Landmark Study Suggests Efficacy of Autoimmune Paleo Protocol

Landmark Study Suggests Efficacy of Autoimmune Paleo Protocol

Posted on: Friday, October 27th 2017 at 11:00 am

Written By: Ali Le Vere, B.S., B.S.

This article is copyrighted by GreenMedInfo LLC, 2017

Visit our Re-post guidelines

Many people following the autoimmune paleo (AIP) protocol witness objective measures of improvement, but now we have a bonafide clinical trial revealing its efficacy in inflammatory bowel disease (IBD). These results may be applicable to all autoimmune disorders, since these conditions share common etiological origins.

Diminished Antigenic Burden: A Tenet of the Time-Honored Elimination Diet

Until now, most of the evidence for the efficacy of the autoimmune paleo (AIP) diet in inducing remission of autoimmune disorders has been anecdotal. An extension of the paleolithic diet, the autoimmune paleo diet not only excludes grains, dairy, and legumes, but it also removes other potentially immunogenic substances including eggs, nuts, seeds, refined sugar, alcohol, food additives, and nightshade vegetables such as sweet and hot peppers, tomatoes, potatoes, eggplant, and goji berries (1).

This represents an adaptation of the gold standard oligoantigenic elimination diet that nutritional professionals have long implemented to produce abatement in symptoms recalcitrant to other interventions. Allergenic and immunogenic foods are removed from the diet for a trial period of a month or longer, and then sequentially re-introduced in a systematic manner to gauge tolerance. Not only does this enable the identification of food reactions, but it also decreases the burden of antigenic foods capable of producing an immune response and imparts opportunities for gut repair and correction of micronutrient deficiencies. Notably, however, most functional medicine practitioners agree that the autoimmune protocol should constitute a short-term intervention and that food re-introductions should commence as soon as significant symptomatic reduction has occurred.

Nutrient Density: A Pillar of the Autoimmune Paleo Diet

Some argue that the therapeutic potential of the autoimmune protocol lies in its exclusion of potentially antigenic foods and its minimization of anti-nutrients, as I previously touched on in my article “Lectins and Autoimmune Disease: Separating Fact from Fiction”. However, the principal strength of the autoimmune protocol is its inclusion of the most nutrient-dense foods—namely, wild-caught seafood, grass-fed meat and offal, roots and tubers, herbs and spices, and fruits and vegetables. The value of eliminating grains and beans, therefore, may actually lie in the fact that they commonly displace these more nutrient-dense foods.

Although the original inception of the paleo diet had its roots in evolutionary biology as well as in anthropological ethnographic studies of contemporary hunter-gatherers and ancient foraging populations, the newfound rationale for adopting a paleo template lies in its emphasis on those foodstuffs delineated in the peer-reviewed literature to have the most nutritive value. Moreover, the autoimmune protocol addresses many of the underlying root causes of aberrant immune responses.

Healing and Sealing the Gut Barrier

The one cell thick lining of the gastrointestinal tract is normally tightly regulated by conformational changes in tight junctions, which supervise the paracellular trafficking of molecules from the intestinal lumen to the submucosa and into systemic circulation (2). Dynamic proteinaceous structures between cells change shape to allow the selective passage of nutrients and water while excluding deleterious foreign elements which exceed a particular molecular radius (2). However, in autoimmune disease, various environmental insults cause the tight junctions to become excessively permeable, enabling undigested food proteins, toxicants, and microbial products to navigate across the gut barrier where they elicit immune reactions that can culminate in autoimmunity (2).

Liver, fatty fish, and shellfish, regarded as nutrient powerhouses on the autoimmune protocol, are particularly essential as they provide nutrients such as vitamins A and D which support regeneration of the gut lining that is compromised in autoimmune disease (3, 4). These fat-soluble vitamins are quintessential for maintenance of mucosal integrity, the violation of which is the precursor to every autoimmune disease in which it has been studied, including multiple sclerosis, celiac disease, ulcerative colitis, Crohn’s disease, type one diabetes, rheumatoid arthritis, ankylosing spondylitis, as well as allergic disorders such as asthma (2, 5, 6, 7, 8, 9, 10, 11).

Vitamin A prevents inappropriate activation of T cells in the immune tissues known as the gut-associated lymphoid tissue (GALT) and Peyer’s patches encircling the digestive tract, therefore reducing risk of chronic gut inflammation (4). It is also instrumental in orchestrating oral tolerance, or the ability to consume an array of foods without adverse reaction (4). Lastly, vitamin A promotes the synthesis of immunoglobulin A (IgA), an antibody in mucosal tissues which confers protection against infection and helps engender healthy gut flora (12). Contrary to popular belief, over half of people do not convert any beta carotene from orange and leafy green vegetables into active vitamin A at all, so consuming preformed vitamin A is essential (13).

Restoration of Immune Homeostasis

It was formerly hypothesized that polarization of the immune system towards dominance of either the Th1 (cellular immunity) or Th2 (humoral or antibody-mediated immunity) pathways was responsible for autoimmune disorders (14). This was later recognized to be an oversimplification, as this paradigm not only failed to elucidate the role of Th17 cells, but it was also discordant with data demonstrating that autoimmune diseases do not always fall into these neat categorical distinctions (14). However, this view still has utility in that regulatory T cells (Tregs) represent an overarching control mechanism that maintains balance between divergent classes of immune cells.

Vitamins A and D, which feature prominent on the autoimmune protocol, display immunomodulatory properties, restoring harmony between the different branches of the immune system. Not only are vitamin D levels commonly deficient in autoimmune disease, but lower levels of vitamin D are directly related to severity of autoimmune manifestations (15, 16, 17). Both vitamin A and D up-regulate expression of a population of immune cells known as toleragenic FoxP3+ regulatory T cells (Tregs), which engender balance between the Th1, Th2, or Th17 arms of the immune system, all of which can perpetuate autoimmunity when their exquisitely fine-tuned balance is disrupted. Likewise, vitamins A and D suppress activation and differentiation of pathogenic interleukin-17 producing Th17 cells, which appear to be the principal mediators of tissue destruction in a host of autoimmune disorders (18).

Balancing Omega-6 to Omega-3 Ratio

As a corollary, the autoimmune protocol emphasizes inclusion of preformed long-chain omega-3s, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), from wild-caught fatty fish such as salmon, mackerel, herring, and sardines, while excluding omega-6 seed oils from corn, canola, cottonseed, soybean, safflower, and sunflower. Compared to dietary omega-6 fatty acids, which generally give rise to more inflammatory thromboxanes, prostaglandins, and leukotrienes, omega-3 fatty acids are metabolized into less inflammatory eicosanoid signaling molecules. Although plant-based sources such as flax, hemp, chia, and walnuts are touted as sources of omega-3s, less than 5-10% of the alpha-linolenic acid (ALA) these foods contain is converted into EPA and less than 2-5% is converted into DHA (19).

Traditional hunter-gatherer populations consuming an ancestral paleolithic diet had the most optimal dietary omega-6 to omega-3 ratio, of 1:1, and were virtually free from the chronic and degenerative diseases of modernity (20, 21, 22). In comparison, the Standard American Diet to which contemporary Western populations are accustomed, where populations are plagued by chronic illness at epidemic proportions, has a dismal omega-6 to omega-3 ratio ranging from 10:1 to 25:1 (21). Incorporating fatty fish, as well as grass-fed meat, the latter of which has been demonstrated to predictably raise plasma and platelet long chain omega-3 status (23), may particularly benefit autoimmune cohorts since omega-3s inhibit multiplication of pathogenic T cell subsets and prevent the synthesis of inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1), and interleukin-2 (IL-2) (24).

Neutralization of Oxidative Stress

The pathophysiological conditions that give rise to autoimmune disorders entail an imbalance between oxidants and antioxidants, the latter of which neutralize oxidative stress. Generation of reactive oxygen species, or free radicals such as superoxide and hydrogen peroxide, is a normal byproduct of metabolism, but can damage cellular machinery when excessive and impair the production of cellular energy, which becomes a vicious cycle as energy-intensive repair processes become untenable (25, 26).

Including an array of colorful plant foods is tantamount to increasing antioxidant intake. Because they function in redox reactions and defend against reactive oxygen and nitrogen species, bioactive constituents in plants known as phytochemicals are categorized as antioxidants (27). Deeply pigmented fruits and vegetables which are staples on the autoimmune protocol include constituents such as stilbenoids, lignans, tannins, carotenoids, phenolic acids, and flavonoids which ensure integrity of genetic material, facilitate cellular repair, and regulate genetic expression in a favorable direction (28, 29, 30). The autoimmune diet is likewise rich in fat-soluble antioxidants such as tocopherols, carotenes, vitamin A and ubiquinol, as well as water-soluble antioxidants such as ascorbate and glutathione (31).

Optimization of Detoxification and Hormone Balance

Many of the fruits, vegetables, herbs and spices included on the autoimmune protocol up-regulate phase II detoxification enzymes, which are required to convert phase I intermediates into their water-soluble counterparts so that they can be excreted. This is important to correct the bottleneck that often occurs in autoimmunity whereby phase I outpaces phase II, creating an accumulation of toxic phase I metabolites and leading to an over-burdening of the liver (32). Many herbs, spices, and phytonutrients, emphasized on the autoimmune protocol, such as ginger (33), curcumin from turmeric (34), cinnamaldehyde from cinnamon (35), resveratrol from grapes, blueberries, and cranberries (36), quercetin concentrated in apples and onions (37) and countless others significantly up-regulate expression of phase II enzymes to enhance excretion of toxins implicated in autoimmunity.

Similarly, an isothiocyanate compound called sulforaphane in cruciferous vegetables, which are often staples of the autoimmune protocol, is the most potent inducer of phase II enzymes identified to date (32, 38). Arugula, broccoli, Brussel sprouts, red, green, Chinese, and savoy cabbage, cauliflower, chard, collard greens, radish, rapini, rutabaga, turnip and turnip greens, wasabi, and watercress are all sources of this compound within the autoimmune protocol.  Another benefit of these vegetables is that they contain indole-3-carbinole (I3C), the biological effects of which are attributed to its oligomeric products, such as 3,3'-diindolylmethane (DIM). Both of these compounds can support healthy estrogen metabolism in the case of estrogen dominance, which is common in autoimmune cohorts.

I3C in particular increases metabolism of estradiol down the 2-hydroxyestrone pathway at the expense of the unfavorable 16-hydroxyestrone pathway (39, 40). In general, 2-hydroxyestrone metabolites have the weakest estrogenic effect, whereas 16-hydroxyestrones are considered proliferative, cancer-promoting estrogen species (41, 42). In addition, I3C inhibits formation of 4-hydroxyestrogen, another potent estrogen possessing growth-promoting effects that has a strong affinity for estrogen receptors (43).

Enrichment of Microbiota Diversity and Inhibition of Pathogens

There is an element of dysbiosis, or bacterial imbalance, in most autoimmune conditions given the inextricable connection between the microbiota and the immune system. Ample substrate to nourish commensal flora, in the form of microbiota-accessible carbohydrates (MACs) or prebiotics, is required to restore a healthy ecosystem. Paleo diets confer a decisive advantage in terms of fiber intake, which is associated with bacterial richness due to prebiotic effects (44).

Prebiotics, or foods that escape digestion and are instead selectively fermented by beneficial bacteria in the colon, are a viable strategy for encouraging microbial diversity and in turn enhance the health of the host (45). Barring any small intestinal bacterial overgrowth (SIBO), liberal use of prebiotics such as asparagus, garlic, onion, artichoke, chicory root, jicama, green bananas, plantain, beetroot, asparagus, leeks, jicama, yacon, and burdock are all permitted on the autoimmune protocol and help to engender a harmonious gut ecology which translates into better immune balance. Studies have shown that changes in the microbiome can materialize in as few as one to two days with increased consumption of plants (46).

In addition, lacto-fermented foods included on the autoimmune protocol such as sauerkraut and coconut kefir are reservoirs of both beneficial bacteria and polyamine compounds, which increase the rate of cellular renewal and regeneration when absorbed by enterocytes and can contribute to gut healing. Re-establishment of healthy gut flora will in turn competitively inhibit attachment of pathogens (47) which can trigger or perpetuate autoimmunity (48).

Improved Cardiometabolic Parameters

Endothelial cell activation, vascular smooth muscle dysfunction, oxidative stress, and inflammation, mechanisms which underlie heart disease, diabetes, and hypertension, are all variables which can precipitate or perpetuate immune imbalances in autoimmune disease. The paleo template has been proven to be superior to the lower fat, higher carbohydrate American Diabetes Association (ADA) diet in correcting these metabolic derangements in type two diabetes (49). For instance, subjects on the paleo diet exhibited improvements in glucose control, as indicated by hemoglobin A1c (HbA1c) (49). The researchers attribute the decrease in blood sugar spikes in subjects on the paleo diet to the greater fiber content they consumed, which was 35 grams per 2500 kcal compared to 12 g per 2500 kcal with the ADA diet (49).

This is complemented by other studies of subjects with hypercholesterolemia, where the paleo diet was found to significantly lower total cholesterol, LDL cholesterol, and triglycerides and to significantly increase HDL cholesterol relative to the traditional grain-based “heart-healthy” diet recommendations (50). Studies have also illuminated that individuals who were most insulin resistant at baseline had the greatest improvement in insulin sensitivity on the paleo diet, which can lower inflammatory burden (51). The paleo diet likewise was more effective than a reference healthy diet for lowering systolic and diastolic blood pressure and other cardiovascular risk factors which often accompany autoimmunity (52).

Repair of Mitochondrial Dysfunction

Malfunctioning mitochondria, the energy powerhouses of the cell, are implicated in almost all pathologic conditions, including most autoimmune disorders (53). Mitochondrial restoration is compatible with the autoimmune protocol since repair of these organelles requires a diet that is nutrient-dense and anti-inflammatory in nature, excluding immunogenic foods and emphasizing micronutrients that sustain aerobic respiration and “facilitate efficient functioning of the biochemical pathways to extract and transform energy into a biological useful form” (54).

Because mitochondrial matrix enzymes function best in an alkaline medium, metabolic processes can be optimized by eating a primarily plant-based autoimmune paleo diet (54). Removing acidic processed foods, sugar, flour, high-glycemic foods, coffee, and alcohol can prevent alterations in membrane potential which compromises mitochondrial function by interfering with the electron transport chain integral to oxygen-based oxidative phosphorylation (55, 56). The autoimmune protocol is likewise rich in cofactors for the citric acid cycle, the process which produces high-energy reduced coenzymes that donate electrons into the electron transport chain in order to generate cellular energy.

For instance, heme molecules required for the complexes of this electron shuttling system are dependent on iron and zinc, both of which are more abundant and bioavailable in organ meats compared to plant sources. By comparison, "The bioavailability of iron and zinc in vegetarian diets is poor because of their higher content of absorption inhibitors such as phytate and polyphenols and the absence of flesh foods" (57, p. 459S). Vegetarian diets have been demonstrated to reduce non-heme iron absorption by 70% and total iron absorption by 85% (58). Similarly, vegetarian diets reduce zinc absorption by 35% compared to omnivorous diets due to phytate content, such that vegetarians may require up to 50% more zinc than omnivores (58). Therefore, the autoimmune protocol is advantageous both in its omission of anti-nutrients which impede mineral absorption and its inclusion of bioavailable vitamins and minerals.

Proven Efficacy in Inflammatory Bowel Disease

A single-center, open-label, uncontrolled study was conducted to assess the efficacy of the autoimmune paleo protocol in inflammatory bowel disease (IBD). The cohort included 9 patients with symptomatic Crohn's disease (CD) and 6 with ulcerative colitis (UC), half of whom were on biologic therapy, with an average disease duration of 19 years (1). Individuals were advised to continue medication therapy during the study duration, with the exception of corticosteroid tapers. Further, a certified health coach and registered dietician were recruited to provide dietary counseling and education on lifestyle facets of the protocol.

73% of subjects were classified as achieving remission by the sixth week of the diet, which persisted through the five-week maintenance phase (1). By week six, fecal bleeding had significantly reduced in patients with UC (1). Not only were endoscopic improvements observed in mucosal appearance, but significant improvements in disease scales such as the mean partial Mayo score for UC and the mean Harvey-Bradshaw index for CD were witnessed (1). In addition, average levels of fecal calprotectin decreased from 471 at week 1 to 112 at week 11 (1). Calprotectin is a marker of intestinal inflammation that is predictive of relapse in quiescent IBD patients when it appears at higher levels (59, 60).

The authors cite, "We did not hypothesize, a priori, that clinical remission would be achieved so early (week 6). Indeed, this proportion of participants with active IBD…achieving clinical remission by week 6 rivals that of most drug therapies for IBD” (1, p. 2058). As a result of the dramatic results produced in the study, the researchers suggest that AIP is a viable adjunctive therapy in IBD, “even among those with moderate-to-severe disease” (1, p. 2056). Despite the significant improvements observed, two Crohn’s subjects with native or anastomotic ileal strictures exhibited partial small bowel obstruction or exacerbation of disease activity with the autoimmune protocol, highlighting the need for physician supervision.

Practical Applications

Although this preliminary study is demonstrative of the efficacy of the autoimmune protocol, it is limited by its design. Not only does it use a small sample size, but it is a non-randomized, non-blinded, prospective observational study that may also be confounded by selection bias—in other words, the subjects may not be representative of the population of individuals with IBD. Therefore, more clinical trials are necessary to reproduce results and extrapolate to other autoimmune conditions. Of course, funding clinical trials is often cost-prohibitive and pharmaceutical industry investors, with legally-binding fiduciary obligations to shareholder interests, have little fiscal incentive to devote resources to dietary protocols for which market exclusivity is an impossibility.

As discussed in my previous installment, some of the dogmatism within the paleo realm does not hold up to scientific scrutiny, and the scientific literature on anti-nutrients is deficient in high-quality human studies. However, many people do not have the luxury of time when it comes to arresting debilitating autoimmune condition, and the clinical experience of many integrative and functional practitioners is a direct testament to the potential efficacy of AIP whether or not biochemical mechanisms have been fully developed.

Moreover, there are many protective lifestyle elements embedded within the autoimmune protocol, such as mobilization of social support, stress management, disease-appropriate exercise, and restorative sleep, all of which are fundamental to healing. Therefore, given the benign, non-invasive nature of the autoimmune protocol and its quintessential nutrient-dense, anti-inflammatory nature, individuals with autoimmune disorders owe it to themselves to explore this regimen as therapeutic option.

References

1. Konijeti, G.G. et al. (2017). Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease. Inflammatory Bowel Diseases, doi: 10.1097/MIB.0000000000001221.

2. Fasano, A. (2012). Leaky gut and autoimmune disease. Clinical Reviews in Allergy and Immunology, 42(1), 71-78.

3. Mora ,J.R., Iwata, M., & von Andrian, U.H. (2008). Vitamin effects on the immune system: vitamins A and D take centre stage. National Reviews in Immunology, 8(9), 685-698.

4. Kim, C.H. (2008). Roles of retinoic acid in induction of immunity and immune tolerance. Endocrine Metabolism Immune Disorders Drug Targets, 8, 289-294.

5. Drago, S. et al. (2006). Gliadin, zonulin and gut permeability: effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scandanavian Journal of Gastroenterology, 41, 408–419.

6. Westall, F.C. (2007) Abnormal hormonal control of gut hydrolytic enzymes causes autoimmune attack on the CNS by production of immune-mimic and adjuvant molecules: a comprehensive explanation for the induction of multiple sclerosis. Medical Hypotheses, 68, 364–369.

7. Edwards, C.J. (2008) Commensal gut bacteria and the etiopathogenesis of rheumatoid arthritis. Journal of Rheumatology, 35, 1477–1497. doi: 10.1007/s12016-011-8291-x.

8. Yacyshyn, B.R., & Meddings, J.B. (1995) CD45RO expression on circulating CD19+ B cells in Crohn’s disease correlates with intestinal permeability. Gastroenterology, 108, 132–138.

9. Martinez-Gonzalez, O. et al. (1994) Intestinal permeability in patients with ankylosing spondylitis and their healthy relatives. British Journal of Rheumatology, 33, 644–648.

10. Schmitz, H., Barmeyer, C., Fromm, M., Runkel, N., Foss, H.D., Bentzel, C.J.,…Schulzke, J.D.(1999) Altered tight junction structure contributes to the impaired epithelial barrier function in ulcerative colitis. Gastroenterology, 116, 301–307.

11. Hijazi, Z et al. (2004) Intestinal permeability is increased in bronchial asthma. Archives of Diseases in Children, 89, 227–229.

12. Macpherson, A.J., & Slack, E. (2007). The functional interactions of commensal bacteria with intestinal secretory IgA. Current Opinions in Gastroenterology, 23, 673-678.

13. Lin, Y. et al. (2000). Variability of the conversion of beta-carotene to vitamin A in women measured by using a double-tracer study design. American Journal of Clinical Nutrition, 71, 1545-1554.

14. Kidd, P. (2002). Th1/Th2 Balance: The Hypothesis, its Limitations, and Implications for Health and Disease. Alternative Medicine Reviews, 8(3), 223-246.

15. Agmon-Levin, N. et al. (2013). Vitamin D in systemic and organ-specific autoimmune diseases. Clinical Reviews in Allergy and Immunology, 45(2),256-266.

16. Finamor, D. et al. (2013). A pilot study assessing the effect of prolonged administration of high daily doses of vitamin D on the clinical course of vitiligo and psoriasis. Dermato-Endocrinology, 5(1), 222-234.

17. Yin, K., & Agrawal, D.K. (2014). Vitamin D and inflammatory diseases. Journal of Inflammation Research, 7, 69–87.

18, Tesmer, L.A. et al. (2012). Th17 cells in human disease. Immunology Reviews, 223, 87-113. doi:  10.1111/j.1600-065X.2008.00628.x

19. Davis, B.C., & Kris-Etherton, P.M. (2003). Achieving optimal essential fatty acid status in vegetarians: current knowledge and practical implications. American Journal of Clinical Nutrition, 78(3 Suppl), 640S-646S.

20. Calder, P.C. (1998). Dietary fatty acids and the immune system. Nutritional Reviews, II, S70-S83.

21. Simopoulos, A.P. (1991). Omega-3 fatty acids in health and disease and in growth and development. American Journal of Clinical Nutrition, 54, 483-463.

22. Sinclair, H. (1981). The relative importance of essential fatty acids of the linoleum and linolenic families: studies with an Eskimo diet. Progress in Lipid Research, 20, 897-899.

23. McAfee, A.J. (2011). Red meat from animals offered a grass diet increases plasma and platelet n-3 PUFA in healthy consumers. British Journal of Nutrition, 105(1), 80-90. doi: 10.1017/S0007114510003090.

24. Das, U.N. (1994). Beneficial effect of eicosapentaenoic and docosahexaenoic acids in the management of systemic lupus erythematosus and its relationship to the cytokine network. Prostaglandins Leukotrienes and Essential Fatty Acids, 51(3), 207-213.

25. James, A.M., & Murphy, M.P. (2002). How mitochondrial damage affects cell function. Journal of Biomedical Science, 9(6 Pt 1), 475–487.

26. Pieczenik, S.R., & Neustadt, J. (2007). Mitochondrial dysfunction and molecular pathways of disease. Experimental and Molecular Pathology, 83, 84-92.

27. Carlsen, M.H. et al. (2010). The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide. Nutrition Journal, 9(3),  doi: 10.1186/1475-2891-9-3

28. Astley, S.B. et al. (2004). Evidence that dietary supplementation with carotenoids and carotenoid-rich foods modulates the DNA damage: repair balance in human lymphocytes. British Journal of Nutrition, 91, 63-72. doi: 10.1079/BJN20031001.

29. Baur, J.A. et al. (2006). Resveratrol improves health and survival of mice on a high-calorie diet. Nature, 444, 337-342.

30. Wood, J.G. et al. (2004). Sirtuin activators mimic caloric restriction and delay ageing in metazoans. Nature, 430, 686-689, doi: 10.1038/nature02789.

31. Sies, H. (1997). Oxidative stress: oxidants and antioxidants. Experimental Physiology, 82(2), 291-295.

32. 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.

33. Tarek, K. et al. (2011). Zingiber officinale acts as a nutraceutical agent against liver fibrosis.  Nutrition and Metabolism, 8, 40. doi: 10.1186/1743-7075-8-40.

34. Lee, G-H. et al. (2017). Protective effect of Curcuma longa L. extract on CCl4-induced acute hepatic stress. BMC Research Notes, 10(1), 77.

35. Petri, S., Körner, S., & Kiaei, M. (2012). Nrf2/ARE Signaling Pathway: Key Mediator in Oxidative Stress and Potential Therapeutic Target in ALS. Neurological Research International, 878030.

36. Spanier, G. et al. (2008). Resveratrol reduces endothelial oxidative stress by modulating the gene expression of superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPx1) and NADPH oxidase subunit (Nox4). Phytochemistry, 69(8), 1732-1738.

37. Yen, G-C. et al. (2011).  Effects of polyphenolic compounds on tumor necrosis factor-α (TNF-α)-induced changes of adipokines and oxidative stress in 3T3-L1 adipocytes. Journal of Agriculture and Food Chemistry, 59(2), 546-551.

38. Riedl, M.A., Saxon, A., & Diaz-Sanchez, D. (2009). Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway. Clinical Immunology, 130(3), 244-251.

39. Michnovicz, J.J., Adlercreutz, H., & Bradlow, H.L. (1997). Changes in levels of urinary estrogen metabolites after oral indole-3-carbinol treatment in humans. Journal of the National Cancer Institute, 89(10), 718-723.

40. Kall, M.A., Vang, O., & Clausen, J. (1997). Effects of dietary broccoli on human drug metabolising activity. Cancer Letters, 114(1-2), 169-170.

41. Fowke et al. (2003). Urinary isothiocyanate levels, brassica, and human breast cancer. Cancer Research, 63(14), 3980-3986.

42. Muti et al. (2000). Estrogen metabolism and risk of breast cancer: a prospective study of the 2:16alpha-hydroxy-estrone ratio in premenopausal and postmenopausal women. Epidemiology, 11(6), 635-640.

43. Sepkovic, D.W., Bradlow, H.L., & Bell, M. (2001). Quantitative determination of 3,3’-diindolylmethane in urine of individuals receiving indole-3-carbinol. Nutrition and Cancer, 41(1-2), 57-63.

44. Cotillard, A., et al. (2013). Dietary intervention impact on gut microbial gene richness. Nature, 500(7464), 585-588.

45. Hawrelak, J.A. (2006). Textbook of Natural Medicine, 3rd ed. St. Louis: Churchill Livingston.

46. David, L.A., et al. (2014). Diet rapidly and reproducibly alters the human gut microbiome. Nature, 505(7484), 559-563.

47. Boermeester, M.A. (2014). A Hypothesis: Important Role for Gut Microbiota in the Etiopathogenesis of Diverticular Disease. Diseases of the Colon and Rectum, 57(4), 539-543.

48. Vojdani, A. (2014). A potential link between environmental triggers and autoimmunity. Autoimmune Disease, 43721.

49. Masharani, U. et al. (2015). Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes. European Journal Of Clinical Nutrition, (8), 944. doi:10.1038/ejcn.2015.39

50. Pastore, R.L., Brooks, J.T., & Carbone, J.W. (2015). Paleolithic nutrition improves plasma lipid concentrations of hypercholesterolemic adults to a greater extent than traditional heart-healthy dietary recommendations. Nutrition Research, 35(6), 474-479.  doi: 10.1016/j.nutres.2015.05.002.

51. Frassetto, L.A. et al. (2009). Metabolic and physiologic improvement from consuming a paleolithic, hunger-gatherer type diet. European Journal of Clinical Nutrition, 63, 947-955.

52. Boers, I. et al. (2014). Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study. Lipids, Health, and Disease, 13, 160. doi: 10.1186/1476-511X-13-160.

53. Aw, T. Y., & Jones, D. P. (1989). Nutrient supply and mitochondrial function. Annual Reviews in Nutrition, 9, 229 – 251.

54. Zeviar, D.D. et al. (2014). The role of mitochondria in cancer and other chronic diseases. Journal of Orthomolecular Medicine, 29(4), 157-166.

55. Hansen, S.H., Andersen, M.L., Cornett, C., Gradinau, R., & Grunnet, N. (2010). A role for taurine in mitochondrial function. Journal of Biomedical Science, 17(Suppl 1), S23.

56. Minich, D., & Bland, J. (2007). Acid-alkaline balance: Role in chronic disease and detoxification. Alternative Therapies in Health and Medicine, 13, 62-65.

57. Gibson, R.S., Heath, A.L., & Szymlek-Gay, E.A. (2014). Is iron and zinc nutrition a concern for vegetarian infants and young children in industrialized countries? American Journal of Clinical Nutrition, 100 Suppl 1, 459S-468S. doi: 10.3945/ajcn.113.071241.

58. Hunt, J.R. (2003). Bioavailability of iron, zinc, and other trace minerals from vegetarian diets. American Society for Clinical Nutrition, 78(3), 633S-639S.

59. Kao, D. et al. (2014). Fecal microbiota transplantation inducing remission in Crohn's colitis and the associated changes in fecal microbial profile. Journal of Clinical Gastroenterology, 48(7), 625-628. doi: 10.1097/MCG.0000000000000131.

60. Mao, R. et al. (2012). Fecal calprotectin in predicting relapse of inflammatory bowel diseases: a meta-analysis of prospective studies. Inflammatory Bowel Diseases, 18(10), 1894-1899.

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 www.EmpoweredAutoimmune.com: 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.

Internal Site Commenting is limited to members. 

Disqus commenting is available to everyone.

To comment:

Can Adults Develop Food Allergies?

Can Adults Develop Food Allergies?

269	October 28, 2017 • 9,592 views

Story at-a-glance

• Most of the processed foods on your grocery store shelves are laden with additives, preservatives, colorings, flavorings and other chemicals that may increase your risk of an allergic reaction
• Today, 1 in every 13 children has a food allergy and more adults are experiencing new food allergies
• Researchers are unsure of why the rate of food allergies continues to grow each year, but associations have been found between eating foods laced with antibiotics, impaired gut microbiome, low levels of vitamin D and food allergies
• If you or someone with you begins to have a severe reaction to food, it is vital you call your local emergency number (911 in the U.S.), administer an autoinjector of epinephrine if available, and remain quiet and calm until emergency personnel arrive

By Dr. Mercola

Most of the processed and packaged foods you find on your grocery store shelves are laden with additives, preservatives, colorings, flavorings and a number of other chemicals designed to make the product look and taste good. However, each of these additional chemicals increases your risk you'll have an adverse reaction.

Food allergies are the fifth leading cause of chronic illness in the U.S.,1 and the number of people who suffer from them is on the rise. In the decade between 1997 and 2007, the incidence of food allergies rose by nearly 18 percent in children under 18.2 Today, nearly 1 in every 13 children has some type of food allergy.3

Some of the more common foods that spark an allergic reaction in children are nuts, soy, wheat, shellfish and milk. Why those particular foods are the leading triggers is still not fully understood. Dr. Kari Nadeau, director for the Stanford Alliance for Food Allergy Research, points out there is no one protein similar between the foods, and that 30 percent of people who do have food allergies often are allergic to more than one food in that group.4

Scientists have found that allergies may run in families, meaning there may be a genetic factor, as well as environmental factors in the development of food allergies. However, at this point, there is no complete answer as to why some people develop a highly sensitive reaction to some foods and others don't. In the past, many of the cases of food allergies began in childhood, but today, it is not uncommon for those over 18 to develop an allergic reaction to foods, even those they have been eating their whole life.

Adult Onset Food Allergies Are Not Uncommon

Preliminary data from a national study shows that nearly 52 percent of Americans who have food allergies developed them after the age of 18.5 These same results showed that shellfish is the most common food allergy, followed by peanuts and then tree nuts, such as walnuts, pecans and cashews. Interestingly, when children are allergic to eggs, milk or wheat products, they may grow out of the reaction as they age. However, adults who develop a food allergy usually continue to suffer for the remainder of their life.

Dr. Ruchi Gupta, a food allergy researcher at Ann and Robert H. Lurie Children's Hospital, led this national study. She had found that in medical meetings around the world there appeared to be a higher number of adults reporting food allergies. However, as this was anecdotal evidence, Gupta and her team set out to quantify the information.6 The researchers surveyed over 40,000 adults from a national sample and found the foods that triggered allergic reactions in adults were the same as those affecting children.

Once the data was compiled, Gupta expressed interest in "why" adults develop food allergies. While gathering data from the sample, researchers asked the participants why they thought they had developed food allergies as an adult. The answers ranged from changing hormonal levels, moving to another area of the country or a viral illness.7 Gupta hopes to answer questions about why children maintain allergies through adulthood, and how adults are developing new ones, as these answers may have a significant public health impact.

The results of this study confirmed results of another study by FAIR Health that found a 377 percent jump in severe food reactions in the past decade.8 FAIR Health9 is a nonprofit, national repository of insurance claims data. The group looked through 24 billion insurance claims filed by 150 million people for diagnoses where anaphylaxis was caused by food reactions.

They discovered that not only had the number of individuals who experienced a severe food allergy jumped nearly fivefold from a decade ago, but nearly 25 percent of the claims were made in 2016.10 Another study by Food, Allergy, Research and Education (FARE), found that at least 15 percent of people who suffer from food allergies will develop them after age 18.11 Medical records of over 1,100 people diagnosed with food allergies were reviewed. The researchers found:12

• The age of the first reaction peaked in the individual's 30s
• The older the person at the time of the first reaction, the more severe the reaction
• A higher percentage were female
• Approximately 16 percent were allergic to more than one food

Do You Have a Food Allergy or Food Intolerance?

There is a difference between allergic food reactions and food intolerances. Although some of the symptoms may be similar, the differences are very important. If you are intolerant to a food, you may be miserable for hours to days after eating.13 However, if you are allergic, it could lead to a life-threatening situation. A food intolerance occurs in the digestive tract, while a food allergy triggers a systemic immune response.

The job of your immune system is to identify foreign invaders, separate them and destroy them. When your immune system overreacts to food or other allergens, it can result in a systemic allergic reaction. During an allergic reaction, your immune system mistakenly identifies specific a molecule as dangerous and produces immunoglobulin E (IgE) in an effort to neutralize the threat.14 Researchers suggest that childhood food allergies might be prevented with prenatal or early postnatal strategies toward desensitization.

Symptoms of a food allergy include hives, swelling, nausea and vomiting.15 If it progresses to cause life-threatening symptoms such as difficulty breathing or a drop in your blood pressure, it is called anaphylaxis. Some allergic reactions are less obvious, especially in children. Colic, reflux, eczema and chronic diarrhea may be signs of a food allergy in young children. One study found that up to 50 percent of cases of eczema in young children are the result of a food allergy.16

Symptoms of a food intolerance may be the result of an inability to digest the food from an enzyme deficiency or sensitivity to any of the food additives or chemicals. Sometimes, if you are intolerant, you may be able to eat small amounts of the food without experiencing a reaction. However, if you have a food allergy, you aren't able to eat any of the food without experiencing a reaction.17

A food intolerance does not involve the immune system and may be immediate or be triggered up to 20 hours after you've eaten the food. Symptoms of a food intolerance may be vague, such as bloating, passing gas, diarrhea or indigestion.  Another type of intolerance is called oral-allergy syndrome, during which you may get tingling or swelling around your mouth after eating some fruits and vegetables.18

This reaction is common in 50 to 75 percent of people who are allergic to birch tree pollen as the proteins in some fruits and vegetables are the same as those in the birch tree. Oral-allergy syndrome is a type of contact allergic reaction that usually appears immediately after eating the offending fruit or vegetable, does not usually lead to swelling of the throat and neck, and often disappears within hours.

Symptoms of Food Allergies May Not Be Obvious

In some instances, symptoms of a food allergy may not be as obvious as hives or swelling. For instance, an exercise-induced food allergy19 occurs when specific foods are eaten just before exercise, which may increase your potential for experiencing an allergic reaction, including serious or life-threatening reactions. Carefully track the foods you ate before the reaction and avoid them in the future. Not eating for two hours or more before exercise can help prevent this problem.

In many cases, gastrointestinal (GI) symptoms, such as bloating or gas, are related to a food intolerance. During a systemic immune response, histamine is released in your body. If the histamine is released to your skin, you develop hives that may progress to an anaphylactic response. However, if the histamine is released into your GI tract, it can cause nausea, diarrhea, vomiting and abdominal pain,20 in much the same way a food intolerance may present.

A rare food allergy to a protein in red meat may lead to GI symptoms, hives or anaphylactic shock.21 Many times, the allergic reaction is delayed by four to six hours, but not always. You may develop an allergic reaction to a protein molecule in red meat after being bitten by a Lone Star tick.22

In this case, something in the saliva of the tick prompts your body to create antibodies against galactose-alpha-1, 3-galactose carbohydrate molecule. Symptoms that develop after eating red meat include nausea, vomiting, stuffy nose, asthma or anaphylaxis. When you search medical studies in PubMed23 using the terms "food allergies" and "migraines" you are presented with over 150 studies associating migraine headaches with specific food allergies. Some of the top foods identified that induce migraines include:

Milk	Wheat	Yeast	Corn
Citrus	Cane sugar	Eggs	Grain cereals

The Number of Food Allergies Is on the Rise

Although the cause behind rising prevalence of adult-onset allergies is unknown, there may be several contributing factors. For example, there is a known association between food allergies and individuals with low levels of vitamin D.24 Since 75 percent of U.S. citizens are deficient in vitamin D,25 it makes sense the number of people suffering from food allergies is also rising.

In the past decade, food manufacturers have increased the number of additives, pesticides, herbicides and chemicals to packaged and whole foods, which also increases the number of potential allergens to which you are exposed at each meal. Genetic modification of foods may also increase the number of protein allergens found in plants, or create new ones.

Another common allergen that is added to many processed and packaged foods is soy. Although many Asian cultures eat soy each day in their diet, the soy they eat is fermented and quite unlike the soy fillers used in Western food. According to leading GMO expert, Jeffrey Smith:

"Levels of one known soy allergen, trypsin inhibitor, were up to seven times higher in cooked GM soy compared to cooked non-GM soy. Another study discovered a unique, unexpected protein in GM soy, likely to trigger allergies. In addition, of eight human subjects who had a skin-prick (allergy-type) reaction to GM soy, one did not also react to non-GM soy, suggesting that GM soy is uniquely dangerous.

… Documents made public from a lawsuit revealed that FDA scientists were uniformly concerned that GM foods might create hard-to-detect allergies, toxins, new diseases, and nutritional problems. Their urgent requests for required long-term feeding studies fell on deaf ears. The FDA doesn't require a single safety test."

Dr. Jonathan Hemler, pediatric allergy and immunology expert at Vanderbilt University School of Medicine, commented on the rising number of children and adults with food allergies, saying:26

“We have noticed that the prevalence of food allergy has tripled in the last 20 to 30 years. It's very concerning because we don't really have a good explanation as to why this is happening. Along with the increase in food allergy, we're also seeing more severe anaphylaxis events happening where adults have to go to the emergency room to get treatment."

Protection Begins in Your Gut

Protection against developing a food allergy may begin with your intestinal flora. Many of the pesticides in use today have an antibiotic action, including the dangerous, damaging and ever-present glyphosate. A steady diet of chemicals that have a low dose antibiotic action may have a devastating effect on your gut microbiome and trigger the development of food allergies.

Your gut microbiome plays an important role in your immune system and has an effect on your mood, cognitive function and overall health. One common bacteria found in your gut microbiome, Clostridia, may help protect against the development of food allergies. However, when your gut is affected by antibiotic action from your foods or prescribed medications, it may increase your risk of allergic reactions.

In a study using mice, researchers were able to demonstrate a lack of Clostridia in the mouse gut increased the probability the mouse developed food allergies,27 and when the Clostridia was returned, the food allergies subsided.28 When tested against Bacteroides, another bacterium found in the gut, it was only the Clostridia that had an effect against food allergies. The researchers discovered the Clostridia produced a signaling molecule called interleukin-22, known to help reduce the permeability of your gut wall.

This means the bacteria reduced the potential for leaky gut or the condition that allows allergens to enter your bloodstream. This discovery may lead to a formulation of probiotics specifically to treat food allergies and reduce leaky gut syndrome. Disruption of your gut microbiome may be the result of your food choices, past medication, cesarean birth, formula feeding or modern hygienic practices.

Truly, anyone suffering from food sensitivities or allergies would be wise to reconsider the kinds of foods they eat. Ultimately, your best bet is to switch to an all-organic diet. This is particularly important for young children and pregnant women, but I really believe this is the answer for everyone, whether you're prone to allergies or not.

Surviving a Systemic Allergic Reaction

Living with a food allergy may mean preparing to address anaphylactic shock if you unknowingly consume the wrong food. Although you may carry an auto-injector filled with epinephrine used to treat anaphylaxis, every reaction requires a trip to the Emergency Room.29 You may believe the epinephrine eliminated your symptoms, but you also have the risk of a rebound anaphylactic reaction once the effects of the epinephrine wear off. The injection is just part of the treatment as you may have more than one reaction.

If you or someone you're with appears to be having an anaphylactic reaction with symptoms of difficulty breathing, hives, swelling of the tongue or throat, change in voice quality or weak and rapid pulse,30 there are steps you can take to help increase the potential for survival:31

• Immediately call your local emergency medical phone number; 911 in the U.S. Do not hesitate to call as emergency personnel would rather evaluate you and send you home than to find you have died at home.
• If you or the person you are with is carrying an emergency epinephrine pen, use it immediately.
• The person having the reaction should lie quietly until emergency personnel arrive.
• Loosen tight clothing, cover with a blanket and lie on the left side, so aspiration of stomach contents into the lungs is prevented if vomiting occurs.
• If the person you're with stops breathing and no longer responds, start CPR. Do uninterrupted chest compressions, approximately 100 per minute, until the paramedics arrive.

DR. STEVEN GREER / The Fifth Kind Initiative

Former ER Physician Sounds The Alarm On Vaccination Dangers

The Interwoven Global Epidemics of Mercury Toxicity and Autism

OCTOBER 24, 2017

The Interwoven Global Epidemics of Mercury Toxicity and Autism

By Robert F. Kennedy, Jr.

In nature, toxic metals generally are bound with other elements rather than being present in their pure form. However, with the advent of large-scale industrial processes to extract metals from naturally occurring compounds, humans let the genie out of the bottle, contributing significantly to the distribution of mercury, aluminum and other heavy metals in the environment. When released from nature’s semi-protective hold, these “invariably toxic” metals wreak havoc on living systems, including humans, animals and plants alike.

Modern-day scientists have been amassing evidence of mercury’s toxicity for decades, with a growing focus in recent years on the metal’s association with neurodevelopmental disorders, including autism spectrum disorder (ASD). A new review article in the multidisciplinary journal Environmental Research pulls together a wide body of literature with the aim of summing up current research and emerging trends in mercury toxicology. Geir Bjørklund, the study’s lead author, is the founder of Norway’s non-profit Council for Nutritional and Environmental Medicine and has published prolifically on topics related to heavy metals, autoimmune disorders and ASD.

Multiple avenues of exposure

Exposure to mercurial compounds remains widespread, despite feeble attempts to ban some uses. Bjørklund et al.’s review covers all three categories of mercury: elemental, organic and inorganic. Exposure to volatile elemental mercury can come about as a result of occupational contact or vapor from dental amalgam fillings. Organic mercury—the most frequent form of exposure, according to Bjørklund and colleagues—exists as methylmercury (in fish) and ethylmercury (in the vaccine preservative thimerosal). Coal-fired power plants send inorganic mercury into the environment, where the toxic metal works its way up the marine food chain.

Because mercury plays no constructive metabolic role whatsoever, humans have not evolved effective mechanisms to excrete it. Children with ASD have a particularly hard time detoxifying and excreting mercury.

Interconversion between various forms of mercury also occurs. For example, elemental and organic mercury can cross the blood-brain barrier and bioaccumulate in the form of inorganic mercury. Studies also have described “mixed exposure” in the brain to both organic and inorganic mercury compounds. Because mercury plays no constructive metabolic role whatsoever, humans have not evolved effective mechanisms to excrete it. Children with ASD have a particularly hard time detoxifying and excreting mercury.

Multiple mechanisms of toxicity

Mercury exerts toxicity through a number of different mechanisms and has effects at both the molecular and cellular levels. For their purposes, Bjørklund and coauthors zero in on eight interrelated mechanisms, although there are others. Every single one of the toxic mechanisms that they describe has a documented association with ASD.

• Sulfur: A key and widely recognized fact about mercury is that it is “thiophilic,” meaning that it has an affinity for biochemically important sulfur compounds called thiols. Mercury binds to the sulfur-containing amino acid cysteine (which contains a thiol group); this allows mercury to piggy-back into brain cells and other target cells through a phenomenon known as molecular mimicry (meaning that the problematic mercury-cysteine entity “mimics” the useful amino acid methionine). According to leading toxicologists at the Centers for Disease Control and Prevention (CDC), mercury then “blocks or attenuates [the] protein molecule’s range of availability for normal metabolic function.” Mercury also reduces sulfate absorption. Individuals with ASD frequently have low levels of sulfate.
• Immune activation and autoimmunity: Bjørklund et al. outline numerous mercury-related immune system effects, including “immunostimulation, immunosuppression, immunomodulation, delayed-type hypersensitivity…, and autoimmunity.” These effects occur largely due to mercury’s influence on immune cytokines—proteins that are important in helping cells communicate. Chronic elevation of inflammatory cytokines and other immune abnormalities such as activation of microglia (immune cells in the brain) are hallmarks of both mercury exposure and ASD.
• Protein synthesis: Researchers have reported since the late 1960s that mercury inhibits protein synthesis (a fundamental cell process that involves both DNA and RNA), interfering with cells’ ability to build new proteins. Bjørklund and coauthors report that inorganic mercury is particularly disruptive in this regard. Investigators have postulated that dysregulated protein synthesis, which disrupts the balance between excitation and inhibition in brain cells, plays a causal role in ASD.
• Brain microtubules: Neuropsychiatrist Jon Lieff describes microtubules as “the brains of the cell” and suggests that cerebral microtubules may be “the seat of consciousness.” Microtubules form the scaffolding required by axons (nerve fibers that transmit neuronal signals). Mercury preferentially targets axonal microtubules, leading to their “depolymerization and derangement,” according to the Environmental Research authors. Moreover, mercury is unique among toxic metals in having these microtubule effects. Axonal disturbances and the altered brain connectivity that these disturbances promote are widely documented features of ASD.
• Membrane transport: Cell membrane transport refers to the process whereby molecules (such as amino acids) pass into or out of a cell. Mercury can disturb amino acid transport and also “penetrate” across biological membranes. The authors note the need for “approaches to inhibit [mercury’s] transfer both at the placental border and at the blood-brain barrier.” An international research group recently described the relationship between ASD and impaired amino acid transport at the blood-brain barrier.
• Glutathione: Numerous researchers have described how organic mercury, in particular, impairs glutathione activity, thereby lessening protection from oxidative stress and weakening the body’s detoxification capacity. The relationship is bidirectional, according to Bjørklund and coauthors, because when brain glutathione levels drop, the uptake of mercury in brain tissue increases substantially. Lowered glutathione levels, elevated oxidative stress and a higher body burden of mercury have been repeatedly documented as core characteristics of ASD.
• Metallothioneins: Metallothioneins (MTs), a family of proteins, are antioxidants and metal chelators that work to maintain metal homeostasis. MTs also play an important role in neuroprotection and regeneration. Although MTs are present to “protect the brain and gastrointestinal tract against overload by toxic metals,” Bjørklund and coauthors cite evidence showing that common genetic mutations and variations in MTs may increase some individuals’ susceptibility to mercury-induced neurotoxicity, including individuals with ASD. Studies have identified “a significant increase in both metal content and metallothionein expression” in autistic children.
• Zinc and copper: Appropriate metabolism of zinc and copper is important for healthy neurological functioning. When mercury binds to metallothioneins, it can substitute for zinc and copper, “interact with [zinc] and [copper] availability” and thereby disturb the normal zinc-copper ratio. In a previous publication, Bjørklund described mercury’s role in disturbing zinc and copper metabolism and the typically low zinc-copper ratio in autistic children. Other researchers have measured the zinc-copper ratio in plasma as a biomarker for mercury toxicity in ASD children.

Reducing mercury toxicity

Bjørklund and coauthors also devote several paragraphs to a discussion of the essential trace element selenium, which plays an important antioxidant role, among other functions. The authors note that mercury is highly “selenophilic,” binding to selenium “with an extraordinarily high affinity…when compared with the affinity for sulfur.” The welcome implication spelled out by the authors—which has been known to researchers for nearly half a century—is that selenium has a “high capability…to reduce the toxicity of [mercury] compounds.” The authors list several mechanisms whereby selenium can minimize mercury-induced toxicity, such as by improving mercury’s excretion or sequestration and strengthening antioxidative activity. Autism researchers have identified “a significant elevation of [mercury]…together with a significant decrease in the [selenium] levels in [red blood cells] of patients with ASD when compared to…healthy controls.” These researchers agree that selenium has an important role to play in reducing mercury toxicity in ASD patients. 

Translating research into action

It has been over a decade and a half since a seminal publication in Medical Hypotheses described autism as “a novel form of mercury poisoning” and showed how “every major characteristic of autism has been exhibited in…cases of documented mercury poisoning.” Ten years later, Kern and colleagues published a detailed consideration of “parallels between mercury intoxication and the brain pathology in autism” in Acta Neurobiologiae Experimentalis. A 2017 publication in Molecular Neurobiology by autism expert Dr. Richard Frye and others reviews “associations between mercury exposure and ASD subtypes,” even “at doses well below the current reference levels considered to be safe.” Thus, Bjørklund and coauthors are far from alone in synthesizing the evidence base and drawing attention to the global public health epidemics of mercury toxicity and autism.

The CDC authors concluded that there are “many commonalities [and] similarities in the mechanisms of toxic action of methylmercury and ethylmercury,” particularly regarding their association with neurotoxicity and neurodevelopmental disorders such as ASD.

Last year, CDC toxicologists published a comprehensive review that specifically focused on the two forms of organic mercury. The CDC authors concluded that there are “many commonalities [and] similarities in the mechanisms of toxic action of methylmercury and ethylmercury,” particularly regarding their association with neurotoxicity and neurodevelopmental disorders such as ASD. Both forms of organic mercury cause DNA damage (or impair DNA synthesis), affect cell division, decrease glutathione activity and increase oxidative stress, among other similar effects. These findings are particularly noteworthy in light of Bjørklund and coauthors’ observation that “co-exposure with [ethylmercury] and [methylmercury] might induce more adverse neurotoxic effects than each agent alone.” Bjørklund’s team calls on researchers to actively investigate these additive toxicological effects.

At the end of the day, as noted by mercury expert Philippe Grandjean, there is a need to move beyond simply generating “endless replications” in the form of “thousands of toxicology publications every year” on mercury and other well-understood toxic metals. The Bjørklund team’s broad review of over 200 studies—including recent findings as well as articles dating back several decades—shows that we already know more than enough about mercury’s hazards to take decisive action.

Sign up for free news and updates from Robert F. Kennedy, Jr. and the World Mercury Project. Your donation will help to support us in our efforts.

Doctors Issue Warning About LED Streetlights

Doctors Issue Warning About LED Streetlights

4.6K	July 16, 2016 • 170,184 views Disponible en Español

Story at-a-glance

• The American Medical Association (AMA) issued new guidance for communities on how to “reduce the harmful human and environmental effects of high-intensity [LED] street lighting”
• LED streetlights operate at a wavelength that adversely suppresses melatonin at night — five times more so than other types of light
• Discomfort and disability caused by the intense LED lighting may “decrease visual acuity and safety, resulting in concerns and creating a road hazard”
• Migrating birds and other wildlife may be disoriented by LED lighting at night

By Dr. Mercola

The light-emitting diode (LED) is rapidly replacing earlier lighting technology, including incandescent bulbs and compact fluorescent lamps (CFLs). There’s good reason for this, as LEDs are far more energy efficient, longer-lasting and produce excellent light quality compared to other types of lighting.

For instance, according to the U.S. Department of Energy (DOE), LED lights use at least 75 percent less energy, while lasting 25 times longer than incandescent lighting.1

It’s estimated that compared to no LED use, widespread LED use in the U.S. by 2027 could save the equivalent electrical output of 44 large electric power plants each year, which would add up to a total of at least $30 billion in savings, according to DOE.2

LEDs are different from incandescent bulbs in three key ways. One, they emit very little heat compared to incandescent bulbs and CFLs, which release 90 percent and 80 percent of their energy as heat, respectively.

Two, LEDs emit light in a specific direction, which make them very efficient and reduces the need for reflectors and diffusers.

Finally, LEDs contain a mix of red, green and blue light, which is usually combined to make white light.3 The light is brighter, whiter and bluer than incandescent bulbs, which contain far more yellow and red light.

The “white” LED light is so bright and energy efficient that about 10 percent of U.S. municipalities are now using it for their streetlights, with more expected to follow suit.4 Unfortunately, in making this change a new set of potential problems has emerged.

American Medical Association Gives Warning About LED Streetlights

At the 2016 Annual Meeting of the American Medical Association (AMA), the AMA issued new guidance for communities on how to “reduce the harmful human and environmental effects of high-intensity [LED] street lighting.”

AMA Board Member Dr. Maya A. Babu said in a news release, "Despite the energy efficiency benefits, some LED lights are harmful when used as street lighting.”5

The guidance focused on high-intensity LED lighting, which emits a large amount of blue light and appears white to the naked eye. Risks noted by the AMA include risks to nighttime drivers, including:

• Worse nighttime glare than conventional lighting
• Discomfort and disability caused by the intense lighting may “decrease visual acuity and safety, resulting in concerns and creating a road hazard”

The AMA also pointed out that blue-rich LED streetlights operate at a wavelength that adversely suppresses melatonin at night — far more so even than other types of light. The AMA noted white LED lights “have five times greater impact” on circadian sleep rhythms than conventional street lamps.

This in turn, may lead to problems with sleep and related conditions. They cited “recent large surveys” that found brighter nighttime light in communities is linked with:

• Reduced sleep times
• Dissatisfaction with sleep quality
• Excessive sleepiness
• Impaired daytime functioning
• Obesity

Residents Demand Removal of Harsh LED Lighting

Residents living in communities that have made the switch to LED have gone so far as to demand the harsh lighting be removed. Such was the case in Davis, California, where new LED streetlights were installed in January 2014.

By May that year, negative public reactions caused the city council to put the light replacement project on hold. According to the Smart Outdoor Lighting Alliance (SOLA), which promotes ecologically responsible outdoor lighting:6

“The city received 40 comments by residents of which 36 or 90 percent were negative.

The complaints were focused on the new fixtures being too bright, producing too much glare and light trespass, increasing skyglow and light pollution, and resulting in potential negative impact on human health and wildlife.  

… [T]he City of Davis should be commended for listening to the residents once the installation was started and for having the courage to remedy the problems that were communicated.”

Ultimately, the new LED fixtures (some 1,400 that had already been installed) were replaced with lower-intensity bulbs.

A similar scenario occurred in New York City, where hundreds of people launched a petition in protest of LED streetlights, comparing them to “an emergency construction zone,” “a zombie picnic” and “the ‘Close Encounters’ mothership.”7

In response, the city has swapped out some of the lights with lower wattage LED bulbs.

Why LED Lights’ Significant Impact on Melatonin Is a Big Deal

The fact that LED lights suppress the hormone melatonin significantly more so than other lighting is a serious issue — and here’s why. Your brain typically starts secreting melatonin around 9 or 10 p.m., which makes you sleepy.

These regularly occurring secretions help regulate your sleep cycle as well as provide other important health benefits, including helping to prevent cancer.

Melatonin acts as a marker of your circadian phase or biological timing. In a nutshell, this hormone influences what time of day or night your body thinks it is, regardless of what time the clock on the wall displays.

Melatonin is produced by a pea-sized gland in the middle of your brain called the pineal gland. In a normal night's sleep, your melatonin levels stay elevated for about 12 hours.

Then, as the sun rises, your pineal gland reduces your production of melatonin, and the levels in your blood decrease until they're hardly measurable at all. When your circadian rhythms are disrupted, such as from shift work, jet lag or nighttime light exposure, your body produces less melatonin.

Melatonin deficiency may come with some profound biological disadvantages, such as higher levels of inflammation, a weakened immune system and an increased risk of cancer.

If you’re exposed to LED lighting often at night (such as if LED streetlights shine in your bedroom window), it could have a profoundly negative influence on your health.

AMA: Light Pollution Via LED Streetlights Poses Environmental Risks

It’s not only humans that may be harmed by widespread adoption of LED streetlights. Wildlife is also adversely affected. Hundreds of bird species migrate at night, for instance, and bright LED lighting may disorient the birds and draw them toward the light.

Some birds die from colliding with buildings lit up with LED lights while others circle the buildings, seemingly unable to break away from the LED trance. Many die of exhaustion as a result.8 Other species that depend on dark nighttime environments are also harmed by the bright LED lights. AMA explained:

“ … [P]oorly designed LED lighting disorients some bird, insect, turtle and fish species, and U.S. national parks have adopted optimal lighting designs and practices that minimize the effects of light pollution on the environment.”

AMA Recommends Minimizing Use of Blue-Rich Light at Night

Red and amber lights will not suppress melatonin, while blue, green and white lights will. The reason for this is because these are the wavelengths that are the most common outdoors during daytime hours. To protect your melatonin production, it’s important to avoid the blue light wavelength after sunset.

This includes the light emitted by electronics such as your TV, computer and other electronic screens. AMA also recognized the importance of minimizing blue-light exposures, stating:9

“Recognizing the detrimental effects of poorly-designed, high-intensity LED lighting, the AMA encourages communities to minimize and control blue-rich environmental lighting by using the lowest emission of blue light possible to reduce glare. The AMA recommends an intensity threshold for optimal LED lighting that minimizes blue-rich light.

The AMA also recommends all LED lighting should be properly shielded to minimize glare and detrimental human health and environmental effects, and consideration should be given to utilize the ability of LED lighting to be dimmed for off-peak time periods.”

Do This at Sundown to Protect Your Health

In the evening (around 8 p.m.), you’ll want to dim your lights (whether they’re LED, incandescent or CFLs) and turn off electronic devices to reduce your exposure to light that may stifle your melatonin production. After sundown, shift to a low-wattage bulb with yellow, orange or red light if you need illumination. A salt lamp illuminated by a 5-watt bulb is an ideal solution that will not interfere with your melatonin production.

If using a computer or smartphone, install blue light-blocking software like f.lux, which automatically alters the color temperature of your screen as the day goes on, pulling out the blue wavelengths as it gets late. The easiest solution, which I recently started using myself, however, is to simply use amber-colored glasses that block blue light.

I found a Uvex model (S1933X) on Amazon that costs less than $10 and works like a charm to eliminate virtually all blue light. This way you don't have to worry about installing programs on all your devices or buying special light bulbs for evening use.

Once you have your glasses on, it doesn't matter what light sources you have on in your house. You can even wear these glasses outdoors at night if you’ll be traveling in an area with LED streetlights. When you’re ready to climb into bed, make sure your bedroom is pitch black. The slightest bit of light in your bedroom can disrupt your body’s clock and your pineal gland's melatonin production.

It’s a good idea to cover your windows with drapes or blackout shades to achieve this — especially if you have LED streetlights outside your bedroom window. If this isn’t possible, wear an eye mask.

Health Ranger: Why independent science TERRIFIES the food and supplement industries (but shouldn’t)

Wednesday, October 25, 2017 by: Mike Adams
Tags: chemicals, contaminants, Food Forensics, food labels, food science, food testing, Health Ranger, Heavy metals, ingredients, Mike Adams, Natural.news, Organic, pesticides

(Natural News) Over the last few years, Natural News has set something in motion that absolutely terrifies the food and supplement industries. What have we done that’s so frightening? We’ve started to use good science to analyze foods and supplements for heavy metals, pesticides, industrial chemicals and more.

We were instrumental in accelerating the independent food science movement in 2013, first exposing the toxic heavy metals (lead, cadmium, mercury) in organic rice protein products imported from China. Very quickly, the entire protein industry moved away from that contaminated rice material, vastly reducing toxic heavy metals exposure across tens of millions of consumers. That never would have happened without Natural News and my laboratory, CWC Labs.

In the years since, we’ve exposed the shockingly high level of lead in zeolite products, and we’re now publishing summary charts showing analyses of supplements, covering pesticides, pharmacological chemicals, heavy metals and much more. (See example report below.)

What you are witnessing in all this is the “democratization of science.” It is a decentralized revolution in food transparency, and the movement is rapidly proliferating. In addition to the Consumer Wellness Center (where I serve as the executive director) now analyzing and publishing food analysis results, another non-profit group called the Clean Label Project is also conducting laboratory analysis of products. The Organic Consumers Association, Cornucopia and the Environmental Working Group are also engaged in lab analysis of foods and personal care products, and I’m personally aware of at least two more similar projects coming online in 2018.

Four years ago, we were called “conspiracy theorists” for exposing lead in rice protein… now we’re the pioneers of new science

Fascinatingly, the outstanding science we are all conducting was originally rejected as a “conspiracy theory” by dishonest supplement industry hucksters. A few of them desperately tried to silence my own work, and to this day they lie to their own customers and claim their contaminated products are “clean.” Yet, to this day, no one has ever shown my lab results to be incorrect. The lead contamination of organic rice protein products I first spotted in 2013 was a very serious issue for the supplements industry, and that’s why Garden of Life, Vega and most other protein manufacturers changed their formulations to avoid toxic rice protein.

Now, my own lab is ISO accredited (17025), meaning its results are accepted as scientific facts by any court of law in the western world. We were also awarded a Certificate of Excellence in heavy metals tested for environmental water samples. No one argues with the results of the food science we conduct; they simply engage in character assassination to try to avoid admitting the truth: Their products are dirty. And they’ve been lying to their own customers for decades.

Just this week, the Clean Label Project discovered that 80% of infant formula samples tested “positive” for arsenic. Although I disagree with the use of the term “positive” when it comes to heavy metals — a preferred result would report ppb concentrations — nobody is calling the Clean Label Project a group of “conspiracy theorists” for daring to conduct heavy metals analysis on food products.

That’s because the food industry has slowly come to realize they can’t stop independent science. If they put a product on the shelf, we can buy that product, test it, and report the results to the public. Although the extremely high cost and technical difficult of building and running a qualified lab is way beyond the reach of most organizations — I’ve spent over $2 million on my lab, and very few people have the required scientific qualifications to operate mass spec instruments — there are still a growing number of non-profits that are investing in good science to analyze off-the-shelf products in the public interest.

The days of food and supplements hiding toxic ingredients is rapidly coming to an end

For decades, the food and supplements industries hid toxic ingredients behind pleasant-looking labels, tricking consumers into buying heavily contaminated products while making them believe they were “better than organic.” For example, if I hadn’t spearheaded the science investigation into organic rice protein products, even Garden of Life might still be selling “Raw Protein” contaminated with mercury and lead (which is exactly what they were doing up until early 2014, but they since reformulated).

Even today, Whole Foods Market and Amazon.com continue to sell food and supplement products that are routinely contaminated with toxic heavy metals. Isn’t it interesting that the Washington Post — owned by Jeff Bezos, the founder of Amazon — seems to take no interest in reporting that science? Instead, they try to cover it up and pretend such heavy metals don’t exist. But their science denialism is only making them look like fools, as real people are now turning to other independent news sources (like this website) to learn the truth that the Washington Post won’t dare tell them.

There’s a spillover benefit to the public in all this, by the way. The fact that we exposed the heavy metals in rice protein products also served notice to other companies that they, too, should start testing their own finished products for heavy metals. As a result, this independent lab science effort has resulted in a safe, more honest food supply for everyone. That’s part of our mission, of course: To celebrate clean foods while encouraging those who have contaminated materials to clean up their act.

Now, with Natural News, the Clean Label Project, the OCA, EWG and other groups all pursuing the same mission of full transparency for products, the days of food and supplement companies hiding toxic ingredients (or contaminants) in their products is rapidly coming to an end. Now, it’s only a matter of time before everybody’s products get tested by one or more of these independent science groups.

The free market, in other words, has taken over the job of the FDA and is using good science to conduct lifesaving research on the chemical composition of foods and supplements.

Our approach to food science testing and honest reporting

I want to assure the food and supplement manufacturers that I am personally dedicated to honest and accurate reporting on the composition of your products, including recognizing you for your quality control efforts. That’s why the non-profit Consumer Wellness Center, where I serve as the executive director, has come up with the following streamlined reporting format. The example shown below is a real product and the results are also real: (article continues below)

//////////////////////////////////////////////////////////////////////////

LonoLife: Savory Chicken Bone Broth (Paleo) Testing Date: 10/3/2017 Lot Number: 042019 Sample Number:

Certified Organic:
Labeled Non-GMO:
Ingredients Rating:
Low Heavy Metals Rating:
Pesticides/Herbicides:
Fungicides:
Antibiotics / Antibacterials:
Pharmacological Drugs:
Toxicological Drugs:
Industrial Chemicals:

All testing conducted in the public interest by the non-profit Consumer Wellness Center using an ISO-accredited laboratory, via mass spec technology. Consumer Wellness Center testing results explained | Manufacturers: How to dispute these results

//////////////////////////////////////////////////////////////////////////

As you can see from the sample chart shown above, we combine heavy metals testing with other mass spec tests for pesticides and chemicals to arrive at a final algorithmic score for each product. This honest, transparent scoring system does not generate unfounded alarm for very tiny “trace” levels of chemicals, many of which are found in almost every non-organic food product.

The Clean Label Project, I might suggest, should learn from this. They are reporting that baby foods test “positive” for arsenic, but if that arsenic level is just 15 ppb, for example, it poses no real danger to anyone (especially since it’s probably mostly organic arsenic). With sensitive enough instruments, you can find parts per trillion of lead and arsenic in almost everything, so when it comes to reporting heavy metals, concentrations really matter. Eating 10 grams of arsenic at 15 ppb is very different from eating it at 1.5 ppm (which is 100 times higher).

This is why, when food and supplement companies really look around and see how results are being reported, they are going to vastly prefer my reporting approach because I don’t flag products as being dangerous if they only contain trace levels that pose no real risk. Truth be told, if the Clean Label Project were to test every single food item in the grocery store, they would find trace arsenic in almost everything (if they’re running a sensitive enough ICP-MS instrument), including fresh apples.

If you’re feeding your baby anything made from non-organic rice, you are likely poisoning your baby

Note, above, that I sounded the alarm over toxic contaminants in rice protein four years ago. What’s fascinating about the Clean Label Project’s findings is that most of their “worst”-rated baby cereals are made with rice ingredients. Rice is a food material that I’ve consistently found to be heavily polluted (when coming from China, but not the USA, where rice is much cleaner). Here’s the list of the worst baby cereals from the Clean Label Project:

1. Healthy Times Special Nourish Organic Brown Rice Cereal for Baby
2. Organix Raspberry & Banana Muesli
3. Gerber DHA & Probiotic Rice Cereal with Vitablocks
4. Earth’s Best Organic Whole Grain Rice Cereal
5. Parent’s Choice 1st Stage Rice Baby Cereal

This list does not surprise me, since I routinely see arsenic, pesticides and crazy toxic chemicals in products made from rice. Interestingly, I’ve tested U.S.-grown rice vs. China-grown rice and I’ve found that U.S. rice is very clean, including Lundberg rice from California. But rice grown in China tends to be heavily contaminated, and because it’s so cheap to produce in a polluted environment, a lot of China-grown rice ends up in U.S. products made from rice… including baby food products. (Don’t act surprised.)

You can see all my heavy metals testing results, by the way, in my science book called Food Forensics. There, I’ve listed the heavy metals test results for over 800 foods, spices and even dog food products.

Here’s another whopper that terrifies the food industry, and I’m going to be launching some shocking science on this next year: “Organic” in China is largely a fraud. USDA enforcement of organic standards in China-grown food products is a complete joke. It is well known even in the organic industry that China’s “organic” is to real organic what Harvey Weinstein is to women’s dignity.

For those of you eating “Guten-free” products, by the way, you’re also eating a lot of non-organic rice, which means you are gobbling down all sorts of heavy metals and toxic chemicals while falsely believing you’re following a healthy diet. I’ll be testing many gluten-free products very soon and releasing the results via Good Gopher Mail, a free email inbox that bypasses censorship to bring you lab science results for food and supplement products.

To other independent labs: Make sure you’re reporting concentrations and not flagging false alarms over non-significant findings

In contributing to the public discussion about clean foods, I want to encourage all independent science groups and non-profits to carry out honest assessments of the concentrations of various analytes when they are being reported. It’s very easy for a group like the Clean Label Project to get a lot of press for reporting products that test “positive” for arsenic or lead, but without reporting concentration data, the claim of testing “positive” is scientifically lacking useful data.

That’s why we went with our new format that offers letter grades for heavy metals concentrations, and provides four descriptive levels for pesticides and other chemicals:

• CLEAR – None detected
• TRACE – Residual amounts detected
• CONCERN – Significant amounts detected
• AVOID – Potentially dangerous amounts detected

Consumers, meanwhile, need to be educated to understand the difference between “trace” vs. a dangerous concentration of a chemical. To say that some food contains one arsenic element (i.e. tested “positive” for arsenic) is about as useful as saying a sample tested positive for carbon. (Hint: There’s carbon in all foods, in nearly every molecule.)

What I’m concerned about is not so much the very tiny, trace levels of arsenic, pesticides or even glyphosate that might be found in many products. Instead, I’m interested in identifying those products that show extremely high levels (concentrations) of such items, which might pose a genuine danger to public health and safety.

For example, I recently tested some “magical” pills from an Indian guru huckster and found some of them to contain something like 400 – 800 ppm of mercury. (No, that’s not a typo.) These pills are extremely dangerous and may cause extreme harm to consumers who take them. (The woman who sent them to us said she kept vomiting each time after taking them. The Indian guru told her she was “detoxing.”)

That’s why millions of people read Natural News and support our mission: We are rooting out toxic, dangerous and heavily contaminated products across the industry while also highlighting those products which test clean.

That’s why no honest food or supplement company should fear our science. We’re here to confirm your clean products and spread the word, supporting your good work in sourcing clean raw materials. The only companies that have anything to fear are those that refuse to conduct laboratory testing or work to source clean raw materials. To those companies, sooner or later the science is going to catch up with you.

Our goal for 2018 is to test over 1,000 off-the-shelf products for pesticides, heavy metals, industrial chemicals and more. We’ll be publishing results at Good Gopher Mail (actually, we’ve already started publishing there). To sign up for a free inbox there if you want to be kept informed as we release our findings to the public.