Friday, October 20, 2017


Aloe Skin Cancer

Research Finds Aloe Vera May Prevent and Treat Skin Cancer

Posted on: Friday, December 21st 2012 at 5:00 am
This article is copyrighted by GreenMedInfo LLC, 2017

Research from the University of Belgrade School of Medicine has confirmed what other recent studies have been finding – that Aloe vera and its constituents inhibit the process of skin cell proliferation that accompanies skin cancer.
The researchers tested Aloe-emodin, a constituent of Aloe, with human skin cells – keratinocytes – after being treated with radiation. Once radiated, keratinocytes will typically proliferate in the process of forming skin tumors.
The researchers found that the Aloe-emodin significantly stopped the proliferation process. This confirmed Aloe's benefit in halting the progression of tumor formation after radiation by the sun.
This study confirms other recent findings. Researchers from South Korea's Gachon University of Medicine and Science found that Aloe-emodin specifically halted the growth of human cancerous liver cells. The researchers found that Aloe-emodin stimulated a genetic change within the cancerous cells that not only halted their expansion, but induced cell death among tumor cells.
In 2010, researchers from the China Medical University found this anticancer effect was not exclusive to Aloe's Aloe-emodin. The researchers found that Aloe constitents Emodin and Rhein also produced anticancer effects, which included the halting of tumor progression and cell death among cancer cells.
The research actually found this anticancer effect was greater with Emodin, as compared with Aloe-emodin and Rhein. But Aloe-emodin was observed having stronger cell repair abilities – for those cells that had not become cancerous.

This illustrates what researchers from the Pharmacy School of the University of Belgrade found in another study: "Although isolated plant compounds have a high potential in protection of the skin, whole herbs extracts showed better potential due to their complex composition," the scientists concluded.
These studies of human cells confirm similar findings in animal research - showing the application of Aloe vera gel onto the skin significantly inhibits the progression of skin cancer.
The research also has found that Aloe stimulates the production of melanins and other protective factors that protect the skin from radiation and the progression of tumorous cells.
The gel of the Aloe leaf and its other plant parts contain many constituents outside of those tested in these studies, including quercetin, luteolin, apigenin, kaempferol, isoorientin, isovitexin, saponarin, lutonarin, chlorogenic acid, pectic acid, caffeic acid, 5-P-coumaroylquinic acid, caffeoylshikimic acid, feruloylquinic acid, coumaric acid, ferulic acid, as well as glycosylchromone aloeresin B, and aloin, which is a precursor to Aloe-emodin. This mix of polyphenols, glucans and glucomannans, and alkaloids give Aloe its tremendous anti-inflammatory and antioxidant properties, along with its ability to stimulate healing.

In 2007, a Washington, D.C. panel of doctors and skin specialists conducted a review – the Cosmetic Ingredient Review – to study the safety of Aloe vera extracts in consumer products. The research found that some of the extracts – particularly those with higher levels of anthraquinones – should be ingested or applied to the skin with some level of caution and professional advice, especially for those with sensitive skin. Aloe-emodin and Emodin are both anthraquinones.
This must be considered together with the many findings that have illustrated that whole plant herbs are safer than extracts because they contain numerous buffering agents that balance the effects of the plant's active constituents.
Whole Aloe gel is easily taken from the Aloe leaf by taking a cutting and peeling off its outer skin. This gel can be applied directly to the skin. The Aloe vera plant is easy to cultivate at home and grows well both indoors and outdoors – though it likes a warm environment and full sun. It is more than irony that Aloe grows best in sunny areas.

  • Popadic D, Savic E, Ramic Z, Djordjevic V, Trajkovic V, Medenica L, Popadic S. Aloe-emodin inhibits proliferation of adult human keratinocytes in vitro. J Cosmet Sci. 2012 Sep-Oct;63(5):297-302.
  • Cosmetic Ingredient Review Expert Panel. Final report on the safety assessment of AloeAndongensis Extract, Aloe Andongensis Leaf Juice,aloe Arborescens Leaf Extract, Aloe Arborescens Leaf Juice, Aloe Arborescens Leaf Protoplasts, Aloe Barbadensis Flower Extract, Aloe Barbadensis Leaf, Aloe Barbadensis Leaf Extract, Aloe Barbadensis Leaf Juice,aloe Barbadensis Leaf Polysaccharides, Aloe Barbadensis Leaf Water, Aloe Ferox Leaf Extract, Aloe Ferox Leaf Juice, and Aloe Ferox Leaf Juice Extract. Int J Toxicol. 2007;26 Suppl 2:1-50.
  • Saini M, Goyal PK, Chaudhary G. Anti-tumor activity of Aloe vera against DMBA/croton oil-induced skin papillomagenesis in Swiss albino mice. J Environ Pathol Toxicol Oncol. 2010;29(2):127-35.
  • Jeon W, Jeon YK, Nam MJ. Apoptosis by aloe-emodin is mediated through down-regulation of calpain-2 and ubiquitin-protein ligase E3A in human hepatoma Huh-7 cells. Cell Biol Int. 2012 Feb;36(2):163-7.
  • Chen YY, Chiang SY, Lin JG, Yang JS, Ma YS, Liao CL, Lai TY, Tang NY, Chung JG. Emodin, aloe-emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 human tongue cancer cells. Anticancer Res. 2010 Mar;30(3):945-51.
  • Korać RR, Khambholja KM. Potential of herbs in skin protection from ultraviolet radiation. Pharmacogn Rev. 2011 Jul;5(10):164-73.

Case Adams is a California Naturopath, board-certified by the American Alternative Medical Association as an Alternative Medical Practitioner, with a Ph.D. in Natural Health Sciences and a degree in Naturopathy. He is a traditional naturopath - not a licensed medical doctor. His focus is upon researching, writing about and authenticating traditional therapies with clinical evidence. He is the author of 26 books on natural health. His books can be found on Heal Naturally - and many are available for immediate download on GreenMedinfo's book library. Contact Case at
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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Natural Substances that Fight Malignant Melanoma

Natural Substances that Fight Malignant Melanoma

Posted on: Monday, October 16th 2017 at 3:00 pm
This article is copyrighted by GreenMedInfo LLC, 2017

Conventional medicine offers little hope in the fight against deadly malignant melanoma, but there are multiple foods, botanicals, and vitamins with proven anti-melanoma activity within nature’s pharmacopeia
Cutaneous malignant melanoma, one of the most aggressive types of tumors, accounts for 75% of death due to cancer, and its incidence is on the rise worldwide (1, 2). In North America, it has become the most prevalent form of cancer for the demographic aged 25 to 29 (3). When detected early, surgical excision of the primary site is the standard of care. However, metastatic melanoma, wherein the tumor cells detach from the primary growth and disseminate to distant organs, is notoriously resistant to conventional radiation, immunotherapy, and chemotherapy (3).
Even after surgical removal, recurrence is a distinct possibility, and therapies employed by the biomedical paradigm have limited success (4). Commonly employed treatments include the DNA alkylating chemotherapeutic agent, dacarbazine, which have response rates of 10 to 26%, most of which are partial, and are accompanied by side effects including anemia, nausea, neutropenia, and thrombocytopenia (5). More selective therapies such as BRAF inhibitors, targeted for the small percentage of advanced melanoma patients with a genetic BRAF V600 mutation, are associated with widespread resistance and the development of other cancers, including keratoacanthoma and squamous cell carcinoma, as side effects (6).
For metastatic melanoma, the five-year survival rate is dismal at less than 25% (6). However, there are evidence-based natural substances supported by the scientific literature for their anti-melanoma effects, which may be used as an adjunctive approached alongside other multi-pronged strategies.
Although regarded in modernity as a pesky garden weed, dandelion, or Taraxacum officinale, has long been a staple of traditional Chinese, Middle Eastern, and Native American folk medicine (3, 7, 8). It has been used by traditional medical systems for digestive, kidney, liver, and spleen disorders, as well as tumors of the lung, breast, and uterus (7). Dandelion is renowned in holistic medicine as a detoxifying agent, but is also anti-inflammatory, anti-oxidant, anti-angiogenic (prevents growth of blood vessels that supply tumors with nutrients), anti-nociceptive (attenuates sensation of pain), and anti-cancer (3).
Studies have demonstrated that dandelion transforms mouse melanoma cells from a proliferative phenotype, which epitomizes the profligate cell division of cancer growth, to a differentiated phenotype representative of restoration of a normal cell cycle (9, Salem et al., 2004). Lupeol-a, the triterpene compound in dandelion found to elicit this effect, is cytostatic, meaning that it inhibits cell growth and multiplication (9).
Taraxacum japonicum, a species of dandelion native to Japan, has also been shown to suppress two stages of carcinogenesis, namely, tumor initiation and promotion (10). It was concluded that a triterpenoid compound called taxasterol within dandelion is a chemopreventative, meaning an agent that slows or prevents the development of cancer (10). In an in vitro study, researchers propose that dandelion root extract represents a novel chemotherapeutic agent, as it selectively induced apoptosis, or programmed cell death, in human melanoma cells, while preserving noncancerous cells (3). Not only do healthy cells remain unaffected, but “melanoma cells retain the signals to commit suicide long after DRE [dandelion root extract] has been removed from the system” (3).
According to researchers, various compounds in dandelion root, including triterpenes, sesquiterpenes, coumarins, and phenolic compounds likely work synergistically to invoke anti-cancer effects (3). They conclude, “We believe that this nontoxic extract can undergo precipitous translation from bench top to bedside, with dandelion products that are already commercially available in the form of tea and supplements…as a chemotherapeutic against aggressive chemoresistant cancers” (3). For those with ragweed allergies, however, caution may be warranted because dandelion can be cross-reactive since they both reside in the Asteraceae (Compositae) family.
UV-induced sunburn lesions, which represent a potent risk factor for melanoma, are inhibited by caffeine, which elicits a sunscreen-like effect in rodent studies (1). Not only does caffeine suppress growth of melanoma cells in vitro and in vivo, but it also up-regulates cell suicide, also known as apoptosis, induced by UV exposure (1). This effectively enhances clearance of defective precancerous cells (1).
One epidemiological study compiled data from 74,666 women in the Nurses' Health Study, 89,220 women in the Nurses' Health Study II, and 39,424 men in the Health Professionals Follow-up Study, comprising over 4 million person-years of follow-up (1). After adjusting for confounding variables, it was found that a high caffeine intake (≥ 393 mg/day) was associated with a lower risk of cutaneous malignant melanoma than a low intake (< 60 mg/day) (1). This correlation was particularly prominent in women, where high caffeine intake decreased risk by 22% relative to low intake (1).
The inverse relationship between caffeine intake and melanoma risk was likewise more apparent for melanomas occurring on anatomic sites such as the head, neck, and extremities, which receive greater sun exposure, compared to sites on the trunk normally insulated from the sun (1).
A staple in traditional Ayurvedic and Unani medical systems, ashwagandha or Withania somnifera is an adaptogenic herb that increases non-specific resistance to chemical, biological, and physical insults, enhances survival during stress, and counteracts pathology (11). It has historically been used to augment energy and to treat musculoskeletal conditions such as arthritis and rheumatism (12). In addition to its anti-stress effects, ashwagandha is classified as an antioxidant, anti-parkinsonism, anti-ageing, antiulcerogenic, and anti-tumor agent (Halder et al., 2015). In fact, it exhibits anti-tumor effects in human breast, prostate, renal, pancreatic, fibrosarcoma, leukemia, and mouse lung adenoma cells (13).
Notably, a crude water extract of ashwagandha reduced viability of human malignant melanoma cells in a dose- and time-dependent manner (13). Morphological changes in ashwagandha-treated cells appeared, such as formation of apoptotic bodies, nuclear blebbing, and DNA fragmentation, indicating that ashwagandha induced programmed cell death in melanoma cell lines (13). The authors conclude that the ashwagandha extract exhibited a potent chemotherapeutic effect, or cytotoxic effect, on human malignant melanoma cells (13).
Not just limited to holiday romance, the festive plant mistletoe, a hemiparasitic evergreen shrub, is routinely used in complementary cancer therapy in Central Europe (14). Since ancient times, it has been perceived as a mystical plant and was used for ailments of the spleen and kidney in the middle ages (15). Mistletoe likewise demonstrates anti-hypertensive, anti-rheumatic, anti-diabetic, and antioxidant effects, but since the early twentieth century, it has been used as a cancer therapy (15).
Although human trials are conflicting, in vivo and in vitro studies have highlighted anti-tumor effects of mistletoe against acute lymphoblastic leukemia, various carcinomas, and melanoma cells (15, 16, 17). In addition, mistletoe has prolonged survival in patients with pancreatic cancer as well as breast and gynecological cancers in human studies (18). One systematic review analyzed 23 controlled clinical trials of mistletoe in cancer, including cancers of the bladder, breast, colon, genital, head and neck, kidney, lung, and stomach, as well as gliomas and melanoma (19). Although results were mixed and heterogeneity of studies was identified, statistically significant increases in survival and quality of life were reported in eight and three trials, respectively (19).
In another review, 22 of 26 randomized controlled trials (RCTs) and all 10 of 10 non-RCTs analyzed reported that mistletoe improved quality of life in patients with malignant disease (20). Mistletoe likewise reduces the side effects of conventional cytoreductive treatments (20). When used in concert with conventional treatments, mistletoe consistently improved “coping, fatigue, sleep, exhaustion, energy, nausea, vomiting, appetite, depression, anxiety, ability to work, and emotional and functional well-being in general” (20, p.142).
Especially relevant to cancer is the immunomodulatory effect of mistletoe extract, as mistletoe can enhance both humoral (antibody-mediated) and cellular immune responses when injected into cancer patients (21), potentially increasing the ability of the immune system to eliminate cancer. In fact, in a mouse melanoma model, mistletoe exerted its anti-cancer effects by promoting secretion of a signaling molecule called interleukin-12 (IL-12), which causes immune cells in the spleen to proliferate (22), up-regulating immune defenses against cancer. Also, researchers state that, “Polysaccharides present in the herb and in berries increased phagocytic activity of granulocytes and macrophages in in vitro experiments,” which increases the ability of immune cells to eat and dispose of defective or neoplastic cells (15, p. 378)
It is hypothesized that water soluble mistletoe lectins are the active anti-cancer constituents in the plant, along with polysaccharides, phenolic compounds, and viscotoxins (14, 23). Lectins in particular induce programmed cell death, or apoptosis, in cancer cell lines, and exhibit direct cytotoxic (cancer cell killing) activity (15). Commercial methods of aqueous mistletoe purification are not able to extract water insoluble triterpenoids, which have anti-melanoma effects (24).
However, one mouse study using a novel method to produce triterpenoid-enriched mistletoe extracts found that this variety amplified the anti-tumor effects of mistletoe (14). Compared to the control group, which had a dense network of blood vessels surrounding the tumor, the mistletoe extract and solubilized triterpenoids elicited anti-angiogenic effects, causing blood vessels around the tumor to collapse, preventing delivery of nutrients to the tumor (14). In this model, mistletoe extracts led to the significant suppression of tumor growth, which was further enhanced by combined treatment with triterpenoids (14).
Broccoli Sprouts
Sulforaphane is an isothiocyanate compound found in all cruciferous vegetables, such as arugula, broccoli, Brussel sprouts, cabbage, cauliflower, chard, collard greens, radish, rutabaga, turnip, wasabi, and watercress. However, it is particularly concentrated in broccoli sprouts, which contain 10 to 100 times the glucoraphanin content of the mature plants, which is a glucosinolate of sulforaphane (25). In vitro and in vivo models demonstrate that sulforaphane induces apoptosis, or cell suicide, in melanoma cells, as indicated by predictable morphological changes that occur with cell death, such as condensation and fragmentation of genetic material and a step in cellular disassembly called membrane blebbing (26).
In an animal model, when sulforaphane was administered simultaneously with melanoma development, “There was 95.5% inhibition of lung tumour nodule formation and 94.06% increase in the life span of metastatic tumour bearing animals” (27). At a mechanistic level, sulforaphane prevented invasion of melanoma cells to secondary sites by inhibiting the activation of matrix metalloproteinases (MMPs), enzymes which hydrolyze, or degrade extracellular proteins such as collagens and elastin and allow for tumors to migrate (27).
The researchers conclude, “These results raise the possibility that SFN [sulforaphane] may be a promising candidate for molecular-targeting chemotherapy against melanoma” (26, p. 332).
Vitamin C
Gonzalez and colleagues (2012) proposed the revolutionary bioenergetic theory of carcinogenesis, which posits that cancer originates when cells revert to a more primitive phenotype favoring uncontrolled proliferation and cell immortalization (28). This occurs as an adaptive response to ensure survival in the harsh cellular milieu and toxic external environment that so drastically departs from the one in which we evolved (28).
Cancer cells resort to inefficient energy production via cytosol-based glycolysis instead of the mitochondrial-based, oxygen-dependent oxidative phosphorylation, which is the primary generator of energy currency in the body (29). One reason malignant cells switch to fermentation, or anaerobic (oxygen-independent) processes for energy production, is due to defective mitochondrial membrane potential, which can be corrected by vitamin C (29).
In this respect, ascorbate, the water-soluble vitamin C, may be helpful by increasing electron flux through the mitochondria, restoring energy production such that apoptosis of cancer cells, which is an energy-intensive process, can occur (29). Vitamin C also optimizes cellular differentiation and intercellular communication, both of which are compromised in a cancerous state and perpetuate tumor growth (29).
Further, vitamin C up-regulates the proliferation and activity of lymphocytes, or white blood cells, and prevents oxidative damage that would engender further mitochondrial dysfunction (30, 31). In addition, vitamin C increases the anti-malignancy effects of lysosomes, the ‘garbage disposal’ organelles that reside within white blood cells, which control cell death and survival and render cancer cells vulnerable to death pathways (32, 33).
Likewise, vitamin C promotes collagen formation, which can sequester tumors, inhibit their growth, and prevent tumor metastasis (30). Along the same lines, vitamin C interferes with the action of hyaluronidase, an enzyme which degrades connective tissue and allows tumors to spread, in order to wall off the tumor with ground substance (30).
Remarkably, high concentrations of vitamin C are selectively toxic to tumors but not to normal tissues (6). In particular, it elicits anti-cancer effects by facilitating the formation of hydrogen peroxide (a reactive oxygen species) in the extracellular space, which can produce other free radicals such as aldehydes and hydroxyl radicals that in turn jeopardize cell viability (34). Hydrogen peroxide not only generates double-stranded DNA breaks, which induces death of cancer cells, but it also recruits immune cells to the site of the tumor to eliminate cancer cells (35, 36). Whereas normal cells have adequate levels of catalase, an enzyme to detoxify hydrogen peroxide and prevent cellular damage, malignant cells are deficient in this antioxidant enzyme, harboring 10 to 100 fold less catalase content than healthy cells (37).
In the 1970s, Nobel Prize winner Linus Pauling conducted experiments demonstrating that high dose vitamin C therapy elongated survival of cancer patients by four times compared to controls (38). In another study, “all melanoma cell lines were susceptible to ascorbate-mediated cytotoxicity,” and “pharmacologic ascorbate was superior or equivalent to dacarbazine as an anti tumor agent” (6, p. 193). In mouse melanoma cells, ascorbic acid induced apoptosis by acting as a pro-oxidant and increasing intracellular levels of reactive oxygen species, which disrupted membrane potential and lead to cell death (39).

Researchers state, “While AA [ascorbic acid] alone may not be enough of an intervention in the treatment of most active cancers, it appears to improve quality of life and extend survival and it should be considered as part of the treatment protocol for all patients with cancer” (29, p. 31). Intravenous vitamin C is optimal, as oral supplementation is unlikely to generate plasma concentrations required to kill tumor cells (37). The combination of vitamin C with other mitochondrial support such as B vitamins, magnesium, coenzyme Q10 (CoQ10), acetyl L-carnitine, alpha lipoic acid, pyrroloquinoline quinone (PQQ), D-ribose, creatine, and phospholipids, would be ideal for reversing the metabolic derangements observed in cancer (38, 40).
Polyphenols, which represent secondary metabolites of plants that evolved as defense mechanisms against pests and ultraviolet radiation, confer protection from cardiovascular disease, diabetes, osteoporosis, neurodegenerative disorders, and cancers (41). Catechin, a polyphenol in green tea, has been elucidated to render collagen resistant to degradation by the mammalian enzyme collagenase (42). Therefore, researchers tested various polyphenols to see if they could inhibit the basement membrane degradation that is essential to melanoma metastasis to the lungs (43).
For metastasis to take place, tumor cells must be liberated from the primary tumor into circulation, adhere to the extracellular matrix, and invade a secondary site via the proteolytic cleavage of the basement membrane, or the fibrous layer of connective tissue that divides epithelial cells from the underlying lamina propria (43). Finally, the malignant cells attach to the secondary site and tumor growth resumes (43). However, metastasis could be arrested if any one of the steps in this sequential process were prevented (43).
In this experiment, curcumin, from the spice turmeric, and ellagic acid, which is abundant in red grapes, were directly toxic towards melanoma cells even at low concentrations, indicating their anticarcinogen potential (43). Further, many of the polyphenols significantly reduced melanoma metastasis to the lungs, with curcumin, catechin, rutin (from figs, apples, and tea), epicatechin (from dark chocolate), and naringin and naringenin (from grapefruit) reducing lung tumor colonies by 89.28%, 82.2%, 71.2%, 61%, 27.2%, and 26.1%, respectively (43). In order of appearance, these polyphenols increased lifespan of animals by 142.85%, 80.81%, 63.59%, 55.29%, 26.6%, and 27.18% (43).
The best strategy would be to obtain polyphenolic compounds from whole foods sources in order to obtain the synergistic effects of other active constituents. As a general rule, the deeper pigmented the fruit or vegetable, the higher the polyphenolic content. Polyphenols inhibit cancer through pleiotropic mechanisms, including “estrogenic/antiestrogenic activity, antiproliferation, induction of cell cycle arrest or apoptosis, prevention of oxidation, induction of detoxification enzymes, regulation of the host immune system, anti-inflammatory activity and changes in cellular signaling” (41).
Sun Exposure
For those with a family history of melanoma interested in prevention, sun exposure is a contentious topic. According to researchers, “It has been documented that the role of sunlight in melanoma differs according to anatomic site, which is supportive of the hypothesis that melanomas may arise through divergent etiologic pathways” (1).
Although frequency of ultraviolet (UV) radiation-induced sunburns represents one of the primary risk factors for (44), the relationship between sun exposure and melanoma risk is convoluted. A longitudinal study tracking 38,000 women for 15 years, in fact, found that chronic sun exposure was protective against malignant melanoma, whereas intermittent sun exposure elevated melanoma risk (45). Contrary to popular belief, sun exposure was found to be protective, as it was also correlated with significantly reductions in cardiovascular and all-cause mortality (45). Therefore, habitual insulation from the sun is clearly deleterious, but safe sunning practices should still be observed to avoid burning and potential detriment.
Although human trials are deficient, people with cancer now cannot wait for research to be translated into clinical practice and adopted as standard of care. Given the nontoxic nature of the aforementioned interventions, they can easily be incorporated into the arsenal of modalities used to reverse cancer as elements of a multi-faceted approach that addresses diet, exercise, sleep, stress, social support, latent infections, hormonal balance, detoxification, and mitochondrial dysfunction.

1. Shaowei, W. et al. (2015). Caffeine Intake, Coffee Consumption, and Risk of Cutaneous Malignant Melanoma. Epidemiology, 26(6), 898-908.
2. Jerant, A.F., Johnson, J.T., & Caffrey, T.J. (2000). Early detection and treatment of skin cancer. American Family Physician, 62, 357-368.
3. Chatterjee, S.J. et al. (2010). The effect of dandelion root extract in inducing apoptosis in drug-resistant melanoma cells. Evidence Based Complementary and Alternative Medicine. doi: 10.1155/2011/129045
4. Soengas, M.S., & Lowe, S.W. (2003). Apoptosis and melanoma chemoresistance. Oncogene, 22(20), 3138-3151.
5. Chapman, P.B. et al. (1999). Phase III multicenter randomized trial of the Dartmouth regimen versus dacarbazine in patients with metastatic melanoma. Journal of Clinical Oncology, 17, 2745-2751.
6. Serrano, O.K. et al. (2015). Antitumor effect of pharmacologic ascorbate in the B16 murine melanoma model. Free Radical Biology Medicine, 86, 193-203. doi: 10.1016/j.freeradbiomed.2015.06.032.
7. Sigstedt, S.C. et al. (2008). Evaluation of aqueous extracts of Taraxacum officinale on growth and invasion of breast and prostate cancer cells. International Journal of Oncology, 32(5), 1085-1090.
8. Sweeney, B. et al. (2005). Evidence-based systematic review of dandelion (Taraxacum officinale) by natural standard research collaboration. Journal of Herbal Pharmcology, 5(1), 79-93.
9. Hata, K. et al. (2000). Differentiation-inducing activity of lupeol, a lupane-type triterpene from Chinese dandelion root (Hokouei-kon), on a mouse melanoma cell line. Biological and Pharmaceutical Bulletin, 23(8), 962-967.
10. Takasaki, M. et al. (1999). Anti-carcinogenic activity of Taraxacum plant. Biological and Pharmaceutical Bulletin, 22(6), 602-610.
11. Singh, N. et al. (1982). Withania somnifera (Ashwagandha) A rejuvenator herbal drug which enhances survival during stress (An adaptogen). International Journal of Crude Research, 3, 29-35.
12. Singh, N. et al. (1976). Evaluation of ‘adaptogenic’ properties of Withania somnifera. Proceedings of the Indian Pharmacological Society, 17.
13. Halder, B., Singh, S., & Thakur, S.S. (2015). Withania somnifera Root Extract Has Potent Cytotoxic Effect against Human Malignant Melanoma Cells. PLoS One, 10(9), e0137498.
14. Strüh, C.M. et al. (2013). Triterpenoids Amplify Anti-Tumoral Effects of Mistletoe Extracts on Murine B16.F10 Melanoma In Vivo. PLoS One, 8(4), e621688. doi: 10.1371/journal.pone.0062168
15. Nazaruk, J., & Orlikowski, P. (2016). Phytochemical profile and therapeutic potential of Viscum album L. Natural Product Resaerch, 30(4), 373-385.
16. Thies, A. et al. (2005). Influence of mistletoe lectins and cytokines induced by them on cell proliferation of human melanoma cells in vitro. Toxicology, 207, 105–116.
17. Thies, A. et al. (2008). Low-dose mistletoe lectin-I reduces melanoma growth and spread in a scid mouse xenograft model. British Journal of Cancer, 98, 106–112.
18. Kienle, G.S. et al. (2009). Viscum album L. extracts in breast and gynaecological cancers: a systematic review of clinical and preclinical research. Journal of Experimental Clinical Cancer Research, 28(1), 79. doi:10.1186/1756-9966-28-79.
19. Kienle, G.S. et al. (2003). Mistletoe in cancer - a systematic review on controlled clinical trials. European Journal of Medical Research, 8(3), 109-119.
20. Kienle, G.S., & Kiene, H. (2010). Review article: Influence of Viscum album L (European mistletoe) extracts on quality of life in cancer patients: a systematic review of controlled clinical studies. Integrateve Cancer Therapies, 9(2), 142-157. doi: 10.1177/1534735410369673.
21. Gardin, N.E. (2009). Immunological response to mistletoe (Viscum album L.) in cancer patients: a four-case series. Physiotherapy Research, 23(3), 407-411. doi: 10.1002/ptr.2643
22. Duong Van Huyen, J-P. et al. (2006). Interleukin-12 is associated with the in vivo anti-tumor effect of mistletoe extracts in B16 mouse melanoma. Cancer Letters, 243(1), 32-37. doi: 10.1016/j.canlet.2005.11.016
23. Beuth, J. (1997). Clinical relevance of immunoactive mistletoe lectin-I. Anticancer Drugs, 8(Suppl 1), S53-S55.
24. Jäger, S. et al. (2007). Solubility studies of oleanolic acid and betulinic acid in aqueous solutions and plant extracts of Viscum album L. Planta Medicine, 73, 157-162.
25. Fahey, J.W., Zhang, Y., & Talalay, P. (1997). Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proceedings of the National Academy of Sciences (USA), 94, 10367-10372.
26. Hamsa, P. T., Thejass, P., & Kuttan, G. (2011). Induction of apoptosis by sulforaphane in highly metastatic B16F-10 melanoma cells. Drug Chemistry and Toxicology, 34(3), 332-340.
27. Thejass, P., & Kuttan, G. (2006). Antimetastatic activity of sulforaphane. Breast Cancer Research Treatment, 99(3), 333-340.
28. Gonzalez, M.J. et al. (2012). The bio-energetic theory of carcinogenesis. Medical hypotheses, 79(4), 433-439.’
29. Gonzalez, M.J. et al. (2010). Mitochondria, energy and cancer: The relationship with Asocrbic acid. Journal of Orthomolecular Medicine, 25, 29-38.
30. Cameron, E., Pauling, L., & Leibovitz, B. (1979). Ascorbic acid and Cancer: a review. Cancer Research, 39, 663-681.
31. Dumitrescu, C., Belgun, M., & Olinescu, R. (1993). Effect of vitamin administration on the ratio between the pro- and antioxidative factors. Romanian Journal of Endocrinology, 21, 81-84.
32. Kirkegaard, T., & Jäättelä, M. (2009). Lysosomal involvement in cell death and cancer. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1793(4), 746-754.
33. Sakagami, H., & Satoh, K. (1997). Modulating factors of radical intensity and cytotoxic activity of ascorbate (review). Anticancer Research, 17, 3513-3520.
34. Benade, L., Howard, T., & Burke, D. (1969). Synergistic killing of Ehlrich ascites carcinoma cells by ascorbate and amino 1,2,4-triazole. Oncology, 23, 33-43.
35. Frankenberg-Schwager, M. et al. (2008). The role of non homologous DNA end joining, conservative homologous recombination, and single-strand annealing in the cell cycle-dependent repair of DNA double-strand breaks induced by H(2)O(2) in mammalian cells. Radiation Research, 170, 784-793.
36. Hara-Chikuma, M. et al. (2012). Chemokine-dependent T cell migration requires aquaporin-3-mediated hydrogen peroxide uptake. Journal of Experimental Medicine, 209, 1743-1752.
37. Riordan, N.H. et al. (1995). Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent. Medical Hypotheses, 44, 207-213.
38. Zeviar, D.D., et al. (2014). The role of mitochondria in cancer and other chronic diseases. Journal of Orthomolecular Medicine, 29(4), 157-166.
39. Kang, J.S. et al. (2003). L-ascorbic acid (vitamin C) induces the apoptosis of B16 murine melanoma cells via a caspase-8-independent pathway. Cancer Immunology and Immunotherapies, 52, 693-698.
40. Parikh, S. et al. (2009). A modern approach to the treatment of mitochondrial disease, 11(6), 414-430.
41. Pandey, K.B., & Rizvi, S.I. (2009). Plant polyphenols as dietary antioxidants in human health and disease. Oxidative Medicine and Cell Longevity, 2(5), 270-278.
42. Kuttan, R., Donnelly, P.V., & Di Ferrante, N. (1981). Collagen treated with (+)-catechin becomes resistant to the action of mammalian collagenase. Experientia, 37, 221-223.
43. Menon, L.G., Kuttan, R., & Kuttan, G. (1995). Inhibition of lung metastasis in mice induced by B16F10 melanoma cells by polyphenolic compounds. Cancer Letters, 221-225.
44. Cho, E. et al. (2005). Risk factors and individual probabilities of melanoma for whites. Journal of Clinical Oncology, 23, 2669-2675.
45. Berwick, M. (2011). Can UV exposure reduce mortality? Cancer Epidemiology and Biomarkers Prevention, 20(4), 582-584.

Ali Le Vere holds dual Bachelor of Science degrees in Human Biology and Psychology, minors in Health Promotion and in Bioethics, Humanities, and Society, and is a Master of Science in Human Nutrition and Functional Medicine candidate. Having contended with chronic illness, her mission is to educate the public about the transformative potential of therapeutic nutrition and to disseminate information on evidence-based, empirically rooted holistic healing modalities. Read more at @empoweredautoimmune on Instagram and at Science-based natural remedies for autoimmune disease, dysautonomia, Lyme disease, and other chronic, inflammatory illnesses.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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Thursday, October 19, 2017


Top 6 Ways to Heal Thyroid Disease

Top 6 Ways to Heal Thyroid Disease

Posted on: Thursday, October 19th 2017 at 7:30 am

Discover protocols that could lead you into thyroid disease remission.
I didn’t always want to be a thyroid pharmacist!  In fact, I didn’t have much interest in the thyroid until my own thyroid diagnosis in 2009. This diagnosis came after almost a decade of some pretty life-altering symptoms. I was so fatigued I had to sleep for 12 hours each night just to feel human. My sharp mind that kept me on the honor roll during my doctorate program studies was not so sharp anymore! I began to have brain fog and started being forgetful… and then there was the intense anxiety…
I remember levels of anxiety so bizarre that my husband couldn’t go for a jog without me thinking he’d been hit by a car or left with some woman!
I was in pain pretty much everyday, and I ended up being diagnosed with carpal tunnel in both arms. I wore braces on my arms and eventually had to resign from my job because it involved too much computer time. I had irritable bowel syndrome and acid reflux and went to so many doctors, I felt like I had more doctors visits than visits with friends!
Some doctors told me that there was nothing wrong with me, other doctors said it was all in my head and suggested antidepressants, other doctors told me that everyone was tired and stressed. One of the most amusing answers I got from a health care professional was “You’re just getting older”.
Did I mention that I was only 25 years old at the time?
When I first got my diagnosis, I finally felt validated, but sadly, the doctors still didn’t have many solutions for me. I was prescribed synthetic thyroid hormone (Synthroid, the #1 selling drug in the US in 2 of the last three years).
Taking medications wasn’t really a big deal for me, after all, I was a trained pharmacist. The only problem was that the medication didn’t do much for most of my symptoms- instead of sleeping 12 hours, I was only sleeping 11!  And it did absolutely nothing to address the underlying cause of my condition, which was an autoimmune attack against my thyroid gland!
Before my diagnosis, I was very skeptical towards natural healing, but I had exhausted my options in conventional medicine and knew there had to be more than what the doctors were telling me.  
I believe in cause and effect, and I couldn’t shake this feeling that all my symptoms were somehow connected. I felt like I was doing something to evoke these symptoms, but I was doing everything I knew to do to be healthy: exercising, eating low-fat dairy, and whole grains, yet I was very sick.
I took my pharmacy training and poured it into researching Hashimoto’s.
I came across the gluten and thyroid connection, and I found that people with Hashimoto’s antibodies who went on a gluten-free diet were eliminating thyroid antibodies within 3-6 months.
Their antibodies were no longer attacking their thyroid, and they’d normalized their thyroid function. Some of the people didn’t even need thyroid medications anymore. I was fascinated by this information, but I was trained that gluten-free diets were only beneficial for people with Celiac disease and I tested negative for Celiac.  I was so skeptical, that it took me about a year to go gluten-free because I wanted to research more studies and go to all these different specialists before I gave it a try.
When I finally decided to take a plunge and charge of my health, things started turning around really quickly.
I bit the bullet and did a food sensitivity test- and it was positive.
It was my wake-up call because now it was in black and white. I was sensitive to gluten and dairy. I removed both from my diet, and within three days my acid reflux was gone. After that, I became a convert to changing nutrition, looking at root causes of symptoms, and was able to eliminate all of my symptoms and reduce my thyroid antibodies! I dug through each layer and was eventually able to get into remission.
I want to share with everyone who has an autoimmune condition that there are root causes and triggers we can often identify.
Conditions like fibromyalgia, chronic fatigue syndrome, and Hashimoto’s are all friends. They predominantly affect women, and many women suffer on a daily basis when there’s a chance they could go into remission.
What is Hashimoto’s Thyroiditis?
Hashimoto’s sounds like an exotic disease, but it’s not. It’s so common that up to 27% of Americans and up to 34% of Italians may be affected.
Hashimoto's is the number one reason people have underactive thyroid in the United States, Europe, and most industrialized countries.
Depending on which estimates you look at, 97% of people who take thyroid medication for an underactive thyroid, actually have Hashimoto’s and they just don’t know it.
People hear they have a sluggish thyroid or they’re getting older when, in reality, they have an autoimmune condition. This means their immune system recognizes their thyroid as an enemy and starts attacking it. The continual attacks break down the thyroid gland.
Initially, some people may have symptoms of an overactive thyroid. They’ll experience anxiety, palpitation and they’ll be agitated. They might have hair loss and loose bowel movements.
Once the symptoms stabilize, they swing to the next spectrum of underactive thyroid. They won’t be able to lose weight. You’ll see people exercise and eat the same, yet continue to gain weight. This happens because the thyroid controls the metabolism.
Common Symptoms
Thyroid hormones affect every single cell in your body. There are hundreds of symptoms linked to having an underactive thyroid. In the surveys I’ve conducted, the top three biggest issues are trouble losing weight or holding onto excess weight, fatigue, and mood changes like brain fog, apathy or depression.
You might also experience cold intolerance. Let’s say you’re in Southern California on a beautiful day and everybody is wearing shorts, but you’re wearing a ski jacket. That’s a pretty solid sign something is off with your thyroid :-)
Women find the hair loss especially distressful. I remember not being able to keep the hair on my head! Every time you brush, more and more hair comes off.
Mood symptoms are very common and misdiagnosis of depression with anxiety often occurs. I’ve seen people hospitalized with bipolar disorder and psychosis because of overactive or underactive thyroid issues.
Others have reported less stressful symptoms like not sweating as much and not growing body hair, though most don’t complain about these symptoms!

What causes Hashimoto’s?
For Hashimoto’s to occur, three factors need to be present: the person has to have the right genes, the right trigger, and intestinal permeability. This has been described as the “three-legged stool of autoimmunity”. People who have the first leg of the stool, the genetic predisposition, will only develop autoimmunity if leg two and three are also present.
The trigger, or second leg, can be an infection, a toxin, a nutrient deficiency and even stress.  There are various potential “root causes”.
The third “leg” of the puzzle is intestinal permeability, also known as leaky gut. Many autoimmune conditions start with irritable bowel syndrome, acid reflux, bloating and constipation. These symptoms allude to intestinal permeability, although some people do not manifest any symptoms.
It takes a perfect storm for autoimmunity to develop. In most cases, people are under a significant amount of stress and stress weakens our immune systems. The body becomes more susceptible to toxins, infections and triggers and the breeding ground for autoimmunity is formed.
The exciting this is, if you remove one of these two legs, then Hashimoto’s goes into remission. Since you can’t remove your genes, we look at ways to remove the other two legs.
How is Hashimoto’s best diagnosed?
Unfortunately, a lot of doctors use a standard screening test known as the TSH test, otherwise known as thyroid stimulating hormone test. For years doctors kept telling me everything was normal, but when I got copies of my lab tests, I noticed the “normal” was an outdated range. In fact, my labs were showing that my numbers were in range for somebody with thyroid disease!
Researchers determined the normal TSH ranges by gathering blood work from a panel of “healthy” people. They measured the average, but there was a problem. Since thyroid disease is so common, many of the “healthy” people actually had undiagnosed thyroid disease.
Most people feel optimal when their TSH is between 0.5-2, but doctors may not notice unless a TSH is above 4.5. My doctor actually missed my hypothyroidism when my TSH was 4.5 and I was sleeping for 12 hours each day, I was told that my thyroid was just fine!.
The other problem with the TSH test is that it may not show changes until someone has had Hashimoto’s for 5-10 years.
The truth is, there are better tests you can do that will show if you have a thyroid condition. The best tests I recommend are the thyroid antibody tests. There are two, inexpensive tests you can request your doctor to administer. You’re testing thyroid peroxidase antibodies, known as TPO antibodies and the thyroglobulin antibodies, known as TG antibodies. These tests often reveal elevated levels 10 years before you see a change in your TSH.
I recommend everyone get tested for these. Depending on the statistics you look at, roughly 20%-30% of the population will have these kinds of antibodies. If you’re experiencing symptoms and you catch these antibodies early, before medications, you can avoid a lot of damage to your thyroid. You can prevent these symptoms and prevent taking medication for the rest of your life. You can also minimize the chances of developing other autoimmune conditions. These tests are worth it.
My recommendations: I encourage you to get a copy of your labs and get tested. I’m talking about a full panel and not just the TSH test because that test can be all over the place. The TSH test is not a direct measure of the autoimmune attack on your thyroid, and it’s not a direct measure of what’s actually happening inside your thyroid.

Transformative Hashimoto’s Protocols
If you only have thyroid antibodies, I would start with your diet. I’d look to see which foods are causing inflammation. Gluten, dairy, and soy are the biggest foods that confuse your immune system and cause it to attack your thyroid.
I’d recommend removing these three from your diet for at least three months. After three months, re-measure your antibodies, and see if there was an improvement. Usually, 10-20% of people that remove these foods see their antibodies go back to normal range. For some, food sensitivities are the root cause.
Others may have more than one root cause. It’s like peeling back an onion, layer by layer. I often find nutrient deficiencies, food sensitivities, infections, an impaired stress response, and an impaired ability to remove toxins as primary root causes.
#1 Nutrition
Proper nutrition is one of the foundations of recovering our health. Beyond gluten-free, I often recommend a nutrient dense diet like the Paleo or the autoimmune Paleo diet.
If you’re new to this community, all these diet ideas and protocols might sound like a lot. I encourage you to break it down into manageable steps. Start with nutrition by getting on a clean, anti-inflammatory diet, and make sure you’re eating organic. Everybody is different, so I recommend tailoring your diet as you go along as it’s a bit of a learning curve when you initially begin.
A lot of people go gluten-free and buy all this gluten-free junk food. It’s corn and rice based which then sets off the blood sugar swings. Blood sugar imbalance is another symptom associated with Hashimoto’s. People think they are eating healthy when it’s really fueling the antibody attack. I recommend people balance their blood sugar, eat good fats and healthy protein with every meal, and try to limit carbohydrates.
You can get better, but you have to be the one driving the car. As you begin changing your diet, pay attention to what you’re reacting to. The Elimination Diet does a great job of teaching you about your food sensitivities. I used to eat dairy multiple times a day, and I never knew it was harming me. Your body will tell you exactly what it needs and what causes issues. You’ll even get cravings when you’re deficient in nutrients. You can get in sync with your body so be kind to it because we only have one!
#2 Nutrient Deficiencies
Next, I look at different nutrient deficiencies. The top  deficiencies in Hashimoto’s are selenium, B12, and ferritin, which is a storage hormone for iron. Selenium deficiency is a trigger for Hashimoto’s.
Replenishing selenium helps alleviate anxiety and even balances blood sugar. Dosages of 200 mcg have been found to reduce thyroid antibodies by about 50% over a course of 3 months.
People with Hashimoto’s often have low stomach acid which can put them at risk for a deficiency in B12. Low levels of B12 can lead to anemia, impaired digestion, inflammation and underdevelopment of villi. Villi house our digestive enzymes. You can find this nutrient in proteins but not usually in plants. I recommend that vegans and vegetarians take a supplement to ensure they aren’t deficient.
The transport of T3 to cell nuclei and the utilization of the T3 hormone requires ferritin. It’s also the storehouse for iron. Our bodies don’t make iron so we must ingest it and when we do, it needs a place to live. When our levels of ferritin are low, you’ll see an increase in hair loss. I remember when I was deficient, I couldn’t keep my hair on my head!
#3 Adrenal Function and Your Mindset
A big player in thyroid function is adrenal function. Adrenals are tiny little glands that produce our stress hormones and alterations in these hormones are often found in Hashimoto’s.
Symptoms of stress hormone imbalance include, but are not limited to, feeling overwhelmed, tired despite adequate sleep, difficulty waking up in the morning, extreme salty food cravings, low blood pressure, feeling faint when getting up quickly, mental fog, alternating diarrhea/constipation, low blood sugar, decreased sex drive, slowed healing, mild depression, and mood symptoms, feeling worse after skipping meals, increased PMS, poor concentration and poor memory.
I encourage you to look for ways to reduce stress because stress is a major player in adrenal dysfunction. The state of our emotions and our mindset need to be in line for us to heal properly.  People often think they only need to take care of the body, but healing comes from mind and body. If we’re stressed, our body is in fight or flight mode. We’re not resting, digesting or rebuilding. We’re not allowing our body to refuel. I have to admit, getting into the right mindset is always easier said than done.
Choosing to be positive and grateful will set you up for success and remission in Hashimoto’s.
#4 The Gut
I’m passionate about gut infections and the role of the gut microbiota in Hashimoto’s and autoimmunity. I think part of my passion stems from having lived through it. I’m grateful for my journey because now I get to help others.
There’s a lot of research supporting the impact our gut bacteria has on autoimmunity. I’ve noticed that balancing your microbiota helps Hashimoto’s. You can do this by taking probiotics, eating fermented foods and eliminating starchy, sugary foods. Take digestive enzymes to help break down foods that feed the good bacteria and not the bad bacteria and that stabilize your reaction to the gut microbiota. Gut bacteria can cause intestinal permeability if they’re off balance.
#5 Infections
If you’ve eliminated inflammatory food and taken probiotics and still don’t feel well, try looking at gut infections. If you work with a functional doctor, they can test you. Gut infections often cause food sensitivities. I’ve seen people on restrictive diets that continue to lose foods and a lot of times it’s because of a gut infection.
The most common infections that I tend to see are H. pylori, small intestinal bacterial overgrowth (SIBO), and parasites.
A study found 54% of people with hypothyroidism had SIBO. Research links H. pylori to Hashimoto’s and thyroid antibodies. I’ve had a few clients go into remission after treating H. pylori, their symptoms disappeared, and their thyroid antibodies dropped below 35.
Parasites stir up a lot of controversies, some people don’t think people in the Western world have them- we do! 80% of my clients who don’t get into remission with diet test positive for parasites on stool tests!
Other people insist that parasites can’t possibly cause autoimmune disease because they have been found to balance the immune system. But this is only partially true, just as we have good bacteria and bad bacteria, we also have good and bad parasites.
We have parasites that help protect our gut lining and modulate and calm down our immune system. Then we have parasites that cause intestinal permeability and cause immune system confusion.

#6 Support Your Pathways
A lot of people can’t get rid of toxins properly. Supporting detoxification pathways is critical. I always start clients on a gentle liver support detox. This gets their bodies ready for healing. It helps push toxins out as we begin flooding the body with much needed nutrients. It’s not an intense detox, and it’s designed to support your body.
Part of the liver support detox is a green smoothie that I love. I call it the Root Cause Green Smoothie Recipe because once you remove initial toxins, you’re better able to dig for root causes.
Baby Steps
If you’re new to this lifestyle then jumping into a Paleo diet will be overwhelming. Start with gluten, dairy, and soy-free. It will be an easier transition. Eat organic vegetables and small, low glycemic index fruits and organic, grass-fed, free range meats. Grain-free is a big commitment, so take these baby steps toward changing your eating habits to healthier living. If you try this for three months and don’t see improvement, consider moving onto the Paleo diet.
With some people, they go gluten-free and dairy-free and soy-free and things turn around quickly. Sometimes it’s as quick as 90 days. With other people, they may need to do a little bit more digging. They may need to address nutrient depletions and gut infections, and that can take months to two years to stabilize. In other people, they have toxins they need to remove. People who have had mercury fillings, or have toxic exposure through their occupations, may have a longer road back to health.
3 Things I’ve Learned that I Wish I Learned Sooner
  1. Healing starts with your mindset. 
  2. You have to take charge of your health because no one is going to do it for you. 
  3. Food either works for you or against you.
Moving Forward Today
You want to keep moving forward. Celebrate small victories and give yourself the gift of healing.
Invest in yourself because you deserve to get better. Don’t feel bad for taking care of yourself.
When I was really sick in 2011, I worked part time so I could get better. I spent a lot of money on different treatments, and it was worth it because now I feel amazing, and I can follow my passion to help others. I wouldn’t be able to do this if I’d not taken the time to invest in myself, spend time with functional medicine doctors, or done the necessary testing research. I let myself heal and rest.
I encourage you to prioritize yourself and your healing journey. Women especially take care of everyone else before they take care of themselves. We’re often very hard on ourselves so today, right now, start being your best friend. Start taking charge of your health because you are worth it.

For evidence-based reaearch on Hashimoto's Thyroiditis, visit the Research Dashboard.

Izabella Wentz, PharmD, FASCP is an internationally acclaimed thyroid specialist and licensed pharmacist who has dedicated her career to addressing the root causes of autoimmune thyroid disease after being diagnosed with Hashimoto’s Thyroiditis in 2009. She is the author of the New York Times best-selling patient guide Hashimoto’s Thyroiditis: Lifestyle Interventions for Finding and Treating the Root Cause and the protocol-based book Hashimoto’s Protocol: A 90-Day Plan for Reversing Thyroid Symptoms and Getting Your Life Back (March 2017 release). She is the curator and director of The Thyroid Secret-a 9-part Documentary Series.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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Tuesday, October 17, 2017

How Gluten and Modern Food Processing Contribute to Poor Health

How Gluten and Modern Food Processing Contribute to Poor Health

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Story at-a-glance
  • Gluten is a protein made up of glutenin and gliadin molecules, which in the presence of water form an elastic bond. Gluten is found primarily in wheat, rye and barley, but other grains may contain it as well
  • For those with celiac disease, a severe gastrointestinal reaction to gluten, a gluten-free diet is vital. But many have some level of gluten intolerance or sensitivity, and fare better on a gluten-free diet as well
  • Besides gluten, other factors contributing to the rise in gluten intolerance and similar symptoms include wheat hybridization for higher gluten content, other wheat components, the milling or baking process and glyphosate contamination
By Dr. Mercola
"Gluten: A Gut Feeling" investigates the health effects of gluten. In recent years, the benefits of a gluten-free diet have become widely recognized, its popularity fueled by celebrity endorsements and an increasing number of books.
This includes The New York Times Best Seller, "Grain Brain," written by Dr. David Perlmutter, a neurologist, in which he reveals how processed grains can trigger neurological dysfunction and worsen dementia.
My own book on this subject, "The No-Grain Diet," was published 13 years ago in 2003. My clinical recommendation included eliminating gluten as a first line intervention before I would further fine-tune a patient's diet.
For those with celiac disease, a severe gastrointestinal (GI) reaction to gluten, a gluten-free diet is vital. But physicians are also starting to recognize that many have some level of gluten intolerance or sensitivity, and fare better on a gluten-free diet even if they don't have celiac disease.
What Is Gluten?
Gluten is a protein made up of glutenin and gliadin molecules, which in the presence of water form an elastic bond. Gluten is most commonly found in wheat, rye and barley.
Gluten can also be found in countless processed foods without being labeled as such. For example, gluten can hide under a variety of labels, including the following: 
  • Malts
  • Starches
  • Hydrolyzed vegetable protein (HVP)
  • Texturized vegetable protein (TVP)
  • Natural flavoring has a long list of label ingredients that typically contain hidden gluten.1
How Gluten May Damage Your Health
The word "gluten" comes from the Latin word for glue, and its adhesive properties hold bread and cake together. As noted in the video, bread makers may also add extra gluten in order to create a more spongy texture.
But those same "binding" properties also interfere with the breakdown and absorption of nutrients, including the nutrients from other foods in the same meal. The result can be likened to a glued-together constipating lump in your gut, which can impede proper digestion.
The undigested gluten then triggers your immune system to attack the lining of your small intestine, which can cause symptoms like diarrhea or constipation, nausea and abdominal pain.
Over time, your small intestine becomes increasingly damaged and inflamed. This in turn can lead to malabsorption of nutrients and nutrient deficiencies, anemia, osteoporosis and other health problems.
The condition can also cause a wide array of other symptoms that are not gastrointestinal in nature, including neurological or psychological problems, and problems related to the skin, liver, joints, nervous system and more.
Celiac disease is also connected to autoimmunity. If you're diagnosed with celiac's after the age of 20, your chances of developing an autoimmune condition skyrocket from the average 3.5 percent to 34 percent. Undiagnosed celiac disease is also associated with a nearly four-fold increased risk of premature death.2
Wheat Has Changed Dramatically
Wheat is one of the most widely grown crops in the Western world. But the wheat of today is vastly different from the wheat our ancestors grew and ate. This is likely part of the explanation as to why celiac disease and gluten intolerance have risen four-fold since the 1950s.
Some believe the sharp increase is merely a sign of improved diagnosis, but research suggests the rise in prevalence is real, and that dramatic changes in the diet play a distinct role.3
The proportion of gluten protein in wheat has increased enormously as a result of hybridization. Until the 19th century, wheat was also usually mixed with other grains, beans and nuts; pure wheat flour has been milled into refined white flour only during the last 200 years.
The resulting high-gluten, refined grain diet most of you have eaten since infancy was simply not part of the diet of previous generations.
How Gluten Triggers Leaky Gut
According to some experts interviewed in the featured video, including Dr. Alessio Fasano, director of the Center for Celiac Research in Massachusetts, mankind did not evolve to eat gluten and therefore cannot digest it properly.
Research suggests the human gut views gluten as a foreign invader against which it must mount an immune response, and Fasano believes this is true for everyone.
However, that doesn't mean everyone must avoid gluten. Most people, he says, can handle gluten without clinical consequence. Others are not so lucky. People with autoimmune disorders are particularly at risk for complications.
Sixteen years ago, Fasano and his team found that gluten can stimulate a molecule in your gut called zonulin — a protein that triggers the opening of junctures between the cells in your gut lining.
In essence, it makes your gut more permeable, allowing food particles to escape into your bloodstream, causing inflammation, immune reactions and raising your risk of various autoimmune disorders. This is known as leaky gut syndrome, and you don't have to have celiac disease to suffer the consequences of leaky gut.
Glyphosate-Treated Wheat Promotes Celiac Disease, Immune Reactions and More
While the question of whether gluten should be avoided by everyone is a controversial one, it's quite clear that today's wheat is far riskier than the wheat of bygone days, and that it causes problems for many.
Stephanie Seneff, Ph.D., a senior research scientist at the Massachusetts Institute of Technology (MIT), believes the recent rise in celiac disease is related to the use of glyphosate. Together with Anthony Samsel, Ph.D., Seneff has published some fascinating research on this connection.4,5
Glyphosate — one of the most widely used herbicides in the world and an active ingredient in Monsanto's Roundup — has been shown to severely damage your gut flora and cause chronic diseases rooted in gut dysfunction. It's actually patented as an antibiotic.
In March 2015, the International Agency for Research on Cancer (IARC), which is the research arm of the World Health Organization (WHO), determined glyphosate is also a "probable carcinogen" (Class 2A). Their determination was based on "limited evidence" showing it can cause non-Hodgkin's lymphoma and lung cancer in humans, along with "convincing evidence" it can cause cancer in animals.
The use of glyphosate on wheat crops specifically has risen in tandem with the rise in celiac disease. In fact, according to Samsel and Seneff, it correlates to a greater degree than glyphosate usage on corn and soy.
You may not have realized this, but desiccating6 non-organic wheat with glyphosate just before harvest became popular about 15 years ago. When the mature wheat is exposed to a toxic chemical like glyphosate, it releases more seeds. This results in slightly larger yield, which is why most wheat farmers do it.
But it also means that most non-organic wheat — and all the processed foods that contain it — is contaminated with glyphosate. And we now know this may have serious health ramifications.
Not only does the glyphosate seriously impair the villi in your gut, it also inhibits a process that normally helps your body digest wheat proteins. The gliadin in gluten is difficult to break down and digest. Normally a reaction takes place that builds connections between different proteins in the wheat.
Glyphosate appears to attach to the gliadin as a consequence of a chemical reaction, and by interfering with the protein connections, glyphosate makes the wheat highly indigestible — more so than it already is — and more likely to cause an immune reaction and gut dysbiosis.
Other Intolerances Can Mimic Gluten Sensitivity
Researchers are also looking into other ingredients in wheat and have discovered there are a number of other proteins and compounds that can cause sensitivity. So if you find yourself feeling better on a gluten-free diet, even if you've been cleared of celiac disease, you could be sensitive to some of the other ingredients in wheat.
These include proteins like albumins, globulins and amylase trypsin inhibitors, and the carbohydrate fructan, a type of fermentable oligo-di-monosaccharides and polyols (FODMAP).7
FODMAPs (which also include fructose, lactose, galactans and polyols) are sugars that are either poorly absorbed in your small intestine or completely indigestible. They can cause symptoms very similar to those of gluten sensitivity, and FODMAPs are often found in things that contain gluten.
While FODMAPs are typically beneficial for your gut microbes, in those who are sensitive to them, such as those with irritable bowel syndrome (IBS), FODMAPs can cause severe GI distress. The Paleo diet is low in FODMAPs, which is likely one of the many reasons for why people tend to feel better when switching to this kind of diet.
Panification and Wheat Milling — 2 Additional Culprits
Aside from glyphosate contamination, which is not discussed in this video at all, two other explanations for the rise in celiac disease and gluten intolerance have to do with how wheat is milled and bread is baked these days. The way we mill wheat changed significantly with the advent of modern food processing.
The endosperm and the starch are roller milled, but all the other ingredients are first extracted and then added back in at varying proportions, depending on the requirements of the end product. What you end up with is highly refined wheat flour that is more likely to cause GI problems.
Whole grain flour is made by grinding the whole grain using a stone mill. Nothing is taken out and nothing is added in. The end product contains the entire grain, hence the term "whole grain." The process is much simpler and less destructive to the nutritional content of the grain.
While whole grain bread still contains gluten, it might not cause as severe a problem if you don't have celiac disease. Some believe the problems attributed to gluten may in fact be related more so to the chemicals used during the processing of refined wheat flour, than to gluten itself.
"Panification," referring to the process of baking bread, has also undergone dramatic changes. In the past, flour was mixed with water and yeast, and the dough was then left to rise overnight. This process allowed enzymes in the yeast to break down the gluten. Your body lacks these enzymes, and cannot replicate this breakdown process.
Today, bread makers no longer let dough rise for up to 18 hours. The addition of various chemicals has cut down the process to about two hours, which is not long enough for the gluten to be broken down. Hence, most bread today contains far more indigestible gluten than breads in the past.
How to Treat Gluten Intolerance and Celiac Disease
The treatment for celiac disease and gluten intolerance is a gluten-free diet, which means abstaining from any food that contains gluten. In August 2013, the U.S. Food and Drug Administration (FDA) issued a standard for gluten-free labeling. According to the rule, in order for a food to bear the label "gluten-free" it must be:
  • Naturally gluten-free. Naturally gluten-free grains include rice, corn, quinoa, sorghum, flax and amaranth seed.
  • Any gluten-containing grains must have been refined in such a way to remove the gluten. The final product may not contain more than 20 parts per million (ppm) of gluten.
A blood test can verify whether or not you actually have celiac disease. If you do, you'll need to be extremely vigilant, as exposure to gluten could make you severely ill and threaten your long-term health and longevity. If you're gluten intolerant, you do not need to be as strict with your diet, and you may eventually discover your own tolerance level to gluten.
For example, one piece of bread may not result in any discomfort, but two pieces, or bread two days in a row, might. Typically, avoiding gluten for a week or two is enough to see significant improvement. Considering the many potential culprits at play, be it wheat hybridization, gluten, other wheat proteins, fructans, the milling or baking process, or glyphosate contamination, it's not surprising that wheat (and other grains) cause such problems for so many.

In my experience, nearly everyone benefits from avoiding grains, even whole sprouted grains, whether you have a gluten intolerance or not, and that's because grains have high net carbs and avoiding them will help improve your mitochondrial function. Impairing mitochondrial function can exacerbate health problems related to insulin resistance, such as overweight, high blood pressure, type 2 diabetes, and more serious problems like heart disease and cancer.

Prevent and Treat the Common Cold with Strain Specific Probiotics

Prevent and Treat the Common Cold with Strain-Specific Probiotics

Posted on: Tuesday, October 17th 2017 at 6:45 am
This article is copyrighted by GreenMedInfo LLC, 2017

Rather than haphazardly buying probiotics off the shelf, customize your selection this cold and flu season with evidence-based strains proven to boost immunity.
Burgeoning technological innovations and scientific revelations have provided us with unparalleled insight into the inner workings of our universe, from the microcosmic realm of the microbiota to the macrocosmic landscape of planetary interactions and phenomena at the galactic scale. However, mankind has yet to conquer the common cold.
American adults contract between two and four colds per year whereas children under two years of age experience six cold infections per year on average (1, 2). When assessed twenty years ago, annual medical expenditures related to the common cold totaled $17 billion dollars whereas the economic burden due to loss of productivity was $25 billion (3).
Several forms of rhinovirus constitute the causative agent behind the common cold, which engender a self-limiting viral infection confined to the upper respiratory tract involving the nasal passages, sinuses, pharynx, and larynx (1). After exposure, there is a latent incubation period of one to three days before symptoms such as malaise, cough, runny nose, and nasal congestion appear, which can then persist for seven to ten days and occasionally remain for weeks (4, 5).
Although no treatments have been established to treat the common cold, and antiviral pharmaceuticals have proven ineffective, up to one in five adults and one in three children on average visit a physician as a result of upper respiratory tract infections resulting from the common cold, which often culminates in antibiotic overprescribing and ensuing antibiotic resistance (3, 6). In fact, 75% of all antibiotic use in high-income countries is attributed to upper respiratory tract infections in which antibiotics have no efficacy if the infection is viral in origin (7).
In addition to micronutrient sufficiency, managing stress, ensuring restorative sleep, and handwashing, all of which mitigate risk of the cold, there are several natural substances that can prevent colds or shorten cold duration (8, 9, 10). Although the field is still in its infancy, strain-specific probiotic therapies, for example, are promising for boosting immunity and fighting infection both prophylactically and acutely.
Mechanisms Whereby Probiotics Affect Immunity
Although re-inoculation of commensal bacteria that have been extinguished due to antibiotic usage is not plausible with most oral probiotics, administration of probiotics which transiently pass through the digestive tract exert immunomodulatory effects (11). At the local level, short-chain fatty acids such as butyrate which are a byproduct of bacterial fermentation reinforce the gut barrier, maintaining tight junction integrity (12). Thus, probiotics prevent the intestinal hyper-permeability that is colloquially known as leaky gut syndrome, interfering with the translocation of toxicants and virulent microbes across the gut barrier (12). Probiotics likewise enhance the production of intercellular signaling messengers known as cytokines, such as interleukins, interferon, and tumor necrosis factor, all of which amplify the immune response to pathogens (13, 14).
Systemically, probiotics improve the innate, non-specific immune system which constitutes the first line of defense against pathogen invasion. Probiotics have been demonstrated to improve activity of phagocytes or ‘big eaters’ which function in clearance of microbe-infected cells and enhance the expression of receptors required for phagocytosis, the process by which cells engulf and eliminate viral particles or bacterial elements (15, 16, 17). For instance, studies exemplify that lactic acid bacteria augment the phagocytic functions of various leukocytes including monocytes, macrophages, natural killer cells, and neutrophils (18).
Similarly, probiotics increase the respiratory burst, a process by which reactive oxygen species (ROS) such as the superoxide radical and hydrogen peroxide are rapidly released from immune cells to neutralize and degrade internalized particles, viruses, and bacteria (15). By the same token, probiotics improve the peripheral pool and activity of natural killer (NK) cells, a specialized cytotoxic cell essential to the early immune response that kills cells infected with viruses (19). The microbiocidal (microbe-killing) action of neutrophils, an immune cell which is one of the first at the scene of infection, ingests microorganisms, and secretes enzymes to kill invading microbes, is also enhanced by probiotics (20).
Secondarily, adaptive immunity, which occurs later on in infection and tailors the immune response to target the microbial entity at hand, is improved with probiotic administration as evidenced by higher levels of IgG, IgM, and IgA immunoglobulins (21, 22). Immunoglobulins are antibodies which bind to and neutralize antigens, or specific molecular patterns on pathogens, in order to eliminate infection. Lastly, probiotics may favorably influence the immune system through interaction with toll-like receptors, a class of proteins expressed on sentinel cells of the innate immune system which recognize conserved structural motifs on microbes (23).
Evidence-Based Probiotic Strains with Immune-Boosting Effects
A systematic review of 10 pooled randomized controlled trials of 3451 subjects revealed that probiotic therapy, defined as “the feeding of (live) non-pathogenic bacteria, originally derived from the alimentary tract, for disease treatment or health promotion,” was effective in upper respiratory tract infection prophylaxis (24, p. 3). Despite heterogeneity in study design, probiotics reduced the number of subjects afflicted by upper respiratory tract infections by 42%, reduced antibiotic usage by 33%, and reduced the quantity of upper respiratory tract infections per person per year by 12% (11).
However, there were marked differences in formulations, colony-forming units (CFUs), and strains administered, so the following will detail some of the most evidence-based strains. When searching for probiotics, it is important to pay attention to the principle of strain specificity, since according to researchers, generalizability from one strain to another, even within the same species categorization, is impossible (25).
For example, “Shirota” is the strain designation in Lactobacillus casei Shirota, such that any generic Lactobacillus casei should not be expected to elicit the same therapeutic effects elucidated in the scientific literature for the Lactobacillus casei Shirota strain. Although many strains may improve gut terrain and elicit immunomodulation based on the mechanisms previously discussed, ensuring strain specificity is optimal for reliable reproducibility of therapeutic effects.
To put this in perspective, strains are analogous to breeds of dogs. Although a shih tzu and a German shepherd both fall under the same taxonomic genus and species classification of Canis familiaris, they possess dramatically different characteristics. One a lap dog and the other a guard dog, the qualities of one cannot be automatically extrapolated to the other.
Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb-12
Arguably, Lactobacillus rhamnosus GG (LGG) is one of the best researched commercially available probiotic strains which is ubiquitously available over the counter. In one double-blind, randomized, placebo-controlled trial, 742 hospitalized children were administered a fermented milk product containing LGG or a pasteurized milk product without LGG (26). Those who received the LGG treatment had a 62% lower risk of respiratory tract infection and were 60% less likely to have episodes of respiratory tract infections exceeding three days (26). As an aside, LGG likewise reduced gastrointestinal infections by 50%, episodes of gastrointestinal infections exceeding two days by 60%, vomiting episodes by 50%, and diarrheal episodes by 76% compared to those in the placebo group (26).
A seven month randomized, double-blind, placebo controlled study in Helsinki, Finland also illustrated that milk supplemented with LGG reduced risk of respiratory infection complications by 17%, days absent from day care due to illness by 16%, and antibiotic treatments for respiratory infection by 19% (27). Similarly, another randomized, double-blind, placebo-controlled study, recruited formula-fed infants from well-baby clinics and supplemented their formula with a combination of LGG and Bifidobacterium lactis Bb-12 or placebo until a year of age (28). A 56% reduced risk of otitis media (ear infection), 48% reduced risk of antibiotic usage, and 49% reduced risk of recurrent respiratory tract infection was observed with the probiotic treatment compared to controls (28).
Lactobacillus casei DN-114 001/CNCM I-1518
Lactobacillus casei is a probiotic species which has exhibited high survivability in its passage through the intestinal tract, and has been shown to decrease the incidence and duration of both diarrhea and allergic rhinitis (hay fever) in infant and child cohorts (29).
In one double-blinded, randomized, placebo-controlled trial, 638 healthy children between the ages of three and six consumed an active yogurt beverage containing Lactobacillus casei DN-114 001/CNCM I-1518 (also known as Lactobacillus paracasei subspecies paracasei) or a non-fermented control beverage once a day for three months (29). After the intervention, the rate of common infectious diseases was significantly lower in those who had received the probiotic-containing yogurt (29).
For example, the rate of gastrointestinal tract infections was 24% lower in the probiotic group, and the rate of upper respiratory tract infections was 18% lower in the probiotic group compared to controls (29). There was also a trend towards less frequent use of antibiotic and anti-inflammatory drugs in the active group relative to placebo (29). Likewise, parents in the probiotic group missed 33% less work and children in the probiotic group had 24% less absences from school or daycare, but these numbers did not reach statistical significance likely due to the small study size (29).
Lactobacillus fermentum VRI-003 (PCC)
The probiotic species Lactobacillus fermentum has been shown to adhere to Peyer’s patches, the aggregates of lymphoid tissue that consists of immune cells which surround the small intestine and surveil microbiota populations (30). In addition to up-regulating gut immunity, L. fermentum has also been demonstrated to colonize the gastrointestinal tract of healthy participants following a single dose (31).
In one double-blind, placebo-controlled, crossover study, twenty elite distance runners were randomly assigned to receive three capsules of L. fermentum VRI-003 (PCC) or placebo twice daily for one month followed by a one month washout period of no treatment (32). Thereafter, the groups exchanged treatments and the former placebo group received the probiotic whereas the former probiotic group received the placebo (32).
Compared to placebo, the PCC strain incited a two-fold greater change in levels of interferon gamma (IFNγ), a cytokine and surrogate marker for cell-mediated immunity, which triggers a cellular response against viral and microbial infections (32). There was also a modest increase in an immunoglobulin A (IgA) subtype in athletes taking the probiotic, which is correlated with reduced susceptibility to respiratory infection (33). PCC treatment was also accompanied by a dramatic reduction in the number of days and severity of respiratory illness versus placebo (32). The researchers conclude that this strain stimulates a protective immune response in the respiratory tract (32).

Lactobacillus acidophilus NCFM and Bifidobacterium lactis Bi-07
A double-blind, placebo-controlled study of 326 children ages three to five were randomly allocated to receive either a placebo, single strain probiotic therapy with Lactobacillus acidophilus NCFM, or a combination of L. acidophilus NCFM with Bifidobacterium animalis subspecies lactis Bi-07 twice daily for six months (23).
The highest degree of efficacy was found using both strains in tandem, with reductions in incidence of fever, coughing, and rhinorrhea, by 72.7%, 62.1%, and 58.8%, respectively (23). Absenteeism from day care due to illness was reduced by almost a third compared to placebo in the probiotic groups, and the single and combination probiotics reduced antibiotic use by 68.4% and 84.2%, respectively (23).
Lactobacillus gasseri PA 16/8, Bifidobacterium longum SP 07/3, and Bifidobacterium bifidum MF
In a three month study during the winter and spring, 479 adults were supplemented with vitamins and minerals with or without a probiotic combination of Lactobacillus gasseri PA 16/8, Bifidobacterium longum SP 07/3, and Bifidobacterium bifidum MF in a double-blind, randomized, placebo-controlled trial (34).
In this study, the probiotics reduced the duration of the common cold by almost two days and also shortened the number of days with fever during a cold episode (34). Not only were fecal lactobacilli and bifidobacteria counts significantly increased after the probiotic treatment period, but immune cells called T helper cells and T suppressor cells were significantly increased in the probiotic-treated group compared to the group taking vitamins and minerals only (34).
Taken collectively, this data indicates that strain-specific probiotics are a viable adjunctive strategy for both prevention and treatment of upper respiratory tract infections when used alongside other holistic interventions. Most of the aforementioned strains are commercially available and can be purchased in various over the counter and professional grade products. Moreover, this research crystallizes the integral role that our microbial ecology plays in our health, and reinforces the paramount importance of acting as a vigilant custodian of your own microbiota.

1. Allan, G.M., & Arroll, B. (2014). Prevention and treatment of the common cold: making sense of the evidence. Canadian Medical Association Journal,186(3), 190-199.
2. Kawakita, K. et al. (2004). Preventive and curative effects of acupuncture on the common cold: a multicentre randomized controlled trial in Japan. Complementary Therapies in Medicine, 12(4), 181-188.
3. Fendrick, A.M. et al. (2003). The economic burden of non-influenza-related viral respiratory tract infection in the United States. Archives of Internal Medicine, 163, 487-494.
4. Heikkinen, T., & Järvinen, A. (2003) The common cold. Lancet, 361, 51-59.
5. Arruda, E. et al. (1997). Frequency and natural history of rhinovirus infections in adults during autumn. Journal of Clinical Microbiology, 35, 2864-2868.
6. Vingilis, E.R. et al. (1999). Cold/flu knowledge, attitudes and health care practices: results of a two-city telephone survey. Canadian Journal of Public Health, 90, 205-208.
7. Fendrick, A.M. et al. (2001). Diagnosis and treatment of upper respiratory tract infections in the primary care setting. Clinical Therapeutics, 1683-1706.
8. Cohen, S., Tyrrell, D.A., & Smith, A.P. (1991). Psychological stress and susceptibility to the common cold. New England Journal of Medicine, 325, 606-612.
9. Cohen, S. et al. (2009). Sleep habits and susceptibility to the common cold. Archives of Internal Medicine, 169, 62-67.
10. Jefferson, T. et al. (2011). Physical interventions to interrupt or reduce the spread of respiratory viruses. Cochrane Database Systematic Review, 7, CD006207.
11. Hao, Q., Dong, B.R., & Wu, T. (2015). Probiotics for preventing acute upper respiratory tract infections (Review). Cochrane Database of Systemic Reviews, 2, CD006895. doi: 10.1002/14651858.CD006895.pub3.
12. Perdigon, G. et al. (1995). Immune system stimulation by probiotics. Journal of Dairy Science, 78(7), 1597-1606.
13. Gill, H.S. (1998). Stimulation of the immune system by lactic cultures. International Dairy Journal, 8, 535-544.
14. Meydani, S.N., & Ha, W.K. (2000). Immunologic effects of yogurt. American Journal of Clinical Nutrition, 71(4), 861-872.
15. Donnet-Hughes, A. et al. (1999). Modulation of nonspecific mechanisms of defense by lactic acid bacteria: effective dose. Journal of Dairy Science, 92(5), 863-869.
16. Schiffrin, E.J. et al. (1995). Immunomodulation of human blood cells following a negation of lactic acid bacteria. Journal of Dairy Science, 78, 491-497.
17. Shei, Y.H. et al. (2001). Systemic immunity-enhancing effects in healthy subjects following dietary consumption of the lactic acid bacterium lactobacillus rhamnosus HN001. Journal of the American College of Nutrition, 20(Suppl 2), 149-156.
18. Vreese, M.D., & Schrezenmeir, J. (2002). Probiotics and non-intestinal infectious conditions. British Journal of Nutrition, 88(Suppl 1), S59-S66.
19. Drakes, M., Blanchard, T., & Czinn, S. (2004). Bacterial probiotic modulation of dendritic cell. Infection and Immunity, 72(6), 3299-3309.
20. Arunachalam, K., Gill, H.S., & Chandro, R.K. (2000). Enhancement of natural immune function by dietary consumption of Bifidobacterium lactis (HN019). European Journal of Clinical Nutrition, 54(3), 263-267.
21. Majamaa, H. et al. (1995). Lactic acid bacteria in the treatment of acute rotavirus gastroenteritis. Journal of Pediatric Gastroenterology and Nutrition, 20(3), 333-338.
22. Link-Amster, H. et al. (1994). Modulation of specific humoral immune response and changes in intestinal flora mediated through fermented milk intake. Immunology and Medical Microbiology, 10(1), 55-63.
23. Leyer, G.J. et al. (2009). Probiotic effects on cold and influenza-like symptom incidence and duration in children. Pediatrics, 124(2), e172-e179. doi: 10.1542/peds.2008-2666.
24. O’Sullivan, G.C. et al. (2005). Probiotics: an emerging therapy. Current Pharmacological Design, 11, 3–10.
25. Marteau, P. (2011). Evidence of Probiotic Strain Specificity Makes Extrapolation of Results Impossible From a Strain to Another, Even From the Same Species. Annals of Gastroenterology & Hepatology, 1-3.
26. Hojsak, I. et al. (2010). Lactobacillus GG in the prevention of nosocomial gastrointestinal and respiratory tract infections. Pediatrics, 25, e1171–e1177.
27. Hatakka, K. et al. (2001). Effect of long term consumption of probiotic milk on infections in children attending day care centres: double blind, randomised trial. British Medical Journal, 322(7298), 1327.
28. Rautava, S., Salminen, S., & Isolauri, E. (2009). Specific probiotics in reducing the risk of acute infections in infancy--a randomised, double-blind, placebo-controlled study. British Journal of Nutrition, 101(11), 1722-1776.  doi: 10.1017/S0007114508116282.
29. Merenstein, D. et al. (2010). Use of a fermented dairy probiotic drink containing Lactobacillus casei (DN-114 001) to decrease the rate of illness in kids: the DRINK study. A patient-oriented, double-blind, cluster-randomized, placebo-controlled, clinical trial. European Journal of Clinical Nutrition, 64, 669–677.
30. Plant, L.J., & Conway, P.L. (2002). Adjuvant properties and colonization potential of adhering and non-adhering Lactobacillus spp. following oral administration to mice. FEMS Immunological Medicine and Microbiology, 34, 105-111.
31. Plant, L., & Conway, P.L. (2002). Association of Lactobacillus spp with Peyers patches in mice. Clinical Diagnostic Immunology, 8, 320-324.
32. Cox, A.J. et al. (2008). Oral administration of the probiotic Lactobacillus fermentum VRI-003 and mucosal immunity in endurance athletes. British Journal of Sports Medicine, 44(4), 222-226.
33. Gleeson, M., & Pyne, D.B. (2000). Effects of exercise on the immune system: exercise effects on mucosal immunity. Immunology and Cell Biology, 78, 536–544.
34. Vreese, M.D., & Schrezenmeira, J. (2005). Effect of Lactobacillus gasseri PA 16/8, Bifidobacterium longum SP 07/3, B. bifidum MF 20/5 on common cold episodes: A double blind, randomized, controlled trial. Clinical Nutrition, 24(4), 481-489.

Ali Le Vere holds dual Bachelor of Science degrees in Human Biology and Psychology, minors in Health Promotion and in Bioethics, Humanities, and Society, and is a Master of Science in Human Nutrition and Functional Medicine candidate. Having contended with chronic illness, her mission is to educate the public about the transformative potential of therapeutic nutrition and to disseminate information on evidence-based, empirically rooted holistic healing modalities. Read more at @empoweredautoimmune on Instagram and at Science-based natural remedies for autoimmune disease, dysautonomia, Lyme disease, and other chronic, inflammatory illnesses.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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