Vitamin C and A for vision and to fight cancer and other invading organisms

guava car.JPGVitamin C (water soluble) and A (fat soluble) for vision and cancer fighting properties: both from colored fruits and veggies

Signs that you are low in Vitamin C and A is when your vision is weak and you get allergies and get tired or sick easily.

Eat Vit A (afternoon) together with good fatty foods and eat Vit C (morning) with water soluble foods. Vitamin C is important in the absorption of most minerals and nutrients in the body such as Calcium, magnesium, iron and others.

Ascorbic acid becomes widely distributed in body tissues with large concentrations found in the liver, leukocytes, platelets, glandular tissues, and the lens of the eye. In the plasma about 25% of the ascorbic acid is bound to proteins.   Ascorbic acid crosses the placenta; cord blood concentration are generally 2 to 4 times the concentration in maternal blood. Ascorbic acid is distributed into milk. In nursing mothers on a normal diet the milk contains 40 to 70 ug/mL of the vitamin.  Food Sources of Vitamin C ranked by mg of vitamin C per standard amount; also calories in the standard amount. (All provide ≥ 20% of RDA for adult men, which is 90 mg/day.)

Whole Food, Standard Amount Vitamin C (mg) Calories
Guava, raw, ½ cup 188 56
Red sweet pepper, raw, ½cup 142 20
Red sweet pepper, cooked, ½ cup   116 19
Kiwi fruit, 1 medium 70 46
Orange, raw, 1 medium 70 62
Orange juice, ¾ cup 61-93 79-84
Green pepper, sweet, raw, ½ cup 60   15
Green pepper, sweet, cooked, ½ cup 51   19
Grapefruit juice, ¾ cup 50-70 71-86
Vegetable juice cocktail, ¾ cup 50 34
Strawberries, raw, ½ cup 49 27
Brussels sprouts, cooked, ½ cup 48 28
Cantaloupe, ¼ medium 47 51
Papaya, raw, ¼ medium (strong enzyme) 47 30
Kohlrabi, cooked, ½ cup 45 24
Broccoli, raw, ½ cup 39 15
Edible pod peas, cooked, ½ cup 38 34
Broccoli, cooked, ½ cup 37 26
Sweet potato, canned, ½ cup 34   116
Tomato juice, ¾ cup 33 31
Cauliflower, cooked, ½ cup 28 17
Pineapple, raw, ½ cup 28 37
Kale, cooked, ½ cup 27 18
Mango, ½ cup 23 54

Vitamin A for growth and bone development

In humans, an exogenous source of vitamin A is required for growth (hormones and others) and bone development, vision, reproduction, and the integrity of mucosal and epithelial surfaces. In the retina, retinol is converted to the aldehyde, cis-retinal, which combines with opsin to form rhodopsin, and visual pigment. Vitamin A has been reported to act as a cofactor in various biochemical reactions including mucopolysaccharide synthesis, cholesterol synthesis, and hydroxysteroid metabolism.

Cholesterol synthesis happens during the night and so is Vitamin A. Women should especially sleep before 10pm to follow the normal body rhythm and hormone production. Cholesterol and Vitamin A are important in hormone production.

Vitamin A is essential for growth and bone development in children, for vision (particularly in dim light), and for integrity of mucosal and epithelial surfaces.

Vitamin A deficiency leads to xerophthalmia, Bitot’s spots, keratomalacia, night blindness (nyctalopia), hyperkeratosis of the skin, epithelial metaplasia of mucous membranes, and decreased resistance to infections. Administration of vitamin A completely reverses signs of vitamin deficiency unless keratomalacia has resulted in irreversible ocular damage.

Retinol inhibited the mutagenic activity of aflatoxin b1 when added to the Ames salmonella/mammalian microsome assay.

Concurrent use of vitamin E may facilitate absorption, hepatic storage, and utilization of vitamin A, and reduce toxicity; excessive doses may deplete vitamin A stores.

Concurrent use /of tetracycline/ with vitamin A 50,000 Units a day and higher has been reported to cause benign intracranial hypertension.

Vitamin A administration induces a high risk of intoxication in patients with chronic renal failure.

From epidemiological research it is argued that low vitamin A intake is associated with a higher incidence of cancer in different tissues.

Food Sources of Vitamin A ranked by micrograms Retinol Activity Equivalents (RAE) of vitamin A per standard amount; also calories in the standard amount. (All are ≥ 20% of RDA for adult men, which is 900 mg/day RAE.)

Food Sources

Whole Food, Standard Amount Vitamin A
(μg RAE)
Calories
Organ meats (liver, giblets), various, cooked, 3 oza 1490-9126 134-235
Carrot juice, ¾ cup 1692   71
Sweetpotato with peel, baked, 1 medium 1096 103
Pumpkin, canned, ½ cup (and yams are happy food) 953 42
Carrots, cooked from fresh, ½ cup 671 27
Spinach, cooked from frozen, ½ cup 573 30
Collards, cooked from frozen, ½ cup 489 31
Kale, cooked from frozen, ½ cup 478 20
Mixed vegetables, canned, ½ cup 474   40
Turnip greens, cooked from frozen, ½ cup 441 24
Instant cooked cereals, fortified, prepared, 1 packet 285-376 75-97
Various ready-to-eat cereals, with added vit. A, ~1 oz 180-376 100-117
Carrot, raw, 1 small 301 20
Beet greens, cooked, ½ cup (for hormonal balance) 276 19
Winter squash, cooked, ½ cup 268 38
Dandelion greens, cooked, ½ cup 260 18
Cantaloupe, raw, ¼ medium melon 233 46
Mustard greens, cooked, ½ cup 221 11
Pickled herring, 3 oz 219 222
Red sweet pepper, cooked, ½ cup 186 19
Chinese cabbage, cooked, ½ cup 180 10

Note: For those with thyroid problems, cooked your greens and most veggies.

How diet can change your epigenome and affect cancer and chromatin of DNA

Food that shapes you: how diet can change your epigenome

You are what you eat – quite literally. Our diet can influence the tiny changes in our genome that underlie several diseases, including cancer and obesity.

DNA helix
Image courtesy of mstroeck /
Wikimedia Commons

When you look at yourself in the mirror you may ask, ‘How, given that all the cells in my body carry the same DNA, can my organs look so unlike and function so differently?’ With the recent progress in epigenetics, we are beginning to understand. We now know that cells use their genetic material in different ways: genes are switched on and off, resulting in the astonishing level of differentiation within our bodies.

Epigenetics describes the cellular processes that determine whether a certain gene will be transcribed and translated into its corresponding protein. The message can be conveyed through small and reversible chemical modifications to chromatin (figure 1). For example, the addition of acetyl groups (acetylation) to DNA scaffold proteins (histones) enhances transcription. In contrast, the addition of methyl groups (methylation) to some regulatory regions of the DNA itself reduces gene transcription. These modifications, together with other regulatory mechanisms, are particularly important during development – when the exact timing of gene activation is crucial to ensure accurate cellular differentiation – but continue to have an effect into adulthood.

Epigenetic modifications can occur in response to environmental stimuli, one of the most important of which is diet. The mechanisms by which diet affects epigenetics are not fully understood, but some clear examples are well known.

Figure 1: Epigenetic changes
to the chromatin structure
involve mainly histone
acetylation – which enhances
transcription – and DNA
methylation, whereby methyl
groups are covalently bound
to cytosine, making the
chromatin structure less
accessible. These changes are
reversible, allowing gene
activity to be adapted to
changing environmental
conditions or signals.
This image was updated on the
13 May 2014.

Image courtesy of Cristina Florean

During the winter of 1944–1945, the Netherlands suffered a terrible famine as a result of the German occupation, and the population’s nutritional intake dropped to fewer than 1000 calories per day. Women continued to conceive and give birth during these hard times, and these children are now adults in their sixties. Recent studies have revealed that these individuals – exposed to calorie restrictions while in their mother’s uterus – have a higher rate of chronic conditions such as diabetes, cardiovascular disease and obesity than their siblings. The first months of pregnancy seem to have had the greatest effect on disease risk.

How can something that happened before you were even born influence your life as much as 60 years later? The answer appears to lie in the epigenetic adaptations made by the foetus in response to the limited supply of nutrients. The exact epigenetic alterations are still not clear, but it was discovered that people who were exposed to famine in utero have a lower degree of methylation of a gene implicated in insulin metabolism (the insulin-like growth factor II gene) than their unexposed siblings (Heijmans et al., 2008). This has some startling implications: although epigenetic changes are in theory reversible, useful changes that take place during embryonic development can nonetheless persist in adult life, even when they are no longer useful and could even be detrimental. Some of these changes may even persist through generations, affecting the grandchildren of the exposed women (Painter et al., 2008).

Figure 2: Two queen
honeybee larvae floating in
royal jelly in their queen cell.
Queen larvae are fed
exclusively with royal jelly,
which triggers the
development of the queen
phenotype, allowing
reproduction 

Image courtesy of Waugsberg /
Wikimedia Commons

The effects of early diet on epigenetics are also clearly visible among honeybees. What differentiates the sterile worker bees from the fertile queen is not genetics, but the diet that they follow as larvae (figure 2). Larvae designated to become queens are fed exclusively with royal jelly, a substance secreted by worker bees, which switches on the gene programme that results in the bee becoming fertile.

Another striking example of how nutrition influences epigenetics during development is found in mice. Individuals with an active agouti gene have a yellow coat and a propensity to become obese. This gene, however, can be switched off by DNA methylation. If a pregnant agouti mouse receives dietary supplements that can release methyl groups – such as folic acid or choline – the pups’ agouti genes become methylated and thus inactive. These pups still carry the agouti gene but they lose the agouti phenotype: they have brown fur and no increased tendency towards obesity (figure 3).

Figure 3: The agouti mouse
model. The phenotype
depends on the mother’s diet
during pregnancy. A:
Normally, the agouti gene is
associated with yellow fur
and a tendency towards
obesity. B: Mice born to a
mother receiving dietary
supplements of methyl
donors, however, have a
methylated and thus
inactivated agouti gene,
resulting in a thin, brown-
fur phenotype.

Image courtesy of Cristina
Florean

An insufficient uptake of folic acid is also implicated in developmental conditions in humans, such as spina bifida and other neural tube defects. To prevent such problems, folic acid supplements are widely recommended for pregnant women and for those hoping to conceive (see Hayes et al., 2009).

What about the dietary effect on epigenetics in adult life? Many components of food have the potential to cause epigenetic changes in humans. For example, broccoli and other cruciferous vegetables contain isothiocyanates, which are able to increase histone acetylation. Soya, on the other hand, is a source of the isoflavone genistein, which is thought to decrease DNA methylation in certain genes. Found in green tea, the polyphenol compound epigallocatechin-3-gallate has many biological activities, including the inhibition of DNA methylation. Curcumin, a compound found in turmeric (Curcuma longa), can have multiple effects on gene activation, because it inhibits DNA methylation but also modulates histone acetylation. Figure 4 shows further examples of epigenetically active molecules.

Fruit market in Spain
Image courtesy of Marcel
Theisen / Wikimedia Commons

Most of the data collected so far about these compounds come from in vitro experiments. The purified molecules were tested on cellular lines, and their effects on epigenetic targets were measured. It remains to be proved if eating the corresponding foods has the same detectable effect as has been seen in cellular models (Gerhauser, 2013).

Epidemiological studies, however, suggest that populations that consume large amounts of some of these foods appear to be less prone to certain diseases (Siddiqui et al., 2007). However, most of these compounds not only have epigenetic effects but also affect other biological functions. A food may contain many different biologically active molecules, making it difficult to draw a direct correlation between epigenetic activity and the overall effect on the body. Finally, all foods undergo many transformations in our digestive system, so it is not clear how much of the active compounds actually reach their molecular targets.

As a result of their far-reaching effects, epigenetic changes are involved in the development of many illnesses, including some cancers and neurological diseases. As cells become malignant, or cancerous, epigenetic modifications can deactivate tumour suppressor genes, which prevent excessive cell proliferation (Esteller, 2007). Because these epigenetic modifications are reversible, there is great interest in finding molecules – especially dietary sources – that might undo these damaging changes and prevent the development of the tumour.

We all know that a diet rich in fruit and vegetables is healthy for our everyday life, but it is becoming increasingly clear that it might be much more important than that, having significant implications for our long-term health and life expectancy.

References

Resources

Connie’s Comments:

  • Eat colored fruits and Veggies.
  • For quality supplementation that resets your gene expression to a younger you:
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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

 

 

 

Inflammatory bowel disease in pets

Inflammatory bowel disease in pets can give us  health cues as humans have similar body functions. Pets do not eat sugar, dairies, trans fat, smoke or stress out like we do.
We can start with cleansing and then nourishment. Do drink raw carrots juice with garlic and ginger. Limit refined foods, sugar, alcohol, smoking and unhealthy fats/trans fat. Email motherhealth@gmail.com for personal health coaching.
Connie
———-
Listen as Dr. Karen Becker discusses the very common problem of IBD in companion animals – how it starts, what to look for, treatment options and how to prevent this miserable disorder in your furry family member.

Dr. Becker’s Comments:

Inflammatory bowel disease (IBD) is a condition of inflammation of the intestines.

There are four common types of IBD, classified by what kind of white blood cells infiltrate the intestine: lymphocytes, plasmacytes, eosinophils and neutrophils. Without a doubt, the most common cause of IBD in pets is lymphocytic-plasmacytic enteritis, gastritis and colitis.

If your pet’s intestines are inflamed long enough, the situation can create a host of other debilitating health conditions.

IBD and Leaky Gut

Both cats and dogs get IBD. Both are susceptible to dysbiosis or ‘leaky gut,’ which means the balance of bad to good intestinal bacteria gets out of whack.

Leaky or permeable gut is a condition in which inflammation weakens the tight junctions of the cells of the GI tract, allowing partially digested proteins and potential allergens to escape into your pet’s bloodstream.

Allergens in the bloodstream trigger a systemic immune reaction – your pet’s body senses foreign invading substances and mounts a powerful defense. The result is allergies or worse – autoimmune or immune-mediated disease. A simple explanation for this condition is that your pet’s body is attacking itself.

IBD Leads to Secondary Infections, Organ Degeneration, Nutritional Deficiencies and Even Cancer

Secondary infections are very common in dogs and cats with inflammatory bowel disease. This is the result of not having a balanced, healthy digestive system.

Over half your pet’s immune function is located in his GI tract, so if the intestines are inflamed and compromised, the immune system is compromised right along with it.

Secondary organ degeneration is common with IBD, especially in the kidneys and liver.

Nutritional deficiencies are also typical in IBD pets because inflammation disrupts the normal absorption and processing of nutrients from food.

With kitties, there’s a correlation between GI cancer (lymphoma of the GI tract) and chronic IBD.

A Common Cause of IBD – GI Parasites

There are a few common causes of inflammatory bowel disease in dogs and cats.

One that is often overlooked is the presence of parasites.

My estimate is the vast majority of puppy mill pets and abandoned/rescued animals left at shelters are positive for parasites – roundworms, hookworms, tapeworms, coccidia, and Giardia. Parasites cause GI inflammation.

Another source for parasite infestation is in litters whose mothers were not tested or treated prior to being bred. Responsible breeders arrange for testing and deworming of females before they are bred, which insures litters will be parasite free.

Less responsible or unknowledgeable breeders don’t take the same precautions and end up selling litter after litter of puppies and kittens that have GI parasites.

The next problem arises at the veterinary clinic, where broad spectrum dewormers are given to infected animals at regular intervals until 16 weeks. At the end of the 16 weeks, the pets are re-checked to see if the parasites are gone.

But here’s the issue: if the specific parasite isn’t identified, it may not be killed by a broad spectrum dewormer. So pets wind up with several weeks of unnecessary medication that doesn’t even solve the problem.

Many dogs I see at my Natural Pet hospital have been dewormed three or four times but are still having problems. When I check fecal samples for these pups, I often find they are coccidia or Giardia-positive. Broad spectrum dewormers don’t take care of these particular parasites. Giardia, for example, causes intermittent diarrhea and chronic low-grade inflammation of the GI tract. It is not responsive to the dewormers most vets prescribe.

A saner, safer approach is for your vet to do at least three fecal analyses one month apart to determine the type of parasite and to confirm your pet is rid of them. Selecting the appropriate dewormer for the type of parasite, and treating the pet until the parasites are completely resolved is a crucial part of decreasing GI inflammation and preventing full-blown IBD.

By the time these unfortunate pups are seen at my practice, they are over 16 weeks old, with intermittent soft stools indicating GI inflammation, and they typically still have a parasite problem which requires treatment before any other symptoms can be resolved.

Another Root Cause – Antibiotics and Steroids

Another of my frustrations is that animals with low-grade GI inflammation are treated with antibiotics by the traditional veterinary community.

Antibiotics are a second common trigger for inflammatory bowel disease.

GI antibiotics kill the healthy bacteria right along with the bad guys. When all bacteria is obliterated from your pet’s gut, the regrowth often results in an imbalance featuring too many gram-negative, unhealthy bacteria or opportunistic yeast and not enough of the friendly variety. This is the definition of dysbiosis.

Now we have a 16+ week old puppy or kitten that has had several weeks of GI inflammation, ineffective deworming treatments, one or two rounds of antibiotics which have obliterated all the bacteria in his GI tract, and no re-seeding of bacteria with an appropriate probiotic to insure a healthy balance.

This little guy is well on his way to low-grade GI inflammation and IBD.

I’ve also seen dogs and cats that at six months of age are already on Prednisone therapy for GI inflammation. Prednisone is an immunosuppressive steroid, which turns the immune system down or completely off, wiping out troublesome symptoms and giving the appearance of a ‘cure.’ Unfortunately, this treatment doesn’t do a thing to uncover the root cause of the GI inflammation and ultimately postpones true healing.

A Third Culprit: Food Intolerance

In my practice I see many pets brought in for intermittent soft-to-watery stools, a situation many pet parents dub ‘sensitive stomach.’

Typically, this ‘sensitive stomach’ means the dog or cat cannot undergo any sort of dietary change without major GI consequences. This isn’t what nature had in mind when it built your favorite furry friend.

Just as you are designed to eat different foods at every meal without GI disturbance, pets with healthy, resilient GI tracts should be able to tolerate changes in the food they eat without negative consequences.

Probably more than half the pet owners I talk to assume it’s normal for their dog or cat to have GI sensitivity to changes in diet. But what’s really going on is the animal’s gut is in some way compromised and therefore cannot withstand dietary variety. It could be a low-grade inflammation that has been present for weeks, months or even years by that time.

Food intolerance or sensitivity can begin with a poor quality, non-species appropriate diet – one that is high in unnecessary carbohydrates. Processed pet food containing a lot of corn, wheat or rice can create inflammation in the gut of your carnivorous dog or cat, designed to digest meat – not grains.

I also have clients that feed a raw, species-appropriate diet without carbohydrates, which is wonderful, except they feed the same protein source for weeks, months or years.

Many animals (including humans) develop hypersensitivity to a food they eat over and over again. Inflammation is the result and can lead to IBD.

So overfeeding too much of even the right foods can lead to problems in the digestive tract.

Testing for IBD

There are two different diagnostic tests that are commonly done to detect IBD.

One test is what is known as a ‘confirming’ test, in which a biopsy is taken to assess morphologic characteristics common in the GI tracts of animals with inflammatory bowel disease. This is not my first choice because it’s expensive, invasive and involves anesthesia and the inherent risks that come with it.

The other test, which I use often in my practice, is a functional gastrointestinal test using a blood sample.

What we’re looking for with this test is two types of B vitamin absorption, the first of which is folate. Folate is a water-soluble B vitamin that is not easily absorbed in the small intestine unless it is deconjugated there.

If your pet’s small intestine can’t deconjugate folate, meaning it can’t break it down into an absorbable form, she can end up folate-deficient, in which case her blood test will show low or suboptimal levels of folate.

A low folate level means either your pet’s assimilation and absorption of nutrients is poor, or her body is challenged by the deconjugation process, indicating a disease or disorder of the small intestine.

If your pet’s folate is high rather than low, it indicates another type of problem. Your pet’s small intestine contains a small amount of bacteria critical for the production and assimilation of certain B vitamins. If this bacteria blooms into an overgrowth, your pet can wind up with high folate levels and a condition known as SIBO – Small Intestinal Bacterial Overgrowth.

The second blood test I use to assess GI function involves another B vitamin called cobalamin, which is bound to protein.

Cobalamin is released from protein through a complex series of events that starts in the stomach and finishes in the small intestine.

If cobalamin levels are low, we can assume this complex process is not occurring optimally. Cobalamin levels are a measure of digestion. This condition of maldigestion can sometimes also involve the pancreas. The disorder is called EPI – Exocrine Pancreatic Insufficiency and can be diagnosed via another GI blood test called a TLI (Trypsin-like Immunoreactivity).

If you suspect your pet has IBD but you’re not interested in doing a biopsy at this point, ask your vet to perform functional GI testing to determine a diagnosis.

In my practice, I also do two additional functional tests, TLI and PLI, which assess pancreatic function. Secondary pancreatitis is a very common condition in IBD patients, so assessing your dog’s or cat’s pancreatic function is also important.

These functional GI tests are available through the gastrointestinal lab at Texas A&M University.

Dietary Recommendations for IBD

Upon diagnosis, your veterinarian will probably tell you to feed a bland diet if your pet is symptomatic with vomiting, diarrhea or soft stool with mucus and/or blood.

My idea of a bland diet is different from a traditional veterinarian’s. I recommend ground cooked turkey and canned pumpkin or cooked sweet potato. I don’t recommend the traditional beef and rice. Beef is high in fat, which can exacerbate GI inflammation and pancreatitis.

Rice is a complex carb which can be fermented in the GI tract, causing gas, which can lead to additional digestive upset.

I recommend a grain-free, bland diet because in my experience it’s more suitable to pets with active symptoms of IBD.

While feeding your dog or cat a bland diet, you should be thinking about what’s next for her in terms of nutritional requirements. Bland is fine for a short time, but balance in the diet is crucial

I recommend you work with an integrative veterinarian to select a novel protein source — one your pet has either never consumed or hasn’t for a long while. This will give the GI tract and your pet’s immune system a good rest.

You’ll also want to select a novel vegetable or fiber source as well, to create an anti-inflammatory menu that will facilitate healing within both the large and small intestine.

An integrative vet can help you build a comprehensive protocol for your pet that addresses not only dietary issues, but also vaccinations, the use of drug therapy, and any potential toxins in your pet’s environment or lifestyle that could be contributing to unaddressed inflammation.


Connie’s notes: We start with cleansing and then nourishment. Do drink raw carrots juice with garlic and ginger. Limit refined foods, sugar, alcohol, smoking and unhealthy fats/trans fat. Email motherhealth@gmail.com for personal health coaching.

https://www.pxscanner.com/content/microsites/pxscanner/en_US/purchase/01103891.html

NANO CARROT

Pineapple, celery, carrots and Arthritis

arthritisYellow colored fruits and veggies contain sulfur which are cleansing to the body. The enzymes in pineapple and papaya help in breaking down fats and unwanted material in the body. Eat them with meat.

Lemon is rich in Vitamin C, an important vitamin in many chemical processes in the body. Vit C reduces tumor growth and promotes absorption of many important nutrients for the body.

Celery is a plant. The fruit and seeds are dried or pressed into oil for use as medicine. Sometimes celery oil is marketed in capsule form. Some people also take celery juice as medicine. The ancient Greeks used celery to make wine, which was served as an award at athletic games.
Celery is used to treat joint pain (rheumatism), gout, hysteria, nervousness, headache, weight loss due to malnutrition, loss of appetite, and exhaustion. Celery is also to promote relaxation and sleep; to kill bacteria in the urinary tract; as a digestive aid and for regulating bowel movements; to start menstruation; to control intestinal gas (flatulence); to increase sexual desire; to reduce the flow of breast milk; for stimulating glands; treating menstrual discomfort; and for “blood purification.”

How does it work?

It is thought that the chemicals in celery act to cause sleepiness, increase urine to decrease fluid retention, decrease arthritis symptoms, decrease blood pressure, decrease blood sugar, decrease blood clotting, and muscle relaxation.