amyloid beta (Aβ) formation, polymerisation, and pathologies is discussed.

1. Introduction

Rosmarinus officinalis L. (family, Lamiaceae), commonly known as rosemary, is one of the most popular perennial culinary herbs cultivated all over the world. Both fresh and dried leaves of rosemary have been used for their characteristic aroma in food cooking or consumed in small amount as herbal tea, while rosemary extracts are routinely employed as natural antioxidant to improve the shelf life of perishable foods. In the latter case, the European Union has approved rosemary extract (E392) as a safe and effective natural antioxidant for food preservation []. The plant is also known to be employed in traditional medicines in many countries even far beyond its native Mediterranean region where it grows wild. Among the pharmacologically validated medicinal uses of rosemary are antibacterial [], anticancer [], antidiabetic [], anti-inflammatory and antinociceptive [], antioxidant [], antithrombotic [], antiulcerogenic [], improving cognitive deficits [], antidiuretic [], and hepatoprotective [] effects. The other major use of rosemary is in the perfumery industry where the essential oils are employed as natural ingredients of fragrances.

The culinary, medicinal, and fragrance uses of rosemary are attributed to the vast arrays of chemical constituents collectively known as plant secondary metabolites. Of these, one group are small molecular weight aromatic compounds called essential oils which play vital role in the fragrance and culinary properties of the plant. Essential oils of rosemary dominated by 1,8-cineole, α-pinene, camphene, α-terpineol, and borneol as principal constituents [] are also responsible for various pharmacological effects of the general antioxidant [] and antimicrobial [] properties known for many essential oils, as well as other effects including anticarcinogenic activities []. The other group of secondary metabolites of rosemary are polyphenolic compounds including the flavonoids (e.g., homoplantaginin, cirsimaritin, genkwanin, gallocatechin, nepetrin, hesperidin, and luteolin derivatives) and phenolic acid derivatives (e.g., rosmarinic acid) []. By far the most important group of rosemary compounds that gain significant attention in recent years, however, are the unique class of polyphenolic diterpenes. In this review, the chemistry and pharmacology of rosemary diterpenes are scrutinised by giving special emphasis to their therapeutic potential for Alzheimer’s disease (AD).

Accounting for an estimated 60 to 80 percent of dementia cases in the elderly populations, AD has become one of the major global health challenges of the century. The worldwide prevalence of dementia is now estimated to exceed 36 million cases with a further projection of 115 million by 2050 []. One of the current well-accepted pathologies of AD is the “amyloid hypothesis” that puts the accumulation and aggregation of amyloid-beta (Aβ) as the major cause of the progressive neuronal cells deaths in the brain. Neuronal deletion particularly in the cortex region is now known to lead to cognitive impairment including acquired learning skills and memory. The hosts of behavioural symptoms arising from AD include agnosia, aphasia, apraxia, erratic emotion, sleep disorders, and interpersonal/social deterioration []. Numerous studies have shown that these clinical symptoms of AD are associated with the loss of cholinergic neurons induced by toxicants such as Aβ, reactive oxygen species (ROS), inflammatory cascades, and excitotoxicity mechanisms. Critical to the AD pathology is the basal forebrain region from where cortical cholinergic neurons originate. The loss of neurons in the basal forebrain has been shown to correlate with the degree and severity of clinical symptoms of AD []. To date, the handful of drugs available to treat AD are the acetyl cholinesterase (ACHE) inhibitors (e.g., rivastigmine, galantamine, tacrine, and donepezil) and N-methyl-D-aspartate (NMDA) receptor antagonist (memantine) which have some benefit in alleviating the clinical symptoms of AD []. Drug of cure for AD is, however, neither available nor within sight, and the search of new drugs from natural sources should be considered as a viable strategy for the future control of the disease. One group of compounds of interest are the rosemary diterpenes which are comprehensively assessed in this communication for their therapeutic potential for AD. Special emphasis is given to the structural features of the compounds with respect to their effects against specific AD target.

2. Overview of Rosemary Diterpenes

2.1. Biosynthetic Perspective

Biosynthetically, diterpenes are derived from the terpenoids or mevalonate pathway and hence composed of repeating 5-carbon backbone skeleton, isoprene unit(s). The two known isoprene building blocks are isopentenyl pyrophosphate (IPP, 1Figure 1) and dimethylallyl pyrophosphate (DMAPP, 2) that polymerises in head-to-tail fashion to form the 20-carbon diterpene precursor (4 isoprene units) called geranylgeranyl pyrophosphate (GGPP, 3). The processing of the GGPP through reactions including cyclization, aromatisation, rearrangements, and a series of reaction steps emanating from the loss of the phosphate group, including removal of the carbonium ion, results in the formation of the diterpene subgroups. The class of diterpenes in rosemary identified so far is the abietane type (57) which is composed of six–membered tricyclic ring system of which one is aromatic (e.g., 7) []. Biosynthetically, abietane-type diterpenes are known to derive from their immediate precursor, labdane subclass (4), as shown in Figure 1. The labdane group of diterpenes on their own are diverse natural products that have been shown to include compounds of novel structural and biological significances [].

Figure 1

Schematic presentation of the biosynthetic pathway of rosemary diterpenes.

2.2. Diversity of Rosemary Diterpenes

The various types of diterpenes isolated from rosemary are shown in Figure 2. The basic skeleton of all of these diterpenes in rosemary appears to be carnosic acid (7) which was first isolated from the plant by Wenkert et al. [] in 1965. It is now well known that this compound is the major constituent of rosemary that accounts to 1.5–2.5% of the dried leaves though even higher amounts have been reported []. Like many other secondary metabolites, the concentration of carnosic acid (7) and other diterpenes in rosemary could vary due to a host of environmental factors (e.g., sun light intensity and water stress) and growth conditions [] as well as genetic factors as there are now several varieties that could yield the compound in up to 10% yield by dry weight []. Carnosic acid (7) is not unique to rosemary and its distribution in sage and other taxonomically related species has been revived recently by Birtić et al. []. Other taxonomically unrelated plants such as Premna species have also shown to synthesise pharmacologically significant abietane-type diterpenoids with even more aromatisation than those shown for rosemary diterpenoids in Figure 2 [].

Figure 2

Carnosic acid and related abietane-type diterpenes of rosemary.

Although carnosic acid (7) is the principal constituent of rosemary extracts, it is not a very stable compound once extracted and may undergo oxidation to form the γ-lactone diterpene, carnosol (8). In fact, the conversion of (7) to (8) in extracts of R. officinalis and Salvia officinalis has been well documented [], and the latter was considered as the principal constituent of the plant in earlier studies. In addition to carnosol (8), the oxidation of (7) is also known to yield rosmanol (9) which differs from carnosol by possessing a free hydroxyl group at C-7 position and the γ-lactone formed via the C-20-C-6 route []. The epimeric form of rosmanol with stereochemistry difference at C-7 position has also been demonstrated by the identification of (11) (epirosmanol []). An enzyme catalysed conversion of carnosic acid (7) to lactone derivatives via singlet oxygen-mediated reactions has been suggested as a possible mechanism of these diterpene lactones formation []. Enzymatic dehydrogenation and free radical attack are now also generally considered as a common route for the formation of various oxidation products of (7) []. An alternative structure, isorosmanol (12) [], where the lactone ring is formed via the C-6 instead of the C-7 hydroxyl position, has also been identified in rosemary extract. The further route of structural diversification in rosemary diterpenes comes through methoxylation and hence the 12-methoxyl derivative of carnosic acid (14) and 11,12-dimethoxy isorosmanol (15) have been identified. Methoxylation at the 7-position is also evident as 7-methoxy-rosmanol (10) has been identified from rosemary []. All these diterpenes are relatively polar and are not found in the essential oil of rosemary [].

The other structurally interesting group of rosemary diterpene derivatives are diterpene quinones (16)–(19) (Figure 3). Mahmoud et al. [] reported the isolation and structural elucidation of two new abietane-type diterpenoid O-quinones, rosmaquinone A (16) and rosmaquinone B, (17) along with another known diterpene quinone, royleanonic acid (18) and rosmanol. Another example of diterpene quinone identified from rosemary was rosmariquinone (19) [].

Glycosylation is the common route of structural diversification in natural products. The study by Zhang et al. [] has resulted in the identification of polar diterpene glycosides named as officinoterpenosides A1 (20) and A2 (21) (Figure 4). These polar compounds also differ from the carnosic acid derivatives (715) not only by their glycosylation and different oxygenation pattern but also by having an altered side chain whereby the 16-methyl group has migrated to the C17 position.

Munné-Bosch and Alegre [] have analysed the relative concentrations of diterpenes in rosemary tissues. In general, the level of carnosic acid (7) was about 6-fold higher than other derivatives such as 12-O-methylcarnosic acid (14) and carnosol (8), which (the latter two) were found in similar concentrations. On the other hand, isorosmanol (11) was found at slightly lower concentrations than carnosol (8) while the 11,12-di-O-methylisorosmanol (15) was about 10 times less abundant than isorosmanol (11). The rosmanol (9) concentration is regarded as a trace amount []. The most important diterpenes in terms of biological significance of the rosemary however remain to be carnosic acid (7) and carnosol (8) which are most abundant (~5% the dry weight) and shown to account for over 90% of rosemary’s antioxidant effects []. Dried rosemary could contain about 0.2–1% carnosol (8) [] while many commercially available extracts may be optimised to contain approximately 10.3% carnosol (8) [].

Bioavailability. Doolaege et al. [] have studied the absorption, distribution, and elimination of carnosic acid (7) in rats following administration via the intravenous (20.5 ± 4.2 mg/kg) and oral (64.3 ± 5.8 mg/kg) routes. Their study revealed that the bioavailability of (7) after 360 min following the intravenous dosage was 40.1%. The study also showed that traces of (7) were found in various organs in its free form while elimination in the faeces after 24 h after oral administration was 15.6 ± 8.2% []. Another study by Vaquero et al. [] emphasised on the oral route of (7) where the glucuronide conjugates were found to be the main metabolites detected in the gut, liver, and plasma. The other metabolites identified were the 12-methyl ether and 5,6,7,10-tetrahydro-7-hydroxyrosmariquinone of (7) []. Since these metabolites were detected as early as 25 min following oral administration, it was reasonable to conclude that rosemary diterpenes are bioavailable. Interestingly, the free form of (7) as well as its metabolites was detected in the brain [] suggesting possible effect in this vital organ.

3. Pharmacological Targets of Rosemary Diterpenes Related to AD Therapy

3.1. General Pharmacological Effect of Rosemary Diterpenes on the Brain and Memory

In an attempt to investigate the effect of rosemary tea consumption on brain function, Ferlemi et al. [] have recently tested the potential anxiolytic- and antidepressant-like behaviour effect on adult male mice. The result showed that oral intake of rosemary tea for 4 weeks has shown a positive effect without altering memory/learning when assessed by passive avoidance, elevated plus maze and forced swimming tests. In an olfactory bulbectomy procedure in mice, MacHado et al. [] have also demonstrated that rosemary extract possesses antidepressant-like effect and is also able to abolish ACHE alterations although the spatial learning deficit induced by the procedure was not altered. Carnosic acid (7) has also shown to have neuroprotective effects on cyanide-induced brain damage in cultured rodent and human-induced pluripotent stem cell-derived neurons in vitro and in vivo in various brain areas of a non-Swiss albino mouse model []. As discussed in the later sections, this effect is likely to be mediated via upregulation of transcriptional pathways related to antioxidant and anti-inflammatory mechanisms []. Protective effects of carnosol (8) on rotenone-induced neurotoxicity in cultured dopaminergic cells were also observed in vitro in parallel with downregulation of apoptotic mechanisms []. It is also worth noting that other components of rosemary, such as essential oil constituents, are known to alter brain function at therapeutic doses. For example, the cognitive enhancing power of rosemary component, 1,8-cineole, has been well documented []. In agreement with these observed effects of the isolated compounds (7, 8), the crude extract of rosemary has been shown to improve memory impairment when tested in vivo using the scopolamine-induced dementia model of AD [].

3.2. Antioxidant Mechanisms

A number of simple in vitro experiments where the antioxidant potential of rosemary diterpenes is demonstrated include lipid peroxidation and protection of cells from oxidative cell death []. Readers must however bear in mind that the antioxidant potential of rosemary extracts and diterpenes on food preservation and various biological models have been established up to the level of large-scale commercial exploitations. The emphasis in this communication is therefore limited to highlighting mechanisms relevant to neurodegenerative diseases. In this respect, Hou et al. [] have shown that carnosic acid (7) protects neuronal cells from ischemic injury by scavenging ROS. The antioxidant mechanisms of (7) and carnosol (8) are dependent on the loss of hydrogen from their phenolic hydroxyl groups leading to formation of quinone derivatives []. Through this antioxidant mechanism, (7) can protect neuronal cells from oxidative damage both in vitro and in vivo. Numerous reports during the last few decades including ours have shown that the antioxidant mechanism and/or radical scavenging effect of polyphenolic natural products is exceptionally prominent when the compounds possess the catechol functional group []. The formation of the various diterpene derivatives as the oxidation products of (7) is also inherently related to its ability to interact with ROS [].

The induction of phase II detoxifying enzymes is an important defence mechanism for the removal of xenobiotics and other toxicants of internal and external origin. A large body of evidence to date indicates that the erythroid derived 2-related factor 2 (Nrf-2) is involved in the antioxidant response elements- (AREs-) mediated induction of genes for a variety of antioxidant enzymes, including phase II detoxifying enzymes []. The expression of many thiol-regulating enzymes, such as glutathione S-transferase, glutamylcysteine synthetase, and thioredoxin reductase, has also shown to be dependent on Nrf-2 []. Of the various mechanisms described for these antioxidant effects is direct S-alkylation of the cysteine thiol of the Kelch-like ECH-associated protein 1 (Keap1) protein by the “electrophilic” quinone derivative of (7) []. Keap1 is a regulatory protein associated with the transcriptional factor Nrf2 that binds to the ARE []. The binding of electrophiles compounds with the cysteine residues on Keap1 protein and the subsequent S-alkyl adduct formation will allow the migration of the Nrf2 to the nucleus. Nrf2 can then promote genes expression by binding to AREs of phase II genes. Through this mechanism, the application of electrophile compounds as antioxidant and neuroprotective agents has been well documented in the various literature [].

Carnosol (8) possesses high electrophilic activity and has been reported to activate Nrf2, phase II detoxifying enzyme genes, and antioxidant enzymes []. Direct interaction of (8) with cysteine residues of the nuclear factor kappa B (NF-κB) has also been demonstrated []. In a similar manor, carnosic acid (7) has been shown to protect neuronal HT22 cells through activation of the antioxidant-responsive element []. The free carboxylic acid and catechol hydroxyl moieties have been shown to play critical role in these effects []. All the available evidence now therefore suggests that the major rosemary constituents (7 and 8) protect neurons against oxidative stress by activating the Keap1/Nrf2 pathway. Xiang et al. [], for example, have demonstrated that (7) and (8) could protect HT22 cells against oxidative glutamate toxicity through mechanisms involving activation of the transcriptional ARE of phase II genes including heme oxygenase-1, NADPH-dependent quinone oxidoreductase, and γ-glutamyl cysteine ligase, all of which provide neuroprotection by regulating the cellular redox system. Through antioxidant mechanism, (7) does also protect the lipopolysaccharide- (LPS-) induced liver injury through enhancement of the body’s cellular antioxidant defence system as the levels of superoxide dismutase, glutathione peroxidase, and glutathione in serum and liver after the LPS challenge were restored []. Pretreatments of RAW264.7 macrophages with (7) also resulted in a significant reduction of the hydrogen peroxide- or LPS-induced generation of ROS and nitric oxide while the heme oxygenase-1 (HO-1) protein expression was time- and dose-dependently upregulated []. Moreover, carnosol (8) has been shown to enhance the glutathione S-transferase (GST) and quinone reductase activity in vivo [].

The therapeutic potential of rosemary diterpenes for AD must be seen in conjunction with the role of oxidant-antioxidant mechanisms in the pathology of the disease. A number of studies have clearly outlined the direct association between ROS-mediated macromolecular cell damage and neuronal cell death in AD, particularly in brain regions where Aβ is highly prevalent []. Interestingly, neuronal cells in the brain appear to be more susceptible to ROS-mediated cell damage than any other cell types for numerous reasons including high oxygen consumption [], high level of polyunsaturated fatty acids content of cell membrane [], association of the NMDA receptor activation with ROS-induced neuronal apoptosis [], and poor level of antioxidant defences including the catalase, glutathione peroxidase, and vitamin E contents []. Furthermore, antioxidant defences in AD have been found to be highly suppressed as low level of SOD [] and reduced form of glutathione (GSH) [] as well as mitochondrial dysfunction [] are all common features of AD. Hence, the numerous reports on the antioxidant effects of rosemary diterpenes along with their specific effect on neuronal cells through the abovementioned antioxidant mechanisms imply that they should be considered for further development as anti-Alzheimer’s agents.

Metal Chelation. High level of metal ions such as copper, zinc, and iron have been found in the amyloid plaques of AD brains []. Higher millimolar level of unregulated metal ions in the brain has also been shown to arise due to age related deterioration of the blood-brain-barrier leading to unchecked access of the brain to metal ions []. As described in the later section, these metal ions play critical role in Aβ-induced neurotoxicity in AD. Hence, a potent metal chelative effect of a drug is an important feature of anti-AD therapy. Our own study on polyphenolic compounds in the last two decades has revealed that their biological effect including enzyme inhibition could be partly explained by their ability to chelate iron and other redox metals and, for such effect, one of the best structural features in a molecule is the orthodihydroxyl functional moiety [].

The structural features of (7) and (8) are in favour of strong metal chelation properties. Carnosol (8) has been shown to inhibit Cu2+-induced LDL oxidation [] but, most importantly, metal (e.g., iron) chelation is one of the known mechanisms of antioxidant effects. Furthermore, iron absorption from the gut is strongly suppressed by rosemary extract [].

3.3. Anti-Inflammatory Mechanisms

The roles of Nrf2 and the antioxidant protein HO-1 in neuroinflammatory response have been well established. The search for effective Nrf2/HO-1 activators that modulate the microglia inflammatory response in AD would therefore have significant therapeutic value. A recent study has further revealed that Nrf2 activation inhibits inflammatory gene expression [] through mechanisms involving HO-1 []. Lian et al. [] have also shown that carnosol (8) and rosemary essential oils inhibit the adhesion of tumour necrosis factor-α– (TNF-α-) induced monocytes to endothelial cells and suppress the expression of intercellular adhesion molecule (ICAM-1) at the transcriptional level in vitro. The anti-inflammatory effect of (8) via inhibition of the TNF-α-induced protein expression of ICAM-1 was also shown to be extended to other cell surface molecules such as the vascular cell adhesion molecule- (VCAM-) 1 and E-selectin in endothelial cells as well as interleukin- (IL-) 8 and the monocyte chemoattractant protein- (MCP-) 1 []. Moreover, Foresti et al. [] have shown that (8) inhibits the TNF-α-induced signaling pathways through inhibition of inhibitor of nuclear factor kappa-B (IKK-β) activity as well as the upregulation of HO-1 expression. At the concentration of 5–20 μM, (8) was demonstrated to upregulate Nrf2 and HO-1 leading to downregulation of the inflammatory response (TNF-α, prostaglandin E-2, and nitrite) []. Carnosic acid (7) was similarly shown to inhibit the expression of cytokine-induced adhesion molecules on endothelial cells surface leading to inhibition of monocyte-cell adhesions []. It does also potently inhibit the LPS-induced rise in serum levels of the proinflammatory cytokines (TNF-α and IL-6) in vivo []. Both (7) and (8) have also shown to inhibit the phorbol 12-myristate 13-acetate- (PMA-) induced ear inflammation in mice with EC50 of 10.20 μg/cm2 and 10.70 μg/cm2, respectively. This activity was coupled with reduced level of expression of IL-1β and TNF-α and cyclooxygenase-2 (COX-2). In another study [], both (7) and (8) inhibited the formation of proinflammatory leukotrienes in cells with IC50 of 7–20 μM as well as purified recombinant 5-lipoxygenase (IC50 = 0.1–1 μM). The study also showed that both (7) and (8) potently antagonise intracellular Ca2+ mobilisation induced by a chemotactic stimulus, coupled with inhibition of ROS generation []. The LPS-induced nitric oxide production in Raw 264.7 cells was also shown to be inhibited by (8) with IC50 of 9.4 μM []. In an in vitro model of brain inflammation, (7) inhibited the LPS-induced activation of cells of the mouse microglial cell line MG6 [], releasing inflammatory cytokines such as IL-1β and IL-6. The nitric oxide production associated with a decrease in the level of inducible nitric oxide synthase has also been reported for (7) [].

Glial cells are the major inflammatory cells of the brain which produce massive amount of proinflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α) upon activation. Numerous studies have highlighted the fact that high levels of these inflammatory cytokines are critical in the coordination of brain inflammation in AD []. Moreover, both microglia and astrocytes have been shown to be highly regulated in AD brains []. The potent anti-inflammatory activity of rosemary diterpenes in both the microglial cells [] and other inflammatory models therefore suggests their potential in tackling AD.

3.4. Aβ Mechanisms

Generally, amyloid plaques and neurofibrillary tangles (NFT), which are closely linked to the formation of toxic insoluble aggregates of Aβ, have shown to be the two most common pathological hallmarks of AD []. The Aβ is formed from the neuronal transmembrane glycoprotein (100–130 kDa) called the amyloid precursor protein (APP). The α-, β-, and γ-secretases are the three major proteolytic enzymes that process APP [] through two major pathways: the amyloidogenic and nonamyloidogenic pathways. The non-amyloidogenic-dependent pathway involves APP processing through α-secretase leading to the generation of nonpathogenic amyloid products. In the amyloidogenic pathway, β-secretase processes APP at the N-terminus of the Aβ domain to generate the membrane-attached fragment, C99, and the sAPPβfragment []. Further cleavage of the C99 fragment by γ-secretase leads to the formation of the two most common forms of Aβ peptides, Aβ1–40 (90%) and Aβ1–42 (10%), along with other fragments. To date, a number of therapeutic agents that inhibit APP processing have been identified and some appear to be in clinical trials []. Of these, inhibitors of β-secretase 1 (BACE1) appear to be most important as this enzyme takes the first rate limiting step in APP processing []. To the best of the author’s knowledge, an inhibitory effect of rosemary diterpenes on β-secretase activity has not been demonstrated but a promising effect on α-secretase has been reported by Meng et al. []. In their study using the SH-SY5Y human neuroblastoma cells, carnosic acid (7) showed 61% suppression of Aβ42 secretion when tested at the concentration of 30 μM. The effect was also coupled with enhanced mRNA expressions of α-secretase but not the β-secretase BACE1. Hence, the mechanism of action of (7) for APP processing inhibition appears to be through promotion of the normal non-amyloidogenic-dependent pathway. Similar results were also demonstrated by Yoshida et al. [] where Aβ peptides (1–40, 1–42, and 1–43) production in U373MG human astrocytoma cells was suppressed by (7) (50 μM). The study also revealed a 55 to 71% inhibition of Aβ release coupled with effect on mRNA expressions of an α-secretase, but once again not the β-secretase BACE1 [].

Once Aβ is formed, it undergoes a serious of polymerisation processes leading to the formation of insoluble precipitates. It has been shown that small soluble oligomers as well as amyloid fibril aggregates induce toxicity to neuronal cells in AD []. Hence, various classes of natural and synthetic compounds that inhibit the polymerisation and stability of Aβ aggregates can be employed as viable therapeutic agents for AD. Some of these agents identified to date include chrysamine G [], oligopeptides [], and plant polyphenols such as curcumin, myricetin, morin, quercetin, kaempferol (+)-catechin, (−)-epicatechin, nordihydroguaiaretic acid and tannic acid [], antibiotics (e.g., rifampicin []), and aspirin []. In this connection, Meng et al. [] have recently investigated the effect of carnosic acid (7) on the viability of cultured SH-SY5Y human neuroblastoma cells challenged by Aβ42 or Aβ43. The cellular deletion in these cells treated with Aβ42 or Aβ43 (monomer, 10 μM each) was reported to be partially reversed by treatment with (7) (10 μM). The observed effect was also coupled with reduced level of cellular oligomers of Aβ42 and Aβ43 suggesting inhibition of oligomerisation as the possible mechanism of action []. These data were also in agreement with the in vivo observation where (7) has been demonstrated to show beneficial effect in AD models []. Rasoolijazi et al. [] also provided direct evidence to demonstrate the therapeutic potential of (7) for AD by using Aβ toxicity in vivo. When Aβ (1–40) was injected into the Ca1 region of the hippocampus of rats, neurodegeneration and cognitive impairment were evident as assessed by the passive avoidance learning and spontaneous alternation behaviour tests. Treatment by (7) appears to reverse these Aβ (1–40) mediated changes suggesting the therapeutic potential of this compound for AD []. The association between Aβ formation and aggregation with metal ions such as copper has been reviewed in many literatures []. In agreement with this finding, metal chelators have been shown to decrease Alzheimer Aβ plaques []. It is now also known that Aβ is a redox-active peptide that reduces transition metals like Cu2+ and Fe3+leading to the generation of ROS []. Both the polymerisation and toxicity of Aβ are therefore intimately linked to metal ions and ROS []. The polymerisation of Aβ itself is shown to be enhanced when the antioxidant defence is diminished []. The multifunctional nature of rosemary diterpenes in metal chelation and ROS scavenging is thus likely to contribute to their effect against Aβ polymerisation and toxicity.

3.5. ACHE Activity

The impairment of memory and cognitive power in AD has been shown to be associated with the loss of cholinergic neurons in the cortex []. Under this circumstance where the acetyl choline (ACH) activity in this region is below the normal level, one approach of therapeutic intervention in AD is to minimise the degradation of ACH by its enzyme, ACHE. Even though such drugs have limitation due to their undesirable side effects, an overall beneficial effect in cognitive improvement and behavioural symptoms have been clinically observed []. Szwajgier [] has studied the effect of carnosic acid (7) against ACHE along with 35 other phenolic compounds. Interestingly, CA was identified as the most potent. In silico molecular interaction study approach on AChE inhibitors has also resulted in the identification of (7) as a potential lead drug candidate []. The memory enhancing effect of rosemary extract (200 mg/kg, p.o.) in the scopolamine-induced dementia model of AD has also been shown to be linked with direct effect on ACHE activity []. While the mRNA expression of butyrylcholinesterase (BuChE) in the cortex was inhibited, its expression in the hippocampus was enhanced by rosemary extract []. These effects on the expression of enzymes however could be mediated through indirect effect viaother mechanisms.

4. General Summary and Conclusion

The industrial scale exploitation of rosemary for food preservation and as natural antioxidant additives is attributed to its phenolic constituents. The predominant phenolic compounds that accounts for such effects as well as the various in vitro and in vivo pharmacological properties of the plant are the abietane type of diterpenes. Structurally, these groups of compounds are based on the steroidal-like terpenoid skeleton but have added pharmacophore of a phenolic structure. The rosemary diterpenoids of pharmacological relevance are represented by (7) and (8) where the diorthohydroxyl/catecholic functional group is evident. Through these structural features, these compounds display a vast array of pharmacological effects ranging between antioxidant, metal chelation, and anti-inflammatory properties. These very mechanisms do also appear to be involved in the potential therapeutic effect of the compounds for AD. The further effect of rosemary diterpenes in Aβ formation, aggregation, and toxicity accounts for their additional benefit in tackling AD. Given that AD is a complex disease involving many pathological processes, treatment with multifunctional drugs like those demonstrated by rosemary diterpenes constitutes a viable therapeutic approach. The cascade of neurodegeneration process in AD has lots of similarities with other diseases like Parkinson’s disease. Interestingly, some of the rosemary diterpenes such as carnosic acid (7) have been shown to have beneficial effect in Parkinson’s disease model []. It is also worth noting that only (7) and (8) have been extensively investigated for their possible therapeutic effect related to AD. Other interesting diterpenes including the glycosidic forms could have different bioavailability and therapeutic profile. Further research in this field will therefore provide more evidence on the therapeutic potential of rosemary diterpenes. All the available date to date however suggest that their effect on AD is very promising and further research including clinical trials is well warranted.

The most interesting health benefits of rosemary include its ability to boost memory, improve mood, reduce inflammation, relieve pain, protect the immune system, stimulate circulation, detoxify the body, protect the body from bacterial infections, prevent premature aging, and heal skin conditions.

What Is Rosemary?

Native to the Mediterranean region, rosemary is one of the most commonly found herbs in a spice rack, and for good reason – not only does it have a wonderful taste and aroma, but also a wealth of beneficial health effects if regularly added to our diet. The scientific name of this perennial woody herb is Rosmarinus officinalis. Similar to many other useful herbs, rosemary is in the same taxonomic family as mint, but doesn’t have that characteristic flavor. It has a warmer, bitter, and more astringent taste that gives a wonderful flavor to soups, sauces, stews, roasts, and stuffing. It is particularly prevalent in Italian cultural cuisine.

Although small amounts like those used to flavor food aren’t typically considered large enough to have a major effect on the body, regular addition of the leaves to your food will allow your body to derive accumulated benefits from the organic compounds and unique phytochemicals present in the leaves. There are also usesof rosemary that involves consuming larger quantities or applying the essential oils from rosemary onto the skin directly. Now, let’s take a more detailed look at the health benefits of rosemary.


Health Benefits Of Rosemary

Health benefits of rosemary include:

Memory Booster

One of the earliest documented uses of rosemary for health reasons was as a cognitive stimulant. It was said to improve memory and help to increase intelligence and focus. While many of those claims are still being researched and studied, its effects on the brain do indicate an increase in memory retention. In that same vein, rosemary has been linked to stimulating cognitive activity in the elderly, as well as those suffering from acute cognitive disorders, such as Alzheimer’s or dementia. This is an exciting alternative or supplement to more modern treatment for these yet uncured conditions.

Mood and Stress

The aroma of rosemary alone has been linked to improving mood, clearing mind, and relieving stress in those with chronic anxiety or stress hormone imbalances. When the plant is consumed or applied topically in some sort of salve of the leaves, it can have similar effects. Aromatherapy also uses rosemary essential oil for this purpose, but the concentration of active components may not necessarily have positive effects on stress and mood.

Boosts Immunity

The active components in rosemary are antioxidant, anti-inflammatory, and anti-carcinogenic in nature. This represents a three-pronged attack against many different diseases and pathogens that could threaten the immune system or damage the integrity of the body. Antioxidant compounds make a secondary line of defense behind the body’s own immune system, and rosemary contains a significant amount of those powerful compounds, including rosmarinic acid, caffeic acid, betulic acid, and carnosol.

Antibacterial Potential

While the general immune boosting qualities of rosemary are impressive enough, it is specifically powerful against bacterial infections, particularly those in the stomach. H. pylori bacteria are a dangerous pathogen that can cause stomach ulcers, but rosemary has been shown to prevent its growth when consumed. Similarly, it is linked to preventing staph infections, which kill thousands of people each year.

Stomach Soother

Rosemary has traditionally been used by dozens of cultures as a natural remedy for upset stomachs, constipation, bloating, and diarrhea. Its anti-inflammatory and stimulant effects are largely the cause of these effects, so adding it to your weekly diet can quickly help you regulate your bowel movements and your gastrointestinal system.

Breath Freshener

As a natural antibacterial agent, rosemary works as a wonderful breath freshener that also improves your oral health. Steep rosemary leaves in a glass of hot water and then gargle or swish the water in your mouth to eliminate bacteria, and give you naturally fresh and clean breath all night!

Stimulate Blood Flow

Rosemary acts as a stimulant for the body and boosts the production of red blood cells and blood flow. This helps to oxygenate vital organ systems, ensuring their metabolic activities, in addition to stimulating the movement of nutrients to cells that require repair.

Pain Relief

As an analgesic substance, rosemary has been topically applied in a paste or salve for hundreds of years to the affected area of the pain. When consumed orally, it acts as a pain reliever for harder to reach spots, such as headaches and pain from a condition. In fact, a popular use of rosemary is for the treatment of migraines. Applying a decoction to the temples, or simply smelling the aroma of rosemary has been linked to reducing the severity of migraine symptoms.

Anti-inflammatory Qualities

Perhaps the most important function of rosemary is as an anti-inflammatory agent in the body. Carnosol and Carnosic acid are two powerful antioxidants and anti-inflammatory compounds found in rosemary that have been linked to reducing inflammation of muscles, blood vessels, and joints. This makes it an effective treatment for many things, including blood pressure, goutarthritis, and injuries sustained during physical exertion or surgery. It is effective in oral or topical form for these anti-inflammatory effects. Furthermore, the reduction in inflammation in the cardiovascular system can help to boost heart health and prevent atherosclerosis from appearing.

Detoxifies the Body

Rosemary is slightly diuretic in nature, meaning that it can help flush out toxins efficiently during urination. Furthermore, by increasing the rate at which water leaves the body, it can also help push out pathogens, salts, toxins, and even excess fat when consumed regularly (or when you’re feeling particularly “toxified”). In terms of the particular organ it benefits, it has been linked to lower levels of cirrhosis and a faster healing time of the liver, which is one of the slowest organs to heal.

Skin Health

The anti-aging properties of rosemary are quite well known. Although more commonly thought of in the essential oil form, the leaves of rosemary can also affect the skin internally or topically and have been shown to improve the quality of the skin, while also healing blemishes and increasing the natural shine and hydrated appearance of your body’s largest organ.

Sage is an herb native to the Mediterranean. It belongs to the same family as oregano, lavender, rosemary, thyme, and basil.

Herbs and spices can have extremely high antioxidant capacities and pack extra flavor into a meal. This means that people can use herbs to cut back on sodium intake, as less salt is used to flavor a meal.

The sage plant has gray-green edible leaves and flowers that can range in color from blue and purple to white or pink. There are more than 900 species of sage around the world.

Sage has a long history of medicinal use for ailments ranging from mental disorders to gastrointestinal discomfort. Research has supported some of its medical applications.

This Medical News Today Knowledge Center feature is part of a collection of articles on the health benefits of popular foods. It provides a nutritional profile of sage, an in-depth look at its possible health benefits, ways to incorporate more sage into the diet, and any potential health risks of consuming sage.

Sage essential oil will not be included in this article, as it is not recommended for consumption.

Fast facts on sage

  • Sage is part of the mint family, alongside oregano, lavender, rosemary, thyme, and basil.
  • Over recent years, studies demonstrating the health benefits of sage have grown in number.
  • Sage appears to contain a range of anti-inflammatory and antioxidant compounds.
  • There are more than 900 species of sage.

Possible health benefits

Spoonful of sage
Sage is highly nutritious and flavorsome.

Sage has several proven health benefits.

Sage can help protect the body’s cells from damage caused by free radicals due to its high antioxidant capacity.

Free radicals often cause cells to die and can lead to impaired immunity and chronic disease. Other potential benefits include:

1) Alzheimer’s treatment

recent review of studies showed that species of sage could positively impact cognitive skills and protect against neurological disorders.

The study author maintains that:

In vitro, animal and preliminary human studies have supported the evidence of Salvia plants to enhance cognitive skills and guard against neurodegenerative disorders.”

Other studies have shown that sage can also improve memory in young, healthy adults.

More research is required, as most studies have been carried out on two species of sage, Salvia officinalis (S. officinalis) and S. lavandulaefolia.

2) Lowering blood glucose and cholesterol

Sage can reduce the amount of glucose in the blood.

One study saw 40 people with diabetes and high cholesterol take sage leaf extract for 3 months.

At the end of the trial, the participants had lower fasting glucose, lower average glucose levels over a 3-month period, and lower total cholesterol, triglyceride, and levels of harmful cholesterol. However, the participants had increased levels of HDL or “good” cholesterol.

The researchers concluded:

“[Sage] leaves may be safe and have anti-hyperglycemic and lipid-profile-improving effects in hyperlipidemic type 2 diabetic patients.”

Another double-blind clinical trial was carried out on 80 individuals with poorly controlled type 2 diabetes. The trial also found that sage caused a positive effect on blood sugar levels. After 2 hours of fasting, blood sugar levels in individuals given sage were significantly decreased when compared with the control group.

This study concluded that sage might show benefit for people with diabetes to reduce glucose levels 2 hours after fasting.

3) Controlling inflammation

Although more evidence is needed to confirm this benefit, certain compounds in sage appear to have an anti-inflammatory action. One study investigated the effects of a range of these compounds on the inflammatory response in gingival fibroblasts. These are a common type of cell found in the connective tissue of the gums.

Some of the compounds in sage helped to reduce this type of inflammation.

More recent studies have supported the use of sage in dentistry for its anti-inflammatory properties.

Many other herbs and spices similar to sage also appear to have anti-inflammatory, antifungal, and antimicrobial effects.

The soft, yet sweet savory flavor of sage along with its wonderful health-promoting properties is held in such high esteem that the International Herb Association awarded sage the title of “Herb of the Year” in 2001! Fresh, dried whole or powdered, sage is available throughout the year.

Sage leaves are grayish green in color with a silvery bloom covering. They are lance-shaped and feature prominent veins running throughout. Sage has been held in high regard throughout history both for it culinary and medicinal properties. Its reputation as a panacea is even represented in its scientific name, Salvia officinalis, derived from the Latin word, salvere, which means “to be saved.”

Sage, dried
2.00 tsp
(1.40 grams)
Calories: 4
GI: very low

This chart graphically details the %DV that a serving of Sage provides for each of the nutrients of which it is a good, very good, or excellent source according to our Food Rating System. Additional information about the amount of these nutrients provided by Sage can be found in the Food Rating System Chart. A link that takes you to the In-Depth Nutritional Profile for Sage, featuring information over 80 nutrients, can be found under the Food Rating System Chart.

Health Benefits

Like rosemary, its sister herb in the mint (Labitae) family, sage contains a variety of volatile oils, flavonoids (including apigenindiosmetin, and luteolin), and phenolic acids, including the phenolic acid named after rosemary—rosmarinic acid.

Anti-Oxidant/Anti-Inflammatory Actions

Rosmarinic acid can be readily absorbed from the GI tract, and once inside the body, acts to reduce inflammatory responses by altering the concentrations of inflammatory messaging molecules (like leukotriene B4). The rosmarinic acid in sage and rosemary also functions as an antioxidant. The leaves and stems of the sage plant also contain antioxidant enzymes, including SOD (superoxide dismutase) and peroxidase. When combined, these three components of sage—flavonoids, phenolic acids, and oxygen-handling enzymes—give it a unique capacity for stabilizing oxygen-related metabolism and preventing oxygen-based damage to the cells. Increased intake of sage as a seasoning in food is recommended for persons with inflammatory conditions (like rheumatoid arthritis),as well as bronchial asthma, and atherosclerosis. The ability of sage to protect oils from oxidation has also led some companies to experiment with sage as a natural antioxidant additive to cooking oils that can extend shelf life and help avoid rancidity.

Better Brain Function

Want some sage advice? Boost your wisdom quotient by liberally adding sage to your favorite soups, stews and casserole recipes. Research published in the June 2003 issue of Pharmacological Biochemical Behavior confirms what herbalists have long known: sage is an outstanding memory enhancer. In this placebo-controlled, double-blind, crossover study, two trials were conducted using a total of 45 young adult volunteers. Participants were given either placebo or a standardized essential oil extract of sage in doses ranging from 50 to 150 microls. Cognitive tests were then conducted 1, 2, 4, 5, and 6 hours afterwards. In both trials, even the 50 microl dose of sage significantly improved subjects’ immediate recall.

In other research presented at the British Pharmaceutical Conference in Harrogate (September 15-17, 2003), Professor Peter Houghton from King’s College provided data showing that the dried root of Salvia miltiorrhiza, also known as Danshen or Chinese sage, contains active compounds similar to those developed into modern drugs used to treat Alzheimer’s Disease. Sage has been used in the treatment of cerebrovascular disease for over one thousand years. Four compounds isolated from an extract from the root of Chinese sage were found to be acetylcholinesterase (AChE) inhibitors. The memory loss characteristic of Alzheimer’s disease is accompanied by an increase of AChE activity that leads to its depletion from both cholinergic and noncholinergic neurons of the brain. Amyloid beta-protein (A beta), the major component of amyloid plaques which form in the brain in Alzeeimer’s disease, acts on the expression of AChE, and AChE activity is increased around amyloid plaques. By inhibiting this increase in AChE activity, sage provides a useful therapeutic option to the use of pharmaceutical AChE inhibitors. (October 24, 2003)


You’d be a wise sage to add the herb sage to your recipes. Not only does it have a soft, yet sweet savory flavor, but for millennia, it has also been prized for its health-promoting qualities. Its reputation as a panacea is even represented in its scientific name, Salvia officinalis, derived from the Latin word, salvere, which means “to be saved.”

Sage leaves are grayish green in color with a silvery bloom covering. They are lance-shaped and feature prominent veins running throughout. Sage is available fresh or dried in either whole, rubbed (lightly ground) or powder form.


Sage is native to countries surrounding the Mediterranean Sea and has been consumed in these regions for thousands of years. In medicinal lore, sage has one of the longest histories of use of any medicinal herb.

The Greeks and Romans were said to have highly prized the many healing properties of sage. The Romans treated it as sacred and created a special ceremony for gathering sage. Both civilizations used it as a preservative for meat, a tradition that continued until the beginning of refrigeration. What these cultures knew from experience, that sage could help to reduce spoilage, is now being confirmed by science, which has isolated the herb’s numerous terpene antioxidants.

Sage’s legendary status continued throughout history. Arab physicians in the 10th century believed that it promoted immortality, while 14th century Europeans used it to protect themselves from witchcraft. Sage was in so much demand in China during the 17th century, appreciated for the delicious tea beverage that it makes, that the Chinese are said to have traded three cases of tea leaves (camellia sinensis) to the Dutch for one case of sage leaves.

And the esteem with which sage is regarded has not faded. In 2001, the International Herb Association awarded sage the title of “Herb of the Year.”

Nutritional Profile

Sage contains a variety of volatile oils, flavonoids (including apigenindiosmetin, and luteolin), and phenolic acids, including the phenolic acid named after rosemary—rosmarinic acid. It is also an excellent source of vitamin K and a good source of vitamin A (in the form of provitamin A carotenoid phytonutrients).

Introduction to Food Rating System Chart

In order to better help you identify foods that feature a high concentration of nutrients for the calories they contain, we created a Food Rating System. This system allows us to highlight the foods that are especially rich in particular nutrients. The following chart shows the nutrients for which this food is either an excellent, very good, or good source (below the chart you will find a table that explains these qualifications). If a nutrient is not listed in the chart, it does not necessarily mean that the food doesn’t contain it. It simply means that the nutrient is not provided in a sufficient amount or concentration to meet our rating criteria. (To view this food’s in-depth nutritional profile that includes values for dozens of nutrients – not just the ones rated as excellent, very good, or good – please use the link below the chart.) To read this chart accurately, you’ll need to glance up in the top left corner where you will find the name of the food and the serving size we used to calculate the food’s nutrient composition. This serving size will tell you how much of the food you need to eat to obtain the amount of nutrients found in the chart. Now, returning to the chart itself, you can look next to the nutrient name in order to find the nutrient amount it offers, the percent Daily Value (DV%) that this amount represents, the nutrient density that we calculated for this food and nutrient, and the rating we established in our rating system. For most of our nutrient ratings, we adopted the government standards for food labeling that are found in the U.S. Food and Drug Administration’s “Reference Values for Nutrition Labeling.” Read more background information and details of our rating system.

Sage, dried
2.00 tsp
1.40 grams
Calories: 4
GI: very low
Nutrient Amount DRI/DV
World’s Healthiest
Foods Rating
vitamin K 24.00 mcg 27 108.8 excellent
World’s Healthiest
Foods Rating
excellent DRI/DV>=75% OR
Density>=7.6 AND DRI/DV>=10%
very good DRI/DV>=50% OR
Density>=3.4 AND DRI/DV>=5%
good DRI/DV>=25% OR
Density>=1.5 AND DRI/DV>=2.5%

In-Depth Nutritional Profile

In addition to the nutrients highlighted in our ratings chart, here is an in-depth nutritional profile for Sage. This profile includes information on a full array of nutrients, including carbohydrates, sugar, soluble and insoluble fiber, sodium, vitamins, minerals, fatty acids, amino acids and more.

Sage, dried
(Note: “–” indicates data unavailable)
2.00 tsp
(1.40 g)
GI: very low
nutrient amount DRI/DV
Protein 0.15 g 0
Carbohydrates 0.85 g 0
Fat – total 0.18 g
Dietary Fiber 0.56 g 2
Calories 4.41 0
nutrient amount DRI/DV
Starch — g
Total Sugars 0.02 g
Monosaccharides — g
Fructose — g
Glucose — g
Galactose — g
Disaccharides — g
Lactose — g
Maltose — g
Sucrose — g
Soluble Fiber — g
Insoluble Fiber — g
Other Carbohydrates 0.26 g
Monounsaturated Fat 0.03 g
Polyunsaturated Fat 0.02 g
Saturated Fat 0.10 g
Trans Fat 0.00 g
Calories from Fat 1.61
Calories from Saturated Fat 0.89
Calories from Trans Fat 0.00
Cholesterol 0.00 mg
Water 0.11 g
nutrient amount DRI/DV
Water-Soluble Vitamins
B-Complex Vitamins
Vitamin B1 0.01 mg 1
Vitamin B2 0.00 mg 0
Vitamin B3 0.08 mg 1
Vitamin B3 (Niacin Equivalents) 0.08 mg
Vitamin B6 0.04 mg 2
Vitamin B12 0.00 mcg 0
Biotin — mcg
Choline 0.61 mg 0
Folate 3.84 mcg 1
Folate (DFE) 3.84 mcg
Folate (food) 3.84 mcg
Pantothenic Acid — mg
Vitamin C 0.45 mg 1
Fat-Soluble Vitamins
Vitamin A (Retinoids and Carotenoids)
Vitamin A International Units (IU) 82.60 IU
Vitamin A mcg Retinol Activity Equivalents (RAE) 4.13 mcg (RAE) 0
Vitamin A mcg Retinol Equivalents (RE) 8.26 mcg (RE)
Retinol mcg Retinol Equivalents (RE) 0.00 mcg (RE)
Carotenoid mcg Retinol Equivalents (RE) 8.26 mcg (RE)
Alpha-Carotene 0.00 mcg
Beta-Carotene 48.79 mcg
Beta-Carotene Equivalents 49.55 mcg
Cryptoxanthin 1.53 mcg
Lutein and Zeaxanthin 26.53 mcg
Lycopene 0.00 mcg
Vitamin D
Vitamin D International Units (IU) 0.00 IU 0
Vitamin D mcg 0.00 mcg
Vitamin E
Vitamin E mg Alpha-Tocopherol Equivalents (ATE) 0.10 mg (ATE) 1
Vitamin E International Units (IU) 0.16 IU
Vitamin E mg 0.10 mg
Vitamin K 24.00 mcg 27
nutrient amount DRI/DV
Boron — mcg
Calcium 23.13 mg 2
Chloride — mg
Chromium — mcg
Copper 0.01 mg 1
Fluoride — mg
Iodine — mcg
Iron 0.39 mg 2
Magnesium 5.99 mg 1
Manganese 0.04 mg 2
Molybdenum — mcg
Phosphorus 1.27 mg 0
Potassium 14.98 mg 0
Selenium 0.05 mcg 0
Sodium 0.15 mg 0
Zinc 0.07 mg 1
nutrient amount DRI/DV
Omega-3 Fatty Acids 0.02 g 1
Omega-6 Fatty Acids 0.01 g
Monounsaturated Fats
14:1 Myristoleic 0.00 g
15:1 Pentadecenoic 0.00 g
16:1 Palmitol 0.00 g
17:1 Heptadecenoic 0.00 g
18:1 Oleic 0.02 g
20:1 Eicosenoic 0.00 g
22:1 Erucic 0.00 g
24:1 Nervonic 0.00 g
Polyunsaturated Fatty Acids
18:2 Linoleic 0.01 g
18:2 Conjugated Linoleic (CLA) — g
18:3 Linolenic 0.02 g
18:4 Stearidonic 0.00 g
20:3 Eicosatrienoic 0.00 g
20:4 Arachidonic 0.00 g
20:5 Eicosapentaenoic (EPA) 0.00 g
22:5 Docosapentaenoic (DPA) 0.00 g
22:6 Docosahexaenoic (DHA) 0.00 g
Saturated Fatty Acids
4:0 Butyric — g
6:0 Caproic — g
8:0 Caprylic 0.01 g
10:0 Capric 0.01 g
12:0 Lauric 0.00 g
14:0 Myristic 0.01 g
15:0 Pentadecanoic — g
16:0 Palmitic 0.04 g
17:0 Margaric — g
18:0 Stearic 0.02 g
20:0 Arachidic — g
22:0 Behenate — g
24:0 Lignoceric — g
nutrient amount DRI/DV
Alanine — g
Arginine — g
Aspartic Acid — g
Cysteine — g
Glutamic Acid — g
Glycine — g
Histidine — g
Isoleucine — g
Leucine — g
Lysine — g
Methionine — g
Phenylalanine — g
Proline — g
Serine — g
Threonine — g
Tryptophan — g
Tyrosine — g
Valine — g
nutrient amount DRI/DV
Ash 0.11 g
Organic Acids (Total) — g
Acetic Acid — g
Citric Acid — g
Lactic Acid — g
Malic Acid — g
Taurine — g
Sugar Alcohols (Total) — g
Glycerol — g
Inositol — g
Mannitol — g
Sorbitol — g
Xylitol — g
Artificial Sweeteners (Total) — mg
Aspartame — mg
Saccharin — mg
Alcohol 0.00 g
Caffeine 0.00 mg


The nutrient profiles provided in this website are derived from The Food Processor, Version 10.12.0, ESHA Research, Salem, Oregon, USA. Among the 50,000+ food items in the master database and 163 nutritional components per item, specific nutrient values were frequently missing from any particular food item. We chose the designation “–” to represent those nutrients for which no value was included in this version of the database.

Zinc Supplementation on Trial: What does the Research Say?

By Neel Duggal Apr 02, 2015

Manufacturers of zinc supplements such as ZMA claim that consuming their products will boost your testosterone, strengthen your immunity, and improve your athletic performance. But are these lofty claims backed up by credible research? And is there really a need for athletes and the general population to consume these supplements? Read below to find out why you need to regularly monitor your zinc status and if regularly taking zinc supplements can enhance your health and athletic performance.


Why Do You Need Zinc?

Zinc is required for many biological processes such as cellular growth, maintenance of the nervous system, and immunity [1]. At a molecular level, zinc is involved in processes supporting life such as cellular respiration, DNA reproduction, preservation of cell membranes, and elimination of substances called radicals which contribute to aging [1]. Because of its incredible variety of functions in your body, zinc is required for the activity of over 300 enzymes [2]. Zinc is found in all tissues and fluids and the total zinc content in the human body is estimated to be 2 g [3]. Zinc is also an essential micronutrient.  This means that it cannot be produced by the body itself and can only be acquired through foods or dietary supplements [4]. It is naturally found in protein-rich foods such as meat, shellfish, wholegrains, and legumes (Fun Fact: Oysters are known to have the highest zinc content!).

Un-optimized levels of zinc can wreak havoc in your body. Zinc deficiency can lead to conditions associated with fatigue such as lethargy and anorexia [5]. It can also impair immune function and increase susceptibility to infection, harm kidney function, and hamper tissue growth [6]. Similarly, excess levels of zinc resulting from consuming high dose supplements and too many zinc-heavy foods can result in kidney problems, impair cardiac function, and inhibit digestive enzymes such as lipase (fat-digesting) and amylase (starch-digesting) [5]. Overall, zinc-deficiency is much more common than zinc excess [6].

Getting your zinc levels tested using services such as InsideTracker can determine if your levels of zinc are optimized based on your internal biochemistry and lifestyle factors. But are you at risk for zinc deficiency?

Key Takeaways: Regularly monitoring for adequate levels of zinc is crucial for maintaining proper bodily function

Zinc Deficiency: How Common is it and who is at Risk?

Some researchers claim that 2 billion people- or about 30% of the world’s population- is zinc-deficient [1]. In the US, approximately 12 percent of people do not consume enough zinc in their diets [1]. This isn’t as common compared to other nutrient deficiencies we see at InsideTracker, such as vitamin D, that we observe in over 70% of our clinical population. That being said, certain populations are more likely to suffer than others from zinc deficiency. Older adults tend to eat fewer zinc-rich foods and their bodies no longer use or absorb zinc optimally, making them highly susceptible to zinc deficiency. In fact, of those 65 and older, the literature states that approximately 40 percent consume insufficient zinc [1].

We most commonly observe zinc deficiencies in two other populations: athletes and vegetarians. The nutritional habits of elite athletes, which comprise a little over 10% of our clinical population, are quite different from the recommended diet for the average American. Endurance athletes in particular, such as swimmers and runners, often increase carbohydrates and lower intake of proteins and fat. According to literature, this change may lead to suboptimal zinc intake in up to 90% of athletes [7]. Mild zinc deficiency using your standard physician’s blood test is difficult to detect because of the lack of personalization in these assessments. However, in athletes, zinc deficiency can lead to significant loss of bodyweightfatigue with decreased endurance, and an increased risk of osteoporosis [7]. All of this, of course, leads to deterioration of athletic performance and general health.

Because many zinc-rich foods are animal-based, zinc deficiency is more commonly observed in vegetarians and vegans. A recent meta-analysis of 26 studies comparing males and females consuming vegetarian diets with non-vegetarian groups revealed that vegetarian populations, on average, have 8-12% lower serum zinc concentrations [8]. This deficiency is even more pronounced in female vegetarians, vegetarians from developing countries, and vegans [8].

As one would expect, vegetarian athletes (especially those over the age of 65!) are most at risk for zinc deficiency. However, can zinc supplementation actually improve quality of health and boost athletic performance?

Key Takeaways: Zinc deficiency is a common problem among Americans. Vegetarians, elderly, and athletes are more likely than average to suffer from zinc deficiency due to specialized diets. 

Zinc Supplementation to Treat Deficiency: Does it make a Difference?



Provided the issues vegetarians encounter with zinc, the researchers of the meta-analysis study concluded that:

“Dietary practices that increase zinc bioavailability, the consumption of foods fortified with zinc or low-dose supplementation are strategies that should be considered for improving the zinc status of vegetarians with low zinc intakes or serum zinc concentrations at the lower end of the reference range” [8].

For vegans specifically, another group of researchers stated that “unless vegans regularly consume foods that are fortified with these nutrients, appropriate supplements should be consumed” [9]. It is important to note that there have been no intervention studies assessing the impact of supplementation on zinc-deficient vegetarians. Additionally, not all vegetarians are zinc-deficient; you can only prove that by getting a proper blood test.

Zinc supplements may be particularly helpful in counteracting aging for elderly individuals who are already deficient in zinc. In 2014, researchers recruited 84 elderly volunteers for a 12 week placebo-controlled intervention trial with 42 subjects in the placebo group and 42 subjects in the zinc-supplement intervention group. At the study’s conclusion, plasma Zn was increased by 5.69% in the Zn supplemented group [10]. Researchers also observed significant improvements in key aging indicators in this group including a decrease in micronucleus frequency and reduced telomere damage. Because of these findings, the authors concluded that “Zn supplementation may have a beneficial effect in an elderly population with low Zn levels by improving Zn status, antioxidant profile and lowering DNA damage” [10].

Because zinc is involved in cellular processes related to diabetes- a condition which commonly affects older adults – researchers have recently begun to assess if zinc supplements can help treat symptoms of diabetes. In one study, providing type 2 diabetics with a low dose supplement of 30 mg/day of zinc for six months reduced a common measure of aging without affecting blood glucose [11]. In contrast, a placebo-controlled study in 40 men with type 2 diabetes and normal levels of zinc found that high-dose zinc supplementation (240 mg/day) for three months did not improve measures of aging or vascular function [12]. Given these findings, a low dose supplementation of zinc might be useful in reducing aging-related effects of diseases such as diabetes in zinc-deficient populations. However, more research needs to be done to confirm this.

Key Takeaways: Low dose zinc supplements are useful for populations that suffer from zinc deficiency such as vegetarians and the elderly. However, the benefits of supplementation are not fully understood in treating symptoms of aging-related diseases such as Type II diabetes.

The Other Side of the Zinc Coin: Zinc Excess 


The last time I got my InsideTracker test, I was surprised to see that my zinc levels were no longer in the optimal zone. Instead, they had elevated to the middle of the clinically acceptable range- putting me well above my optimal zone. While clinical zinc deficiency is more common than clinical zinc excess, we observe zinc levels at the high end of the clinically accepted zone in almost 50 % of our clinical population. So, what does the research say about zinc excess?

Research supports the notion that excessive zinc supplementation is known to have adverse effects on the digestive and urinary systems. In a long-term, randomized trial of 3,640 patients over 6 years, researchers experimented with four different treatments: two that included 80 mg zinc supplements and two that didn’t. After analyzing the data, researchers found a significant increase in hospital admissions due to genitourinary causes in the patients who consumed the zinc supplement vs. the ones who did not (11.1% vs 7.6%) [13]. This was even more pronounced in males. When comparing the subjects who took zinc compared to the ones who didn’t, researchers noticed significant increases in urinary tract infections especially in females (2.3% vs 0.4%) [13]. Thus, researchers concluded “these data support the hypothesis that high dose zinc supplementation has a negative effect on select aspects of urinary physiology” [13].

An older but credible study from the Journal of American Medical Association showed that excess zinc supplementation resulted in lower levels of HDL cholesterol– the form of cholesterol that lowers arterial clogging. In their study, twelve healthy adult men ingested an equivalent of 160 mg of zinc per day for five weeks. At the end of the intervention, high-density lipoprotein-cholesterolconcentration decreased 25% below baseline values (40.5 to 30.1 mg/dL) [14]. The authors concluded that “zinc [supplementation] may be atherogenic in men”, meaning that it increases your chance of developing cardiovascular disease [14]. This study was supported by a similar but more precise study in women. In it, researchers provided 32 women for 8 weeks with either a placebo, 15 mg supplement of zinc, 50 mg supplement of zinc, or 100 mg supplement each day. At the end of the study, researchers observed no significant differences in HDL cholesterol levels except in the 100 mg supplement group which experienced an 8.7% decrease in HDL levels [15].

Key Takeaways: Because many people commonly fall under the clinically acceptable range of zinc levels, regularly taking high dose zinc supplements (>50 mg) can harm the health of your urinary, digestive, and cardiovascular systems.

ZMA Supplementation for Athletes: Does it Work?



Of all zinc-related supplements, manufacturers of ZMA have made the boldest claims about its product enhancing your health and athletic performance. ZMA is a natural mineral supplement that contains zinc along with magnesium aspartate (which increases your body’s magnesium) and vitamin B6. According to the company which produces ZMA, daily consumption of ZMA can increase your immunity and metabolism (because of Zinc), optimize your testosterone (because of magnesium), and boost energy for athletic performance (because of B6). Its manufacturers even claim that ZMA can benefit health and fitness even in people who already have adequate levels of zinc- meaning that one need not have zinc deficiency to obtain its proclaimed benefits.

But are these bold claims supported by research? In a 2000 sport science study, researchers provided ZMA supplements to a group of 12 NCAA football players practicing twice a day for 7 weeks and compared them to a placebo group of 15 NCAA football players. At the conclusion of the intervention, they found a significant increase in the players’ levels of testosterone and growth hormone compared to the placebo group [16]. Despite these promising findings, the study was funded by the company that creates ZMA and one of the researchers who conducted the study helped patent the supplement’s formula. This means that its results, while promising, aren’t credible due to financial interest and personal bias. Another studies often cited by ZMA supporters were also funded by private interest groups and used poor methodologies [17].

The only third-party research study assessing ZMA does not support the notion that it benefits athletic performance or weight loss in populations that already have optimized levels of zinc. In 2006, scientists recruited fourteen healthy, regularly exercising men aged 22–33 years with clinically healthy levels of zinc. According to their group assignment, all subjects ingested either three capsules per day of ZMA or placebo for 56 days. At the conclusion of the study’s period, researchers only observed increased levels of zinc in the urine of the population that consumed ZMA- indicating that it may have induced toxicity in the body. As a result, they concluded that “the present data suggest that the use of ZMA has no significant effects regarding serum testosterone levels and the metabolism of testosterone in subjects who consume a zinc-sufficient diet” [18].

Key Takeaways: There are no proven benefits of ZMA on athletes with adequate zinc and magnesium. In fact, consuming it might be harmful. 

The Verdict on ZMA

Because of the inconclusive research on ZMA, InsideTracker does not recommend consuming ZMA if you already have optimized levels of zinc or magnesium or if you are unaware of your levels of these minerals. That being said, if your InsideTracker results show deficiencies in both zinc and magnesium, we recommend that you consume ZMA. Magnesium deficiency is even more common than zinc deficiency and affects an estimated 50% of Americans [19]. Additionally, there is compelling research to suggest that correcting deficiencies in both of these nutrients can help optimize other biomarkers including testosteronec-Reactive Protein, and white blood cell count. Again, it is important to regularly monitor your zinc (and magnesium) levels in order to make sure that you avoid the negative effects of zinc toxicity we mentioned above and look at your other health and biomarker data.