Endothelins are peptides that constrict blood vessels, plant sources prevent hypertesion

Endothelins are the most potent vasoconstrictors known

In a healthy individual, a delicate balance between vasoconstriction and vasodilation is maintained by endothelin and other vasoconstrictors on the one hand and nitric oxide, prostacyclin and other vasodilators on the other.

Overproduction of endothelin in the lungs may cause pulmonary hypertension, which can sometimes be treated by the use of an endothelin receptor antagonist, such as bosentansitaxentan or ambrisentan. The latter drug selectively blocks endothelin A receptors, decreasing the vasoconstrictive actions and allowing for increased beneficial effects of endothelin B stimulation, such as nitric oxide production. The precise effects of endothelin B receptor activation depends on the type of cells involved.

Disease involvement

The ubiquitous distribution of endothelin peptides and receptors implicates its involvement in a wide variety of physiological and pathological processes in the body. Among numerous diseases potentially occurring from endothelin dysregulation are

In insulin resistance the high levels of blood insulin results in increased production and activity of ET-1, which promotes vasoconstriction and elevates blood pressure.[9]ET-1 impairs glucose uptake in the skeletal muscles of insulin resistant subjects, thereby worsening insulin resistance.[

Production of Antihypertensive Peptides from food sources

Antihypertensive peptides have been mainly produced from dairy products such as milk, cheese, etc. However, production from food sources other than dairy has also been carried out recently. These peptides can be produced by one or a combination of following methods [11]:

  1. Enzymatic hydrolysis
  2. Fermentation of protein based food sources
  3. Genetic recombination in bacteria

Enzymatic hydrolysis by digestive enzymes: According to literature the most common way of producing antihypertensive peptides from food proteins is enzymatic hydrolysis. Many of the Angiotensin Converting Enzyme (ACE) inhibitory peptides have been produced using gastrointestinal enzymes, usually pepsin and trypsin [12,13]. Enzymes from plant (e.g. Papain) and animal sources (e.g., pepsin and trypsin), have also been used in producing antihypertensive peptides [14].

A variety of food sources, antihypertensive peptides have been produced using enzymatic hydrolysis. Different enzymes have been used to digest milk proteins to yield antihypertensive peptides. The first study has been conducted in 2004 which yielded lactokin in Ala-Leu-Pro-Met-His-Ile-Arg (ALPMHIR) as ace inhibitory peptides [15]. The latest study on lactoferr in hydrolyzates (LFHs) generated by trypsin and proteinase K yield different antihypertensive peptides which acts on rennin-angiotensin system (RAS) and the endothelin (ET) system [16].

Black-bone silky fowl (Gallus gallus domesticus Brisson) muscle has been treated by multistage separation. The black-bone silky fowl muscle peptides (BSFP) was hydrolyzed with Alcalase and papain has been tested for ACE in hibitiory activities. From a total of 29 peptides two novel potent ACE inhibitory peptides Leu-Glu-Arg and Gly-Ala-Gly- have been found [17]. Hen eggs provide biological functions beyond basic nutrition. In a study, the antihypertensive effect of peptide RVPSL from egg protein decreased the blood pressure of SHRs in 4 weeks. The peptide influenced the expression of major RAS components by down-regulating the renin, ACE, Ang II, and AT1 receptor while upregulating the AT2 receptor in SHRs [18]. In an another study a tri-peptide IRW (Ile-Arg-Trp) from egg white protein ovotransferrin; demonstrated anti-hypertensive effects of IRW in vivo which is mediated through ACE inhibition and endothelial nitric oxide synthase [19]. ACE inhibitory peptides have also been isolated from fish sources. Suetsuna & Osajima [20] identified first ACE inhibitory peptide in sardine over thirty years ago. Since then many other peptides have been isolated from various fish species, including shellfish, tuna, bonito, salmon, etc. [21].

Amongst plant sources, Met-Arg-Trp (MRW) isolated from the pepsin-pancreatin digest of spinach lowers blood pressure via prostaglandin D(2)-dependent vasorelaxation in SHRs [22].

Pea protein isolate, hydrolyzed with alcalase, have proven inhibitory against ACE, renin, and calmodulin-dependent phosphodiesterase 1 (CaMPDE) [23].

Four peptides of sequence: ITP IIP GQY STYQT have been isolated by protease enzyme digestion of sweet potato protein. ITP peptide was found to be the most potent ACE inhibitor as concluded by in vivo study on rats [24].

Edible mushrooms have also yielded ACE inhibitory oligo peptides.

One such peptide with the sequence LSMGSASLSP was isolated in water extracts of mushroom Hypsizygus marmoreus (brown cultivar). The extract from its fruiting body was purified and proven to have antihypertensive action on SHRs [25]. In an another study, two new ACE in hibitiory peptides from the fruiting body of Pleurotus cornucopiae were purified. Their sequences were determined to be RLPSEFDLSAFLRA and RLSGQTIEVTSEYLFRH with the molecular mass of 1622.85 and 2037.26Da, respectively [26]. In vivo study on SHRs validated the antihypertensive activity of both the peptides.

Macro-algae have been part of the staple diet in east Asia for centuries and has wide applications in food and pharmaceutical industries. Papain hydrolysates of the crude Palmaria palmata protein release renin inhibitory peptide of the sequence: IRLIIVLMPILMA. The bioactivity of this peptide was confirmed by renin inhibitory assay [27].

Amongst cereals Wheat gliadin hydrolysates can act as ACE inhibitors. The peptide Ile-Ala-Pro prepared with acid protease decreased the blood pressure in SHRs significantly with intra-peritoneal administration [28]. Arginine-rich peptides from Flaxseed protein isolate (FPI) obtained by enzymatic hydrolysis with trypsin and pronase were observed to produce in vivo vasodilatory effects. The in vivo study on SHRs suggested that the rate of peptide absorption is rapid as compared to amino acids and thus it provides a fast relief from hypertension [29]. Rapeseed protein isolate (RPI) digested with proteinase, thermolysin, flavourzyme and pepsin produced rapeseed protein hydrolyzates which can be separated into different anti hypertensive peptides [30].

At large scale the serine type protease Alcalase is most widely used endo-protease in digests of various plant proteins such as rapeseed, canola, sunflower seed protein, soy protein legumes, rice as well as mung and chick beans showing high potency for ACE inhibition [31].

Antihypertensive peptides produced by fermentation: Many industrially utilized dairy starter cultures are highly proteolytic in nature and can be used for production of antihypertensive peptides by fermentation of dairy products. The proteolytic system of lactic acid bacteria (LAB) such as Lactococcus lactis, Lactobacillus helveticus and L. delbrueckii ssp. Bulgaricus consists of a cell wall-bound proteinase and a number of intracellular peptidases, including endo peptidases, amino peptidases, tri peptidases and dipeptidases [32]. Based on these peptidases, a number of commercial products have been synthesized for clinical trials for efficacy testing using different hypertensive subjects.

Many dietary proteins, especially milk proteins, contain physiologically active peptides encoded in the protein sequence. These peptides may be released during gastrointestinal digestion or food processing and once liberated, cause different physiological functions. Milk-derived bioactive peptides are shown to have antihypertensive, antimicrobial, immune modulatory, anti oxidative and mineral-binding properties [33]. Thus fermentation can yield peptides that are ACE-inhibitory and thus blood pressure–lowering, to be derived from milk proteins. Some of these peptides have also been found to have opioid receptor binding properties [34,35].

A fermented milk product with the biologically active peptides valyl-prolyl-proline (Val-Pro-Pro) and isoleucyl-prolyl-proline (Ile-Pro-Pro) was shown to lower blood pressure in spontaneously hypertensive rats [36]. It was suggested that small peptides are absorbed from the gastrointestinal tract without being degraded further by digestive enzymes [37]. Two other peptides (Tyr-Pro and Lys-Val-Leu-Pro-Val-Pro-Gln) that were purified and characterized from fermented milk were also shown to have ACE-inhibitory activity in SHRs [38,39]. Nurminen et al. [40] found that alpha-lactorphin (Tyr-Gly-Leu-Phe) also reduced blood pressure in normotensive and SHRs.

Seppo et al. [41] reported that fermented milk product named Evolus or Kaiku Vitabrand, lowered the blood pressure in hypertensive human volunteers in 8 weeks by -14.9mm.

Another controlled trial in hypertensive men lowered the systolic blood pressure in two weeks by -4.3mm Hg and -5.2mm Hg in 4 weeks [42]. A study on casein hydrolysate (Ameal Peptide) lowered the blood pressure by -6.3mm Hg in 6 weeks [43].

The whey from milk fermented by LAB, Streptococcus thermophilus and Lactobacillus bulgaricus along with protease treatment was fractionated into four fractions by size exclusion chromatography on a Sephadex G-15 column. The fourth fraction showed the highest inhibitory efficiency ratio (IER) and contains the inhibitory peptide Tyr-Pro-Tyr-Tyr, of which the IC50 was 90.9 lM. The systolic blood pressure (SBP) and diastolic blood pressure (DBP) was reduced by 15.9 and 15.6 mm Hg, respectively, in spontaneously hypertensive rat (SHR), after 8 weeks of oral administration of diluted whey (peptide concentration 4.9 mg/ml). Tri peptides IPP and VPP released from casein inhibit ACE and reduce arterial stiffness in humans at micro molar concentrations produced during the fermentation of milk with lactobacilli [33].

Several novel antihypertensive peptides have been reported in milk fermented with Enterococcus faecalis CECT 5727. Two of the identified peptides LHLPLP and LVYPFPGPIPNSLPQNIPP, showed angiotensin converting enzyme-inhibitory (ACEI) activity with IC50 values as low as 5mM and showed antihypertensive activity in hypertensive rats. In particular, b-casein f (133–138), yielded a significant antihypertensive effect in these animals [44].

A total of 75 peptides included in the fraction with molecular mass below 3000 from an 8-month-old Manchego cheese could be identified using HPLC coupled on line to an ion trap mass spectrometer. Some previously described peptides with antihypertensive and/or angiotensin-converting enzyme (ACE)-inhibitory activity were detected. The formation of five active sequences was followed during cheese ripening in four different batches of Manchego cheese. Two experimental batches of Manchego cheese elaborated with selected bacterial strains with the aim of improve the organoleptic characteristics demonstrated also a good performance in the formation of peptides with ACE-inhibitory activity during cheese ripening [45].

Over the past decade, there has been a growing interest in the use of food sources other than dairy, for production of bioactive peptides with antihypertensive activity. Cereal based fermented products contain peptides which have a BP lowering effect [46]. Studies have shown that common foods from animal and plant origin are important sources of bioactive peptides.

Plant sources usually include cereals (wheat, barley, corn, rice) pseudocereals (buckwheat and amaranth), legumes (soybean, bean, pea), brassica species and others (sunflower).

The presence of bioactive peptides in cereals and legumes can contribute to increase their food protein quality value and add “functionality” to fermented functional foods consumed on a daily basis [47].

Soy protein foods are fast category products in the food industry with demand for soy ingredients with improved processing characteristics. Fermented soy products, traditionally consumed in Eastern countries, have been also found to be an important source of ACE inhibitory and antihypertensive peptides [48-50].

A potent antihypertensive peptide has been identified and characterized in a Korean soy product denominated “chunggugjang” and obtained by soy fermentation with Bacillus subtilis CH-1023 [51]. Other ACE-inhibitory and antihypertensive peptides have been identified in soy paste [52], soy sauce [53,54], natto and tempeh [55], and other fermented soy products [56-58].

Miso paste is a Japanese traditional fermented food, prepared from soy beans mixed with rice fermented with Aspergillus oryzae (rice koji).

Since A. oryzae protease based casein hydrolysate results in production of two antihypertensive peptides, Val-Pro-Pro and Ile-Pro-Pro, Casein was added to miso paste during miso paste fermentation in order to release angiotensin-I converting enzyme (ACE) inhibitory peptides. Casien miso paste had a higher ACE inhibitory activity as compared to casein-free miso paste after 7 days of fermentation. Further, a significant antihypertensive activity of casein miso paste was observed in spontaneously hypertensive rats compared to water and the general miso paste at a dosage of 1.8 g of the casein miso paste/kg of BW [59].

The two ACE inhibitory peptide fractions F2 and F3 were isolated after fermentation of soy protein with Lactobacillus casei spp. pseudoplantarum.

The peptide analogues of LIVTQ were synthesized based on N-terminal sequence of peptide (F2) Leu-Ile-Val-Thr-Gln (LIVTQ) and effect of individual residues on ACE enzyme were studied. The study determined the importance of glutamine (Q) and threonine (T) residues in ACE inhibition [60].

Genetic recombination in bacteria: Apart from the above methods for the production of peptides recombinant DNA techniques have also been explored. As compared to the enzymatic method, the advantages of microbiological genetic engineering techniques to prepare AHP include higher peptide yield and lower cost [61]. The first study involved expression of recombinant human alpha 1-casein in Escherichia coli and its purification [62].

Another antihypertensive peptide multimer (AHPM) was designed and cloned in an expression vector in E. coli. The release of high active fragments was confirmed by the simulated gastrointestinal digestion from the AHPM [63]. Antihypertensive peptides with sequences HHL, HVLPVP, FFVAPFPEVFGK, and GHIATFQER have been expressed successfully in E .coli [64]. Peptides expressed in Escherichia coli by a high throughput recombinant expression system have been designed and used widely, though other bacterial system could be used for the production of peptides at similar yields [65].

http://medcraveonline.com/MOJFPT/MOJFPT-02-00024.php

Pubmed: Dietary modification may affect inflammatory processes

carotenoidI recommend eating colored fruits and vegetables. There are dietary supplements that have anti-aging properties as they contain carotenoid. Below are Pubmed information about inflammation and dietary modifications (foods/supplements rich in carotenoids, tocopherols, anti-oxidants).

For products to help reduce inflammation, go to:

http://clubalthea.pxproducts.com/products-2

Email motherhealth@gmail.com to personalize supplementation based on your health.

Connie Dello Buono

Br J Nutr. 2014 Oct;112(8):1341-52. doi: 10.1017/S0007114514001962.

Patterns of dietary intake and serum carotenoid and tocopherol status are associated with biomarkers of chronic low-grade systemic inflammation and cardiovascular risk.

Wood AD1, Strachan AA1, Thies F1, Aucott LS1, Reid DM1, Hardcastle AC2, Mavroeidi A3, Simpson WG1, Duthie GG4, Macdonald HM1.

Author information

 Abstract

Dietary modification may affect inflammatory processes and protect against chronic disease. In the present study, we examined the relationship between dietary patterns, circulating carotenoid and tocopherol concentrations, and biomarkers of chronic low-grade systemic inflammation in a 10-year longitudinal study of Scottish postmenopausal women. Diet was assessed by FFQ during 1997-2000 (n 3237, mean age 54·8 (sd 2·2) years). Participants (n 2130, mean age 66·0 (sd 2·2) years) returned during 2007-11 for follow-up. Diet was assessed by FFQ (n 1682) and blood was collected for the analysis of serum high-sensitivity C-reactive protein (hs-CRP), IL-6, serum amyloid A, E-selectin, lipid profile and dietary biomarkers (carotenoids, tocopherols and retinol). Dietary pattern and dietary biomarker (serum carotenoid) components were generated by principal components analysis. A past ‘prudent’ dietary pattern predicted serum concentrations of hs-CRP and IL-6 (which decreased across the quintiles of the dietary pattern; P= 0·002 and P= 0·001, respectively; ANCOVA). Contemporary dietary patterns were also associated with inflammatory biomarkers. The concentrations of hs-CRP and IL-6 decreased across the quintiles of the ‘prudent’ dietary pattern (P= 0·030 and P= 0·006, respectively). hs-CRP concentration increased across the quintiles of a ‘meat-dominated’ dietary pattern (P= 0·001). Inflammatory biomarker concentrations decreased markedly across the quintiles of carotenoid component score (P< 0·001 for hs-CRP and IL-6, and P= 0·016 for E-selectin; ANCOVA). Prudent dietary pattern and carotenoid component scores were negatively associated with serum hs-CRP concentration (unstandardised β for prudent component: – 0·053, 95 % CI – 0·102, – 0·003; carotenoid component: – 0·183, 95 % CI – 0·233, – 0·134) independent of study covariates. A prudent dietary pattern (which reflects a diet high in the intakes of fish, yogurt, pulses, rice, pasta and wine, in addition to fruit and vegetable consumption) and a serum carotenoid profile characteristic of a fruit and vegetable-rich diet are associated with lower concentrations of intermediary markers that are indicative of CVD risk reduction.

PMID: 25313576 [PubMed – in process]

 J Nutr Biochem. 2014 Sep 16. pii: S0955-2863(14)00168-5. doi: 10.1016/j.jnutbio.2014.07.004. [Epub ahead of print]

Preventive supplementation with fresh and preserved peach attenuates CCl4-induced oxidative stress, inflammation and tissue damage.

Gasparotto J1, Somensi N2, Bortolin RC2, Girardi CS2, Kunzler A2, Rabelo TK2, Schnorr CE2, Moresco KS2, Bassani VL3, Yatsu FK3, Vizzotto M4, Raseira MD4, Zanotto-Filho A2, Moreira JC2, Gelain DP2.

Author information

 Abstract

The present study was elaborated to comparatively evaluate the preventive effect of different peach-derived products obtained from preserved fruits (Syrup and Preserve Pulp Peach [PPP]) and from fresh peels and pulps (Peel and Fresh Pulp Peach [FPP]) in a model of liver/renal toxicity and inflammation induced by carbon tetrachloride (CCl4) in rats. Tissue damage (carbonyl, thiobarbituric acid reactive species and sulfhydril), antioxidant enzymes activity (catalase and superoxide dismutase) and inflammatory parameters [tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels, and receptor for advanced glycation end-products (RAGE) and nuclear factor (NF)κB-p65 immunocontent] were investigated. Our findings demonstrated that Peel, PPP and FPP (200 or 400 mg/kg) daily administration by oral gavage for 30 days conferred a significant protection against CCl4-induced antioxidant enzymes activation and, most importantly, oxidative damage to lipids and proteins as well as blocked induction of inflammatory mediators such as TNF-α, IL-1β, RAGE and NFκB. This antioxidant/anti-inflammatory effect seems to be associated with the abundance of carotenoids and polyphenols present in peach-derived products, which are enriched in fresh-fruit-derived preparations (Peel and FPP) but are also present in PPP. The Syrup – which was the least enriched in antioxidants – displayed no protective effect in our experiments. These effects cumulated in decreased levels of transaminases and lactate dehydrogenase leakage into serum and maintenance of organ architecture. Therefore, the herein presented results show evidence that supplementation with peach products may be protective against organ damage caused by oxidative stress, being interesting candidates for production of antioxidant-enriched functional foods.

Copyright © 2014. Published by Elsevier Inc.

Nutr Res. 2014 Jul 18. pii: S0271-5317(14)00117-1. doi: 10.1016/j.nutres.2014.07.010. [Epub ahead of print]

Carotenoids, inflammation, and oxidative stress-implications of cellular signaling pathways and relation to chronic disease prevention.

Kaulmann A1, Bohn T2.

Author information

 Abstract

Several epidemiologic studies have shown that diets rich in fruits and vegetables reduce the risk of developing several chronic diseases, such as type 2 diabetes, atherosclerosis, and cancer. These diseases are linked with systemic, low-grade chronic inflammation. Although controversy persists on the bioactive ingredients, several secondary plant metabolites have been associated with these beneficial health effects. Carotenoids represent the most abundant lipid-soluble phytochemicals, and in vitro and in vivo studies have suggested that they have antioxidant, antiapoptotic, and anti-inflammatory properties. Recently, many of these properties have been linked to the effect of carotenoids on intracellular signaling cascades, thereby influencing gene expression and protein translation. By blocking the translocation of nuclear factor κB to the nucleus, carotenoids are able to interact with the nuclear factor κB pathway and thus inhibit the downstream production of inflammatory cytokines, such as interleukin-8 or prostaglandin E2. Carotenoids can also block oxidative stress by interacting with the nuclear factor erythroid 2-related factor 2 pathway, enhancing its translocation into the nucleus, and activating phase II enzymes and antioxidants, such as glutathione-S-transferases. In this review, which is organized into in vitro, animal, and human investigations, we summarized current knowledge on carotenoids and metabolites with respect to their ability to modulate inflammatory and oxidative stress pathways and discuss potential dose-health relations. Although many pathways involved in the bioactivity of carotenoids have been revealed, future research should be directed toward dose-response relations of carotenoids, their metabolites, and their effect on transcription factors and metabolism.

J Neuroinflammation. 2014 Jul 1;11:117. doi: 10.1186/1742-2094-11-117.

Cerebrospinal fluid levels of inflammation, oxidative stress and NAD+ are linked to differences in plasma carotenoid concentrations.

Guest J, Grant R1, Garg M, Mori TA, Croft KD, Bilgin A.

Author information

 Abstract

BACKGROUND:

The consumption of foods rich in carotenoids that possess significant antioxidant and inflammatory modulating properties has been linked to reduced risk of neuropathology. The objective of this study was to evaluate the relationship between plasma carotenoid concentrations and plasma and cerebrospinal fluid (CSF) markers of inflammation, oxidative stress and nicotinamide adenine dinucleotide (NAD+) in an essentially healthy human cohort.

METHODS:

Thirty-eight matched CSF and plasma samples were collected from consenting participants who required a spinal tap for the administration of anaesthetic. Plasma concentrations of carotenoids and both plasma and cerebrospinal fluid (CSF) levels of NAD(H) and markers of inflammation (IL-6, TNF-α) and oxidative stress (F2-isoprostanes, 8-OHdG and total antioxidant capacity) were quantified.

RESULTS:

The average age of participants was 53 years (SD=20, interquartile range=38). Both α-carotene (P=0.01) and β-carotene (P<0.001) correlated positively with plasma total antioxidant capacity. A positive correlation was observed between α-carotene and CSF TNF-α levels (P=0.02). β-cryptoxanthin (P=0.04) and lycopene (P=0.02) inversely correlated with CSF and plasma IL-6 respectively. A positive correlation was also observed between lycopene and both plasma (P<0.001) and CSF (P<0.01) [NAD(H)]. Surprisingly no statistically significant associations were found between the most abundant carotenoids, lutein and zeaxanthin and either plasma or CSF markers of oxidative stress.

CONCLUSION:

Together these findings suggest that consumption of carotenoids may modulate inflammation and enhance antioxidant defences within both the central nervous system (CNS) and systemic circulation. Increased levels of lycopene also appear to moderate decline in the essential pyridine nucleotide [NAD(H)] in both the plasma and the CSF.

PMID: 24985027 [PubMed – in process] PMCID: PMC4096526 Free PMC Article

 

Glob Adv Health Med. 2014 Mar;3(2):34-9. doi: 10.7453/gahmj.2013.098.

A Phytochemical-rich Multivitamin-multimineral Supplement Is Bioavailable and Reduces Serum Oxidized Low-density Lipoprotein, Myeloperoxidase, and Plasminogen Activator Inhibitor-1 in a Four-week Pilot trial of Healthy Individuals.

Lerman RH1, Desai A1, Lamb JJ1, Chang JL1, Darland G1, Konda VR2.

Author information

 BACKGROUND:

A multivitamin-multimineral supplement combined with a diverse blend of bioactive phytochemicals may provide additional antioxidant capacity and anti-inflammatory property for overall health. This convenient feature may be useful for individuals who want to increase their intake of phytochemicals.

METHODS:

We conducted a pilot study in 15 healthy individuals (8 women and 7 men, mean age 41.7±14.9 years, mean body mass index 28.0±5.6) to investigate the effects of this novel formulation on biomarkers associated with oxidative stress and inflammation. After a 2-week diet that limited intake of fruits and vegetables to 2 servings/day, participants continued with the same restricted diet but began consuming 2 tablets of the study product for the subsequent 4 weeks. Fasting blood samples collected at Week 2 and Week 6 were analyzed and compared using paired t-tests for levels of carotenoids, folate, vitamin B12, homocysteine, oxidized low-density lipoprotein cholesterol (oxLDL), high-sensitivity C-reactive protein (hs-CRP), F2-isoprostane, plasminogen activator inhibitor-1 (PAI-1), and myeloperoxidase. Noninvasive peripheral arterial tonometry (EndoPAT) was also measured.

RESULTS:

After 4 weeks of supplementation, plasma levels of carotenoids, folate, and vitamin B12, but not homocysteine, were significantly increased (P<.05). Serum levels of oxLDL, PAI-1 and myeloperoxidase were significantly reduced (P<.05), but F2-isoprostane, hs-CRP, and EndoPAT measures were unchanged compared with baseline. The study product was well tolerated.

CONCLUSIONS:

This nutritional supplement is bioavailable as indicated by the significant increase in plasma carotenoids, vitamin B12, and folate levels and may provide health benefits by significantly reducing serum levels of oxLDL, myeloperoxidase, and PAI-1 in healthy individuals.

KEYWORDS:

Multivitamin; cardiovascular disease; low-density lipoprotein; multimineral

PMID: 24808980 [PubMed] PMCID: PMC4010963 [Available on 2015/3/1]

J Surg Res. 2014 Nov;192(1):206-13. doi: 10.1016/j.jss.2014.05.029. Epub 2014 May 21.

Astaxanthin offers neuroprotection and reduces neuroinflammation in experimental subarachnoid hemorrhage.

Zhang XS1, Zhang X2, Wu Q1, Li W1, Wang CX1, Xie GB1, Zhou XM1, Shi JX1, Zhou ML3.

 

BACKGROUND:

Neuroinflammation has been proven to play a crucial role in early brain injury pathogenesis and represents a target for treatment of subarachnoid hemorrhage (SAH). Astaxanthin (ATX), a dietary carotenoid, has been shown to have powerful anti-inflammation property in various models of tissue injury. However, the potential effects of ATX on neuroinflammation in SAH remain uninvestigated. The goal of this study was to investigate the protective effects of ATX on neuroinflammation in a rat prechiasmatic cistern SAH model.

METHODS:

Rats were randomly distributed into multiple groups undergoing the sham surgery or SAH procedures, and ATX (25 mg/kg or 75 mg/kg) or equal volume of vehicle was given by oral gavage at 30 min after SAH. All rats were sacrificed at 24 h after SAH. Neurologic scores, brain water content, blood-brain barrier permeability, and neuronal cell death were examined. Brain inflammation was evaluated by means of expression changes in myeloperoxidase, cytokines (interleukin-1β, tumor necrosis factor-α), adhesion molecules (intercellular adhesion molecule-1), and nuclear factor kappa B DNA-binding activity.

RESULTS:

Our data indicated that post-SAH treatment with high dose of ATX could significantly downregulate the increased nuclear factor kappa B activity and the expression of inflammatory cytokines and intercellular adhesion molecule-1 in both messenger RNA transcription and protein synthesis. Moreover, these beneficial effects lead to the amelioration of the secondary brain injury cascades including cerebral edema, blood-brain barrier disruption, neurological dysfunction, and neuronal degeneration.

CONCLUSIONS:

These results indicate that ATX treatment is neuroprotective against SAH, possibly through suppression of cerebral inflammation.

Nutr J. 2013 Dec 5;12(1):157. doi: 10.1186/1475-2891-12-157.

Extracellular micronutrient levels and pro-/antioxidant status in trauma patients with wound healing disorders: results of a cross-sectional study.

Blass SC, Goost H, Burger C, Tolba RH, Stoffel-Wagner B, Stehle P, Ellinger S1.

Abstract

BACKGROUND:

Disorders in wound healing (DWH) are common in trauma patients, the reasons being not completely understood. Inadequate nutritional status may favor DWH, partly by means of oxidative stress. Reliable data, however, are lacking. This study should investigate the status of extracellular micronutrients in patients with DWH within routine setting.

METHODS:

Within a cross-sectional study, the plasma/serum status of several micronutrients (retinol, ascorbic acid, 25-hydroxycholecalciferol, α-tocopherol, β-carotene, selenium, and zinc) were determined in 44 trauma patients with DWH in addition to selected proteins (albumin, prealbumin, and C-reactive protein; CRP) and markers of pro-/antioxidant balance (antioxidant capacity, peroxides, and malondialdehyde). Values were compared to reference values to calculate the prevalence for biochemical deficiency. Correlations between CRP, albumin and prealbumin, and selected micronutrients were analyzed by Pearson’s test. Statistical significance was set at P < 0.05.

RESULTS:

Mean concentrations of ascorbic acid (23.1 ± 15.9 μmol/L), 25-hydroxycholecalciferol (46.2±30.6 nmol/L), β-carotene (0.6 ± 0.4 μmol/L), selenium (0.79±0.19 μmol/L), and prealbumin (24.8 ± 8.2 mg/dL) were relatively low. Most patients showed levels of ascorbic acid (<28 μmol/L; 64%), 25-hydroxycholecalciferol (<50 μmol/L; 59%), selenium (≤ 94 μmol/L; 71%) and β-carotene (<0.9 μmol/L; 86%) below the reference range. Albumin and prealbumin were in the lower normal range and CRP was mostly above the reference range. Plasma antioxidant capacity was decreased, whereas peroxides and malondialdehyde were increased compared to normal values. Inverse correlations were found between CRP and albumin (P < 0.05) and between CRP and prealbumin (P < 0.01). Retinol (P < 0.001), ascorbic acid (P < 0.01), zinc (P < 0.001), and selenium (P < 0.001) were negatively correlated with CRP.

CONCLUSIONS:

Trauma patients with DWH frequently suffer from protein malnutrition and reduced plasma concentrations of several micronutrients probably due to inflammation, increased requirement, and oxidative burden. Thus, adequate nutritional measures are strongly recommended to trauma patients.

PMID: 24314073 [PubMed – indexed for MEDLINE] PMCID: PMC4028853

J Biomed Biotechnol. 2012;2012:524019. doi: 10.1155/2012/524019. Epub 2012 Oct 2.

Antioxidant, antinociceptive, and anti-inflammatory effects of carotenoids extracted from dried pepper (Capsicum annuum L.).

Hernández-Ortega M1, Ortiz-Moreno A, Hernández-Navarro MD, Chamorro-Cevallos G, Dorantes-Alvarez L, Necoechea-Mondragón H.

Abstract

Carotenoids extracted from dried peppers were evaluated for their antioxidant, analgesic, and anti-inflammatory activities. Peppers had a substantial carotenoid content: guajillo 3406 ± 4 μg/g, pasilla 2933 ± 1 μg/g, and ancho 1437 ± 6 μg/g of sample in dry weight basis. A complex mixture of carotenoids was discovered in each pepper extract. The TLC analysis revealed the presence of chlorophylls in the pigment extract from pasilla and ancho peppers. Guajillo pepper carotenoid extracts exhibited good antioxidant activity and had the best scavenging capacity for the DPPH(+) cation (24.2%). They also exhibited significant peripheral analgesic activity at 5, 20, and 80 mg/kg and induced central analgesia at 80 mg/kg. The results suggest that the carotenoids in dried guajillo peppers have significant analgesic and anti-inflammatory benefits and could be useful for pain and inflammation relief.

PMID: 23091348 [PubMed – indexed for MEDLINE] PMCID: PMC3468166

Biochimie. 2012 Dec;94(12):2723-33. doi: 10.1016/j.biochi.2012.08.013. Epub 2012 Aug 24.

A dietary colorant crocin mitigates arthritis and associated secondary complications by modulating cartilage deteriorating enzymes, inflammatory mediators and antioxidant status.

Hemshekhar M1, Sebastin Santhosh M, Sunitha K, Thushara RM, Kemparaju K, Rangappa KS, Girish KS.

Abstract

Articular cartilage degeneration and inflammation are the hallmark of progressive arthritis and is the leading cause of disability in 10-15% of middle aged individuals across the world. Cartilage and synovium are mainly degraded by either enzymatic or non-enzymatic ways. Matrix metalloproteinases (MMPs), hyaluronidases (HAases) and aggrecanases are the enzymatic mediators and inflammatory cytokines and reactive oxygen species being non-enzymatic mediators. In addition, MMPs and HAases generated end-products act as inflammation inducers via CD44 and TLR-4 receptors involved NF-κB pathway. Although several drugs have been used to treat arthritis, numerous reports describe the side effects of these drugs that may turn fatal. On this account several medicinal plants and their isolated molecules have been involved in modern medicine strategies to fight against arthritis. In view of this, the present study investigated the antiarthritic potentiality of Crocin, a dietary colorant carotenoid isolated from stigma of Crocus sativus. Crocin effectively neutralized the augmented serum levels of enzymatic (MMP-13, MMP-3 and MMP-9 and HAases) and non-enzymatic (TNF-α, IL-1β, NF-κB, IL-6, COX-2, PGE(2) and ROS) inflammatory mediators. Further, Crocin re-established the arthritis altered antioxidant status of the system (GSH, SOD, CAT and GST). It also protected the bone resorption by inhibiting the elevated levels of bone joint exoglycosidases, cathepsin-D and tartrate resistant acid phosphatases. Taken together, Crocin revitalized the arthritis induced cartilage and bone deterioration along with inflammation and oxidative damage that could be accredited to its antioxidant nature. Thus, Crocin could be an effective antiarthritic agent which can equally nullify the arthritis associated secondary complication.

Cell Stress Chaperones. 2014 Mar;19(2):183-91. doi: 10.1007/s12192-013-0443-x. Epub 2013 Jul 14.

Astaxanthin reduces hepatic endoplasmic reticulum stress and nuclear factor-κB-mediated inflammation in high fructose and high fat diet-fed mice.

Bhuvaneswari S1, Yogalakshmi B, Sreeja S, Anuradha CV.

Abstract

We recently showed that astaxanthin (ASX), a xanthophyll carotenoid, activates phosphatidylinositol 3-kinase pathway of insulin signaling and improves glucose metabolism in liver of high fructose-fat diet (HFFD)-fed mice. The aim of this study is to investigate whether ASX influences phosphorylation of c-Jun-N-terminal kinase 1 (JNK1), reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, and inflammation in liver of HFFD-fed mice. Adult male Mus musculus mice were fed either with control diet or HFFD for 15 days. After this period, mice in each group were divided into two and administered ASX (2 mg/kg/day, p.o) in 0.3 ml olive oil or 0.3 ml olive oil alone for the next 45 days. At the end of 60 days, liver tissue was excised and examined for lipid accumulation (Oil red O staining), intracellular ROS production, ER stress, and inflammatory markers. Elevated ROS production, lipid accumulation, and increased hepatic expression of ER stress markers such as Ig-binding protein, PKR-like ER kinase, phosphorylated eukaryotic initiation factor 2α, X-box binding protein 1, activating transcription factor 6, and the apoptotic marker caspase 12 were observed in the liver of the HFFD group. ASX significantly reversed these changes. This reduction was accompanied by reduced activation of JNK1 and I kappa B kinase β phosphorylation and nuclear factor-kappa B p65 nuclear translocation in ASX-treated HFFD mice. These findings suggest that alleviation of inflammation and ER stress by ASX could be a mechanism responsible for its beneficial effect in this model. ASX could be a promising treatment strategy for insulin resistant patients.

PMID: 23852435 [PubMed – indexed for MEDLINE] PMCID: PMC3933623

Clin Nutr. 2012 Oct;31(5):659-65. doi: 10.1016/j.clnu.2012.01.013. Epub 2012 Feb 25.

Higher serum concentrations of dietary antioxidants are associated with lower levels of inflammatory biomarkers during the year after hip fracture.

D’Adamo CR1, Miller RR, Shardell MD, Orwig DL, Hochberg MC, Ferrucci L, Semba RD, Yu-Yahiro JA, Magaziner J, Hicks GE.

 

BACKGROUND & AIMS:

Chronic inflammation impairs recovery among the 1.6 million people who suffer from hip fracture annually. Vitamin E and the carotenoids are two classes of dietary antioxidants with profound anti-inflammatory effects, and the goal of this study was to assess whether higher post-fracture concentrations of these antioxidants were associated with lower levels of interleukin 6 (IL-6) and the soluble receptor for tumor necrosis factor-alpha (sTNF-αR1), two common markers of inflammation.

METHODS:

Serum concentrations of the dietary antioxidants and inflammatory markers were assessed at baseline and 2, 6, and 12 month follow-up visits among 148 hip fracture patients from The Baltimore Hip Studies. Generalized estimating equations modeled the relationship between baseline and time-varying antioxidant concentrations and inflammatory markers.

RESULTS:

Higher post-fracture concentrations of vitamin E and the carotenoids were associated with lower levels of inflammatory markers. Associations were strongest at baseline, particularly between the α-tocopherol form of vitamin E and sTNF-αR1 (p = 0.05) and total carotenoids and both sTNF-αR1(p = 0.01) and IL-6 (p = 0.05). Higher baseline and time-varying α-carotene and time-varying lutein concentrations were also associated with lower sTNF-αR1 at all post-fracture visits (p ≤ 0.05).

CONCLUSIONS:

These findings suggest that a clinical trial increasing post-fracture intake of vitamin E and the carotenoids may be warranted.

Copyright © 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

PMID: 22365613 [PubMed – indexed for MEDLINE] PMCID: PMC3412071

Mar Drugs. 2012 Apr;10(4):890-9. doi: 10.3390/md10040890. Epub 2012 Apr 10.

Astaxanthin treatment reduced oxidative induced pro-inflammatory cytokines secretion in U937: SHP-1 as a novel biological target.

Speranza L1, Pesce M, Patruno A, Franceschelli S, de Lutiis MA, Grilli A, Felaco M.

Abstract

It has been suggested that oxidative stress activates various intracellular signaling pathways leading to secretion of a variety of pro-inflammatory cytokines and chemokines. SHP-1 is a protein tyrosine phosphatase (PTP) which acts as a negative regulator of immune cytokine signaling. However, intracellular hydrogen peroxide (H(2)O(2)), generated endogenously upon stimulation and exogenously from environmental oxidants, has been known to be involved in the process of intracellular signaling through inhibiting various PTPs, including SHP-1. In this study, we investigated the potential role of astaxanthin, an antioxidant marine carotenoid, in re-establishing SHP-1 negative regulation on pro-inflammatory cytokines secretion in U-937 cell line stimulated with oxidative stimulus. ELISA measurement suggested that ASTA treatment (10 µM) reduced pro-inflammatory cytokines secretion (IL-1β, IL-6 and TNF-α) induced through H(2)O(2), (100 µM). Furthermore, this property is elicited by restoration of basal SHP-1 protein expression level and reduced NF-κB (p65) nuclear expression, as showed by western blotting experiments.

KEYWORDS:

SHP-1 protein; astaxanthin; carotenoids; inflammation

PMID: 22690149 [PubMed – indexed for MEDLINE] PMCID: PMC3366681

Mol Cell Biol. 2012 Dec;32(24):5103-15. doi: 10.1128/MCB.00820-12. Epub 2012 Oct 15.

Retinol-binding protein 4 induces inflammation in human endothelial cells by an NADPH oxidase- and nuclear factor kappa B-dependent and retinol-independent mechanism.

Farjo KM1, Farjo RA, Halsey S, Moiseyev G, Ma JX.

Abstract

Serum retinol-binding protein 4 (RBP4) is the sole specific vitamin A (retinol) transporter in blood. Elevation of serum RBP4 in patients has been linked to cardiovascular disease and diabetic retinopathy. However, the significance of RBP4 elevation in the pathogenesis of these vascular diseases is unknown. Here we show that RBP4 induces inflammation in primary human retinal capillary endothelial cells (HRCEC) and human umbilical vein endothelial cells (HUVEC) by stimulating expression of proinflammatory molecules involved in leukocyte recruitment and adherence to endothelium, including vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-selectin, monocyte chemoattractant protein 1 (MCP-1), and interleukin-6 (IL-6). We demonstrate that these novel effects of RBP4 are independent of retinol and the RBP4 membrane receptor STRA6 and occur in part via activation of NADPH oxidase and NF-κB. Importantly, retinol-free RBP4 (apo-RBP4) was as potent as retinol-bound RBP4 (holo-RBP4) in inducing proinflammatory molecules in both HRCEC and HUVEC. These studies reveal that RBP4 elevation can directly contribute to endothelial inflammation and therefore may play a causative role in the development or progression of vascular inflammation during cardiovascular disease and microvascular complications of diabetes.

PMID: 23071093 [PubMed – indexed for MEDLINE] PMCID: PMC3510526

 

 

 

Blue bions – high energy whole foods kills T-bacilli cancer cells

Orgone Experiments

The new observations with a superior microscope also validate the orgone experiments of Wilhelm Reich who described similar microbial processes in the 1940’s (The Cancer Biopathy. Farrar, Straus and Giroux, NY, 1973). He accepted only ‘terminal’ cancer patients and treatment was free. Commonly pain diminished, blood and weight improved, and tumours shrank or disappeared. Despite this, the patients died. From this he concluded that tumours are not an important part of the disease.

Reich’s work was so threatening to the medical establishment that all of Reich’s published books were burned and equipment destroyed under FDA supervision. Because he maintained that a court was not a proper place to discuss a scientific theory, he died 1957 in an US jail (www.wilhelmreichtrust.org/biography.html).

Bion

His most important achievement, which I regard as the greatest scientific discovery of the last century, was the bion as the basic unit of biological life. He found that every kind of food and vegetable matter when heated to incandescence and then dropped into a sterile nutrient solution evolved into round moving or pulsating bions that appeared blue in dark-field or when viewed with a fluorescent microscope. Reich sacrificed fine structure details and observed mainly at 3000 – 5000x in order to better see colour and movements.

Higher the vitality of the entity – blue Bions

The stronger the blue colour, the higher the vitality of the entity. Under these conditions healthy erythrocytes have a blue appearance while dead ones are black. According to Reich this blue glimmer is the characteristic of bio-energy or life-force which he called orgone. It is present not only in all living matter but also in water and air. Orgone originates in the sun and is transmitted by sunlight. Bions, the biological units of orgone, may gradually aggregate and evolve into amoeba-like or protozoan structures.

Degenerating proteins as T-bacilli

Reich described another formation derived from degenerating proteins as T-bacilli, which stands for the German ‘Todes Bacilli’ or ‘death bacilli’. These can easily be cultivated from cancer tissue, the blood of patients with cancer or precancerous conditions, and also from degenerating blood. Injected in high doses they can kill mice within 24 hours, in lower doses they produce cancerous growths. They are black, lancet shaped and of similar size as described by Olbrich.

Blue bions paralysed and killed the black T-bacilli

Also interesting is the observation that the blue bions paralysed and killed the black T-bacilli and even the much bigger proteus bacilli. In the same way strongly blue erythrocytes killed T-cells and pathogenic bacteria, but thereby the erythrocytes lost some of their blue colour, indicating that their vitality diminished in the process.

When strongly charged red blood cells entered a tumour, cancer tissue started to disintegrate into non-motile T-bodies. But in addition also the red blood cells disappeared and only T-bodies remained visible. The tumour developed large cavities which filled up with T-bodies. Macroscopically the originally blood-red cavities turned into a rust brown colour from the disintegrating tumour and blood cells.

Sunlight

Reich observed that weak erythrocytes could be charged to become strongly blue and vital by using sunlight, and especially his orgone accumulator which concentrates orgone from the atmosphere. Some healers have the ability to channel strong bio-energy with their hands and to some degree even remotely with their mind.

Growth hormone DHEA increases libido/anti-aging

 DHEA is the most common hormone in the human blood. Like steroids it has also been grossly misunderstood, with it being crucially restricted in empowering the art of love making. Blood levels are highest during our late teens and these begin to decline by the time we are 25 years of age. By 70 years of age, DHEA production is only a small fraction of what it was when we were younger. This is most commonly seen in women whose libido decreases, especially after pregnancy. There are many reasons why this happens, one amongst them is the presence of DHEA.

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Research has shown a correlation between low DHEA levels and a declining immune system as well. As such, DHEA is being used in the fight against HIV, cancer, and senile dementia. But DHEA’s most overlooked but vital role may be its relationship with cortisol. DHEA has an inverse relationship to cortisol, i.e. when DHEA is low cortisol levels are elevated and vice-versa. Now what in the world is cortisol, you may well ask! Cortisol is one of the few hormones that increases with age. Known to induce stress, especially when its levels are elevated for long periods, most bodily functions get negatively affected by it. For example, the body may become more insulin resistant and damage to other systems may damage other vital organs in our body.

Maintaining Healthy DHEA Levels
Maintaining healthy DHEA levels while keeping coritisol levels under control may help slow physical aging and reduce stress. In short it may also decrease the pace at which we might observe aging signs in our body. To sum it up, DHEA, in reality is more like a growth hormone that fills in the void that gets created with the passage of time in our body. The first few signs of aging in any human, be it wrinkles, or hair loss, or even dryness in our skin is due to the shrinkage of the growth hormone. Usage of DHEA helps you revive it all over again.

The average production of DHEA from healthy adrenal glands is approximately 25mg per day. Men produce more DHEA on an average than women. This may also be so because women are endowed with the ability to give birth to a child, an activity, which in varying mannerisms drags a certain weakness in a woman’s body, even though she chooses to live a healthy lifestyle.

Although there is no-known down-regulation (a situation whereby the adrenal glands would slow or stop their own production of DHEA in response to the continuous high levels caused by long-term DHEA supplementation), it is advisable to stop DHEA use for periods of time on a regular basis to prevent this possibility (or have DHEA levels monitored by blood tests). Of course you need to see your physician before you start popping in DHEA pills, but it’s advisable that you monitor your health file before doing so to avoid dangerous consequences.

Needless to mention that DHEA should NOT be used by people suffering from prostate or testicular cancer. It is best if you consult a physician before using it on yourself, as these are hormones that you are dealing with and any side effect could possibly have a serious negative effect on you! Moreover, the advancement of Science is to move you to a platter that’s most desirable not one that is most detested!

Dehydroepiandrosterone (DHEA) is a steroid hormone that’s produced naturally by the adrenal glands. The body converts DHEA into male and female sex hormones, such as estrogen and testosterone. DHEA is also available in supplement form.

DHEA supplements are made from a substance called diosgenin, which is found in soy and wild yams. Wild yam cream and supplements are often touted as natural sources of DHEA, but the body can’t convert wild yam to DHEA on its own—it must be done in a laboratory.

DHEA supplements were taken off the U.S. market in 1985 because of concerns about false claims regarding their benefits. It became available only by prescription, but was reintroduced as a nutritional supplement after the Dietary Supplement Health and Education Act was passed in 1994.

Health Effects of DHEA Supplements?

DHEA levels typically peak by the time people are in their 20s and decline with age, which is why there has been considerable interest in DHEA and its role in aging. What’s more, low levels of DHEA have been detected in some people with type 2 diabetes, breast cancer, heart disease, osteoporosis and kidney disease. Some individuals use DHEA supplements in order to protect against these and other health conditions.

Certain medications may also deplete DHEA, such as corticosteroids, insulin, opiates and danazol.

DHEA is often taken to slow or reverse the aging process, enhance exercise performance, prevent Alzheimer’s disease, improve libido, fight fatigue, enhance health in people with HIV/AIDS, soothe menopausal symptoms, treat erectile dysfunction and stimulate the immune system.

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Can Taking DHEA Supplements Improve Your Health?

There are very few large, well-designed human studies testing the health effects of DHEA supplements. For example, there is not enough scientific evidence to rate the effectiveness of DHEA supplements in treating adrenal insufficiency, metabolic syndrome, depression, HIV/AIDS, Addison’s disease, chronic fatigue syndrome, menopausal symptoms, heart disease, breast cancer, infertility, diabetes, or Parkinson’s disease according to the National Institutes of Health (NIH).

In addition, there isn’t enough evidence to support the use of DHEA supplements as an anti-aging remedy or weight-loss aid. The NIH also cautions that DHEA supplements appear to be ineffective for boosting libido, enhancing muscle strength in elderly people, protecting against Alzheimer’s disease and improving thinking in healthy older people.

However, some research suggests that DHEA supplements may be useful for certain conditions. Here’s a look at several key study findings:

1) Osteoporosis

Taking DHEA by mouth daily seems to improve bone mineral density in older women and men with osteoporosis or osteopenia, according to the NIH. Indeed, a 2002 study from the Chinese Medical Journal deemed DHEA safe and effective in the treatment of osteoporosis. After six months of treatment with DHEA, 44 male osteoporosis patients experienced a significant increase in bone mineral density (compared to 42 male osteoporosis patients assigned to a control group for the same time period).

2) Lupus

Studies indicate that DHEA may enhance mental function and increase bone mass in women with systemic lupus erythematosus (SLE), an autoimmune disease affecting connective tissue. Many of those studies focused on the use of a form of synthetic DHEA called prasterone (Prestara).

For example, a 2004 study in Arthritis and Rheumatism found that daily intake of prasterone improved or stabilized symptoms among patients with SLE. The study involved 381 women with SLE, each of whom received 200 mg of prasterone or a placebo each day (in addition to their standard treatments) for up to 12 months. Although some members of the prasterone group developed acne and/or hirsutism (excess facial and body hair), most cases were mild and did not require the patients to discontinue their use of prasterone.

For a 2007 report in the Cochrane Database of Systematic Reviews, scientists analyzed seven clinical trials (with a total of 842 participants) that tested the use of DHEA in treating SLE. The report’s authors concluded that DHEA may have a “modest but clinically significant impact” on health-related quality of life in the short-term for people with SLE.

3) Schizophrenia

Increasing DHEA levels may help lessen anxiety and depressive symptoms in people with schizophrenia, according to a 2003 study from the Archives of General Psychiatry. The study involved 30 people with schizophrenia, each of whom received either DHEA or a placebo for six weeks (in addition to their regular antipsychotic medication).

DHEA may also help improve mood, enhance well being and boost energy in people with schizophrenia, according to the study’s authors. It’s important to note that DHEA appeared to be more effective in women than in men.

4) Erectile Dysfunction

For people with sexual dysfunction, DHEA may improve the ability to achieve an erection. However, DHEA does not appear to benefit men whose erectile dysfunction is caused by diabetes or nerve disorders.

Some research shows that decreased DHEA levels may be common among men with erectile dysfunction. In a 2000 study from Urology, for example, researchers examined 442 men (including 309 patients with erectile dysfunction and 133 healthy volunteers) and found that DHEA levels were lower in those with erectile dysfunction until age 60.

Although few trials have tested the effects of DHEA supplementation on patients with erectile dysfunction, there’s some evidence that increasing DHEA levels may treat this condition. For instance, in a 1999 study of 40 erectile dysfunction patients, men who received a daily dose of DHEA for six months experienced significant improvement in their ability achieve or maintain an erection sufficient for satisfactory sexual performance. Published in Urology, the study found that the 20 participants who received a placebo for the same time period had no improvement in their erectile dysfunction.

DHEA is a hormone, so it should only be used under the supervision of a qualified health practitioner. Children and pregnant or nursing women should not use DHEA. There have been no studies on the long-term safety of DHEA.

One of the more common side effects of DHEA supplements is acne. Other side effects include insomnia, fatigue, oily skin, abdominal pain, hair loss, nasal congestion, rapid or irregular heartbeats and heart palpitations.

DHEA supplements may alter liver function, so people with liver disease shouldn’t use the hormone. People with mood disorders (such as depression) should only use DHEA under the supervision of their healthcare provider, as DHEA supplementation may worsen mood. High levels of the body’s natural DHEA has been associated with psychotic disorders, so people with or at risk for psychotic disorders shouldn’t use DHEA unless under the supervision of their healthcare provider.

Since DHEA supplements may influence the production of male and female hormones, acne, greasy skin, facial hair growth, hair loss, weight gain around the waist, a deepening of the voice and other signs of masculinization may occur in women. Men may develop aggressiveness, high blood pressure, male pattern baldness, breast enlargement (gynecomastia), breast tenderness and shrinkage of the testicles.

DHEA supplements may also affect the levels of other hormones, such as insulin and thyroid hormone, as well as affect cholesterol levels. People with diabetes or hyperglycemia, high cholesterol, thyroid disorders, Cushing’s disease and other hormonal disorders should be particularly cautious.

DHEA supplements may alter the levels estrogen and testosterone, which can theoretically increase the risk of hormone-sensitive cancers such as breast, prostate and ovarian cancer.

People taking DHEA supplements may be more likely to develop blood clots, so people with clotting disorders, heart disease and those with a history of stroke should avoid DHEA supplements.

It’s also not known whether DHEA supplements may inhibit the body’s ability to make its own DHEA.

DHEA rich foods

  • Wild yam and soybean products

  • Vegetables and fruits: Seaweed
    contains anti-aging minerals and vitamins
    example: kelp (lithium and other minerals) – recent anti-aging mineral for nerve growth

  • Fish oil

  • SOD

SOD is an enzyme naturally found in every cell in your body and is considered one of the most important antioxidants, according to Dr. Mark Rosenberg from the website Foodtrients. Its primary role is to protect your cells against the cell-damaging free radical superoxide. As you age, the amount of SOD in your body decreases, says Rosenberg. However, filling your diet with foods that contain nutrients needed for the production of SOD may help improve your levels.

SOD-Rich Melons

Both honeydew and cantaloupe melon contain high amounts of SOD. Although your body is unable to use the SOD in these fruits, they are also excellent sources of vitamin C, which may help up your production of the super antioxidant. These fruits also contain small amounts of copper, zinc and manganese, which are trace minerals your body needs to make SOD.

Green Vegetables With SOD

The cruciferous vegetables broccoli, cabbage and Brussels sprouts are naturally rich in SOD. They are also excellent sources of vitamin C and contain small amounts of essential trace minerals that boost SOD production, including copper, manganese and zinc. For overall good health, you should try to eat at least 1 1/2 cups to 2 cups of dark green vegetables a week, says ChooseMyPlate.gov.

Copper, Manganese and Zinc

In addition to the healthy food sources of SOD, be sure to include foods rich in the necessary trace minerals. Up your zinc intake by eating more oysters, lobster, chicken, chickpeas, cashews and peas. Good sources of manganese include hazelnuts, tofu, pumpkin seeds, mussels and spinach. Grains, beans, nuts and potatoes are all good sources of copper.

Phytonutrients found naturally in fruits and vegetables can significantly reduce the risk of cancer because of their antioxidant and anti-inflammatory properties. Aspirin was originally extracted from the bark of the White Willow Tree and is now synthetically produced has pain-relieving and anti-inflammatory properties. Taxol was initially extracted from the Pacific Yew Tree and is the number one drug used for treating Cancer.

Diindolylemthane is another Phytonutrients found in vegetables such as Broccoli, Cauliflower, Cabbage, Kale and Brussels sprouts used in the treatment of cancers caused the Human Papilloma Virus. The National Cancer Institute of the United States is testing this compound in the treatment of prostate, lung, colon, and cervical cancers. Phytonutrients is believed to be destroyed by cooking and by modern food processing techniques. For this reason only fresh uncooked Phytonutrients should be consumed.

Lycopene found in tomatoes is in clinical trials for Prostate cancer and Heart disease. It has been shown to improve blood flow throughout the human body. A nutritional study has shown that a diet rich and broccoli and tomatoes was more effective in limiting prostate cancer growth than any of the leading drugs for prostate cancer.

Bioflavanoids provide visible benefits to the anti-aging process such as reducing wrinkles, improving skin tone, helping to prevent sagging skin as well as improves pigmentation.

Substances called Antioxidants can neutralize free radical by pairing up or binding with the free radical elections thus inhibiting them from damaging cells in the human body. Natural Antioxidants are abundant in fruits and vegetables such as, apples, blueberries, broccoli, cherries, cranberries, Grapes, spinach, and Spirulina a blue-green algae.

Studies of the Greenland Eskimos lack of heart attacks have show that Eico-Sapentaenoic Acid (EPA) lowers blood cholesterol considerably, even more than polyunsaturated fat does. It also triggers a major drop in triglycerides . Salmon Oil is one of the best known sources of natural EPA.

Fish Oil

Fish oil contains omega 3 and fatty acids, which have been shown to stimulate the brain and increase memory and mental awareness.

Foti also called He Shou Wu in China is legendary in its ability to lengthen life. Modern studies have show that Foti has the ability to lower serum cholesterol, prevent premature gray hair, promote red blood cell growth, and to increase longevity on a cellular level. This herb raises the level of the naturally occurring antioxidant Superoxide Dismutase (SOD) in the body.

Anti-Aging supplement can be very effective but they must be used in conjunction with a healthy diet. Care must be taken to also ensure that you remain active both physically as well as mentally. If you just feel that you need vitamins, supplements or herbs to fight the aging process then find a good health care professional prior to starting any type of home treatment.

Always consult your doctor before using this information.

This Article is nutritional in nature and is not to be construed as medical advice.

————————————-

Connie Dello Buono 
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Connie Dello Buono, health coach and health author of Birthing Ways Healing Ways
Owner of Motherhealth , Health Mobile Outpatient application (in development , http://www.careme.live ) to match, monitor and report health data, reduce chronic care costs and integrate patient generated health data to facilitate health promotion and doctor’s communication. Investors and doctors are welcome to join , email motherhealth@gmail.com

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