Sunday, September 3, 2017

Toxic Tattoos links to Inflammatory and autoImmune Disorders


Toxic Chemicals Found in Tattoos: Links to Autoimmune and Inflammatory Diseases
2786

3Posted on: Thursday, August 31st 2017 at 7:15 pm

Tattooing is a long-standing human ritual that transcends historical and sociocultural boundaries, but more regulatory oversight is needed to ensure inks are not contaminated with dangerous chemical byproducts.
Debunking Tattoo Mythology: A Short History of The Tattooing Ritual
Tattoos represent a cultural rite of passage, a mode of self-expression, and a means of cultivating one’s unique identity (1). British captain, explorer, and navigator James Cook introduced the word tattoo into the European vernacular, as an amalgamation of the Polynesian word ‘ta’ to ‘strike something’ and the Tahitian word ‘tatau’ meaning ‘to mark something’ (2). 
The historical use of tattoos extends back at least seven thousand years ago, as tattoos were discovered on the extremities of a mummy from that period found in Northern Chile (3). Also, the five thousand year-old mummified remains of Ötzi the Iceman were found to contain osteochondrosis, or abnormal bone growth, in body sites where tattoos were present (2). Pesapane and colleagues (2014) likewise note that documentation of tattoos dates back to records by Roman emperor Constantine the Great in 313 AD, Pope Hadrian 1 in 787 AD, and the Old Testament (2).
Historically, tattoos were used to demarcate group identity, to protect the internal body from the exterior world, as a symbol of religious indoctrination, and in branding rituals as a form of medieval punishment. As an example of tattoos signifying group affiliation, “Crusaders used mostly Christian motifs to ensure that they received a Christian funeral in case they died in a foreign country” (3). In Japan, on the other hand, criminals were branded with tattoos as a mark of social stigmatization from the eighteenth century onward, which led to the rise of a tattooed demographic called the Yakuza (3).
Although condemned as marks of defilement by monotheistic religions, tattoos were a venerated practice in ancient Egypt and Rome, and remained a secret practice in some Christian sects such as the Sanctuary of Loreto (2). Ocean expeditions of the eighteenth century heralded a resurgence in the popularity of the tattoo, as interaction of colonialists with local South Pacific cultures led to adoption of local tattoo motifs by the former, and the eventual replacement of native designs with European-themed tattoos (3).
In the nineteenth century, a veritable “tattoo mania” was embraced by elite aristocratic European social classes (2). Celebrity figures including Tsar Nicholas II, Sir Winston Churchill, and Empress Elisabeth of Austria all sported tattoos (2, 3). However, in the late nineteenth century, the law profession contributed to the demise of the traditional meanings of the tattoo in their attempts to “conclude from the physiognomy of the exterior appearance as to the moral standards or criminal intent of a person” (3). The public perception of tattoos was also influenced by the display of tattooed persons as elements in circuses and carnivals (3).
Today, popularity of tattooing once again soars, as studies have demonstrated that nearly a third of university students, and 80 million people in the United States, are tattooed (4, 5). With its origins in pre-industrial cultural traditions and supernatural mythology, tattooing and other body modifications have been a long-standing component of the human condition. Clearly, “Tattoos and piercings can no longer be regarded as destructive acts of self mutilation practiced by fringe groups” (1, p. 115).
Histologic Reactions Secondary to Tattoos
Although the age of moralizing tattoos as an indictment of character should be long passed, concerns linger over health implications. According to Wenzel and colleagues (2013), “Medical complications after tattooing are often seen by physicians, but are generally unknown to the public” (6, p. 138). Tattoos have been associated with “allergic, lichenoid, granulomatous, and pseudolymphomatous reactions or induction of skin diseases” (2, p. 145). Other localized skin diseases, including the autoimmune disorders lichen planus and psoriasis, as well as eczema and morphea, have also been induced by tattoos (7). 
In one nationwide survey of German-speaking countries, for example, 67.5% of individuals with tattoos reported skin problems, 6% reported systemic reactions resulting from tattoos, with 1.3% reporting light sensitivity of the tattooed skin (8). The survey similarly revealed that chronic problems including burning, itching, erythema, papules, nodules, and eczema occurred in 6% of subjects (8). It is estimated that five million people in the United States have persistent skin problems secondary to tattoos, but data on toxicant-induced health problems related to tattoos has not been systematically collected (9).
According to Goldstein (1979), “The injection of any foreign material into the skin produces an inflammatory response, and some degree of necrosis, due to mechanical disruption of the tissue” (10, p. 896). Although this initial reaction normally subsides, subsequent sensitization reactions can occur along with mild fibrosis of the papillary dermis, meaning thickening and scarring of collagenous connective tissue (10). 
In addition, perivascular infiltration of lymphocytes and macrophages, meaning migration of white blood cells of the immune system to sites around slightly dilated blood vessels, is also a feature of tattooed tissues (10). Various histological abnormalities can occur, such as foreign-body type or sarcoid type granulomatous formations, comprised of aggregates of macrophage cells known as histiocytes (10). Inflammatory infiltrates characterized by significant fibroplasia, or the growth of fibrous tissue, creating nodules known as dermatofibroma and keratoses can also occur (10).
Pathological skin pigmentation, known as cutaneous dyschromia, can likewise occur due to deposition of heavy metals such as bismuth and mercury in the basement membranes of sebaceous glands and sweat ducts (10). 
Tattoo Safety: A Need For More Regulatory Oversight
Researchers state, "Tattoo inks are typically composed of negligibly soluble or insoluble pigments, dispersants in which the pigments are suspended and other additives for preservation or to alter the viscosity of the ink" (11). Although some contemporary inks can contain organic pigments, colored ink conventionally contains metals (12). Because other industrial applications of tattoo inks include paint and printing, they can harbor up to 10% impurities (9). Further, studies show that the "vast majority of tested tattoo inks contained significant amounts of NPs [nanoparticles],” which are associated with a litany of ill health effects (13).
A recent study published in the Journal of Hazardous Materials revealed that chemicals present in tattoo ink induced cytotoxicity (cell death), genotoxicity (DNA mutation), and adaptive stress response pathways (11).  Adaptive stress pathways are activated to restore cellular homeostasis, or balance, following damage incurred to cell structure, indicating that tattoo ink disrupts cellular integrity (34). Chemicals in tattoo ink can contribute to deleterious health outcomes by different modes, including binding of chemicals to enzymes and biological molecules and partitioning of chemicals into cell membranes (11).
Safety Hazards of Colored Inks
Because no color additives are approved for intradermal injection, no tattoo pigments are approved for use by the Food and Drug Administration (FDA). As articulated in a study by Arisa and Alster (2012), “The majority of tattoo ink is industrial-grade color intended for use as printer ink or automobile paint” (14).
Colored pigments, on the one hand, can decompose following light exposure into dangerous aromatic amines which are subsequently disseminated throughout the body and accumulate in lymphatic system, interfacing directly with components of the immune system (6). In a recent study, the levels of genotoxicity (DNA damage) and oxidative stress (inflammatory) pathways induced by red and yellow tattoo ink were particularly troublesome, as they generated the greatest response (11). Another study by Falconi and colleagues (2009) found that red tattoo ink significantly reduced viability of fibroblast cells, which are responsible for production of the extracellular matrix that provides the structural framework for tissues (15). 
When exposed to natural or ultraviolet light, azo pigments contained within red and yellow inks have been demonstrated to emit hazardous compounds, and they also have been shown to contain the probable human carcinogen 3,3-dichlorobenzidine as an intermediary in their production (11). Furthermore, o-anisidine and 4-aminobiphenyl, aromatic amines within red ink, can elicit genotoxic effects, damaging genetic material after metabolic activation (11, 16). Other investigations have elucidated a connection between red tattoo ink, skin irritation, and tumors (6). In various studies, “Coincidental lesions such as sarcoidosis, B-cell lymphoma, pseudolymphoma, melanoma, basal cell carcinoma, non-Hodgkin's lymphoma, and squamous cell carcinoma have also been reported to occur” (14).
Safety Hazards of Black Inks
However, black inks, which predominately consist of soot products, are also problematic (9). Carbon black in black ink is derived from the incomplete combustion of hydrocarbons, which accounts for its polycyclic aromatic hydrocarbon (PAH) content (17). PAHs represent ubiquitous pollutants derived from the burning of organic materials such as wood, petrol, oil, and coal, which elicit well-defined carcinogenic (cancer-causing), mutagenic (DNA-altering), and toxic effects (18). 
Researchers state, "Chemical analysis revealed the presence of polycyclic aromatic hydrocarbons in the tested black tattoo ink at concentrations twice the recommended level" (11). In particular, the PAHs pyrene and fluoranthene were found at the highest levels, and the possible human carcinogen naphthalene was also detected (11). PAHs are capable of absorbing ultraviolet radiation from the sun and producing a cytotoxic reactive oxygen species (ROS), singlet oxygen, as a byproduct, which can result in cell death (6). In another study, 10 of 11 black inks tested had levels of PAH exceeding the concentration recommended by the European Council, and 100% of black inks analyzed had levels of the carcinogen benzo(a)pyrene exceeding safe limits (17). 
One toxic ingredient found in black tattoo ink, hexachloro-1,3-butadiene (HCBD), is a byproduct of manufacturing processes for chlorinated solvents, and has a history of use as a fumigant or pesticide (9). It has been shown to perpetuate skin, kidney, and liver damage in rodent studies (19). 9-fluorenone, acquired from coal tar, has likewise been found in black tattoo ink and may cause phototoxic reactions, or chemically induced skin irritation following sunlight exposure (20, 21).
Hexamethylenetetramine, a preservative used in the manufacture of coatings, resins, rubber, and cosmetics, is another agent contained within some black tattoo inks (9). It releases formaldehyde, the xenobiotic toxic substance used to embalm corpses, which is associated with systemic autoimmune disease (22). It has likwewise been shown in the literature to cause respiratory allergies and contact dermatitis (9). 

Particularly alarming is the occurrence of dibenzofuran (DBF) in black tattooing agents, which is derived from “the incomplete combustion of coal biomass, refuse, diesel fuel, and residual oil, as well as tobacco smoke” 9, p. 236). When polychlorinated, or attached to chlorine atoms, it belongs to a dangerous class of persistent organic pollutants called dioxin-like chemicals (9). Dioxin-like chemicals exert gastrointestinal, hepatic, and dermal toxicity and DBF can cause respiratory irritation (9).
Components of Tattoo Ink Linked to Autoimmunity and Mitochondrial Dysfunction
Another study found that all 14 commercially available black inks analyzed contained the softener dibutyl phthalate, a sensitizing agent which “acts directly on keratinocytes and can drive Th2 responses following skin exposure via induction of thymic stromal lymphopoietin gene expression” (9, p. 231). This is to say, dibutyl phthalate can facilitate expression of a gene that tips the immune system in the direction of Th2-dominant responses, which have been implicated in some autoimmune diseases including systemic lupus erythematosus (SLE) and Sjögren's syndrome (23).
Other chemicals found within tattoos, such as formaldehyde, may induce autoimmunity by either inducing cell death, and exposing antigenic material within the cell against which the immune system may mount an attack, or by covalently binding to tissue and creating ‘neoantigens’ which incite immune responses (24, 25, 26).
Black inks likewise have been shown to induce production of reactive oxygen species (ROS) such as singlet oxygen or peroxyl radicals, which are free-radicals that can steal electrons from neighboring molecules and damage cell constituents (17). One study by Regensberger and colleagues (2010) found that in the presence of ultraviolet light, some black inks reduced activity of the energetic powerhouses of the cell, the mitochondria, of human dermal keratinocytes, the type of cell that predominates in the outermost layer of skin (27). Impaired mitochondrial activity has health implications since mitochondrial dysfunction is implicated in mood disorders, cardiovascular disease, diabetes, neurodegenerative disorders, chronic fatigue syndrome, fibromyalgia, migraine headaches, autoimmune diseases, and cancer (28).
Risk of Infection from Tattoos
Although professional tattooist organizations have improved hygienic standards, concerns about contagious exposure through tattooing remains (29). As articulated by Serup (2017), microbial pathogens such as hepatitis B (HBV), hepatitis C (HCV), and human immunodeficiency viruses (HIV) can be introduced, and “Severity of infection varies from minor to major, ultimately with life-threatening septicemia” (29, p. 30). People who are immunocompromised are often advised to refrain from tattooing (29).
Although sanitation measures are improving and risk of contracting infectious diseases from contaminated tattoo equipment has decreased, the inks themselves may harbor infectious microbes (30). Recent studies reveal that, despite 42% of products claiming sterility on their labels, 10% of unopened and 17% of previously used stock bottles of tattoo ink were contaminated with pathogenic bacteria, and that almost a third of products had leaking physical seals (31). Those inks marketed as nontoxic, which exclude alcohol and preservatives, possess greater risk of microbial contaminants, such as the Starbrite Colors tattoo inks which were removed from the market due to the presence of Pseudomonas aeruginosa and Acremonium mold (14).
How To Ensure Tattoo Safety
As an honored tradition, indelible art form, and means of forging individuation, it is incumbent upon the industry to guarantee safer options for tattoo ink. People should have the bodily autonomy to engage in tattooing practices without sacrificing their health.
For instance, vegetable-based inks, such as yellow pigments derived from turmeric, may represent a safer alternative, although they may need to be special ordered by the tattoo artist. Not dissimilar to cosmetics, the FDA has not traditionally enforced or regulated tattoo inks (32). Further, the level of transparency regarding ingredients is impeded by the proprietary nature of the tattoo inks sold by many manufacturers. 
In addition, because the term non-toxic is not legally regulated, what is advertised as nontoxic ink may still contain deleterious ingredients, such as blue pigments derived from the neurotoxin aluminum and white pigments derived from titanium dioxide nanoparticles. The latter, for example, is not only classified as possessing carcinogenic properties by both the International Agency for Research on Cancer and the National Institute for Occupational Safety and Health, but also elicits oxidative damage that can cause immunogenicity, inflammation, genotoxicity, and problems with cell integrity (33).
Consumers should demand access to safer tattoo inks and also rally for more regulatory oversight not only in this domain, but in the realms of cosmetics and personal care products as well. Further, for those suffering from toxicity as a result of tattoos, natural regimens intended to support biotransformation and elimination may be indicated, and some individuals suffering overt heavy metal toxicity may need to undergo chelation protocols supervised by an environmental medicine physician.
References
1. Stirn, A. (2007). ["My body belongs to me"--cultural history and psychology of piercings and tattoos] [Article in German]. The Umsch, 64(2), 115-119.
2. Pesapane, F. et al. (2014). A short history of tattoo. Journal of the American Medical Association: Dermatology, 150(2), 145. doi:10.1001/jamadermatol.2013.8860
3. Schmid, S. (2013). Tattoos — An historical essay. Travel Medicine and Infectious Disease, 11(6), 444-447.
4. King, K.A., & Vidourek, R.A. (2013). Getting inked: tattoo and risky behavioral involvement among university students. Social Science, Journal, 50, 540-546. 
5. Laumann, A.E., & Derick, A.J. (2006). Tattoos and body piercings in the United States: a national data set. Journal of the American Academy of Dermatology, 413-421.
6. Wenzel, S.M. et al. (2013). Adverse reactions after tattooing: review of the literature and comparison to results of a survey. Dermatology, 226, 138-147.
7. Khunger, N., Molpariya, A., & Khunger, A. (2016). Complications of tattoos and tattoo removal: stop and think before you ink. Journal of Cutaneous and Aesthetic Surgery, 8(1), 30-36.  doi: 10.4103/0974-2077.155072.
8. Klugl, I. et al. (2010). Incidence of health problems associated with tattooed skin: a nation-wide survey of German-speaking countries. Dermatology, 221, 43-50. 
9. Lehner, K. et al. (2011). Black tattoo inks are a source of problematic substances such as dibutyl phthalate. Contact Dermatitis, 231-238.
10. Goldstein, A.P. (1979). VII. Histologic reactions in tattoos. Journal of Dermatology and Surgical Oncology, 5(11), 896-900.
11. Neale, P.A. et al. (2015). Bioanalytical evidence that chemicals in tattoo ink can induce adaptive stress responses. Journal of Hazardous Materials, 296, 192-200. doi: 10.1016/j.jhazmat.2015.04.051.
12. Bäumler, W. et al. (2000). Q-switch laser and tattoo pigments: first results of the chemical and photophysical analysis of 41 compounds. Laser Surgery Medicine, 13-21.
13. Høgsberg, T. et al. (2011). Tattoo inks in general usage contain nanoparticles. British Journal of Dermatology, 165(6), 1210-1218. doi: 10.1111/j.1365-2133.2011.10561.x.
14. Arisa, O.E., & Alster, T.S. (2012). Rising Concern over Cosmetic Tattoos. Dermatologic Survey,  38(3), 424–429. doi: 10.1111/j.1524-4725.2011.02202.x
15. Falconi, M. et al. (2009). Influence of a commercial tattoo ink on protein production in human fibroblasts. Archives of Dermatology Research, 539-547.
16. Oda, Y. (2004). Analysis of the involvement of human N-acetyltransferase 1 in the genotoxic activation of bladder carcinogenic arylamines using a SOS/umu assay system. Mutation Research: Fundamental and Molecular Mechanisms of Mutagenesis, 399-406.
17. Høgsberg, T. et al. (2013). Black tattoo inks induce reactive oxygen species production correlating with aggregation of pigment nanoparticles and product brand but not with the polycyclic aromatic hydrocarbon content. Experimental Dermatology, 464-469.
18. Abdel-Shafy, H.I., & Mansour, M.S.M. (2016). A review on polycyclic aromatic hydrocarbons: Source, environmental impact, effect on human health and remediation. Egyptian Journal of Petroleum, 25(1), 107-123. 
19. Dubrat, P., & Gradiski, D. (1987). Percutaenous toxicity of hexachlorobutadiene. Acta Pharmacol Toxicol (Copenhagen), 43, 346-353.
20. Atsumi, T. et al. (1998). Cytotoxicity of photosensitizers camphorquinone and 9-fluorenone with visible light irradiation on a human submandibular-duct cell line in vitro. Archives of Oral Biology, 43, 73-81.
21. Okada, N. et al. (2008). Effects of visible light-irradiated camphorquinone and 9-fluorenone on murine oral mucosa. Dental Materials Journal, 27, 809-813.
22. Bigazzi, P.E. (1997). Autoimmunity caused by xenobiotics. Toxicology, 119, 1-21.
23. Ishida, H. et al. (1997). [An imbalance between Th1 and Th2-like cytokines in patients with autoimmune diseases--differential diagnosis between Th1 dominant autoimmune diseases and Th2 dominant autoimmune diseases]. Nixon Rinsho, 55(6), 1438-1443.
24. Pollard, K.M. (2012). Gender differences in autoimmunity associated with exposure to environmental factors. Journal of Autoimmunity, 38(2-3), J177–J186.
25. Germolec, D., Kono, D.H., Pfau, J.C. et al. (2012). Animal models used to examine the role of the environment in the deveopment of autoimmune disease: findings from an NIEHS expert panel workshop. Journal of Autoimmunity, 39(4), 285–293.
26. Griem, P. et al. (1998). Allergic and autoimmune reactions to xenobiotics: how do they arise? Immunology Today, 19(3), 133–141.
27. Regensburger, J. et al. (2010). Tattoo inks contain polycyclic aromatic hydrocarbons that additionally generate deleterious singlet oxygen. Experimental Dermatology, 19, 275-281.
28. Pieczenik, S.R., & Neustadt, J. (2007). Mitochondrial dysfunction and molecular pathways of disease. Experimental and Molecular Pathology, 83, 84-92.
29. Serup, J. (2017). Tattoo Infections, Personal Resistance, and Contagious Exposure through Tattooing. Current Problems in Dermatology, 52, 30-41. doi: 10.1159/000450777.
30. Bonadonna, L. (2015). Survey of studies on microbial contamination of marketed tattoo inks. Current Problems in Dermatology, 48, 190-195. doi: 10.1159/000369226. 
31. Høgsberg, T. et al. (2013). Microbial status and product labelling of 58 original tattoo inks. Journal of the European Dermatology and Venereology, 27(1), 73-80. doi: 10.1111/j.1468-3083.2011.04359.x.
32. Ortiz, A.E., & Alster, T.S. (2012). Rising concern over cosmetic tattoos. Dermatologic Surgery, 38(3), 424-429.
33. Skocaj, M. et al. (2011). Titanium dioxide in our everyday life; is it safe? Radiology and Oncology, 45(4), 227-247. 
34. Simmons, S.O. et al. (2009). Cellular stress response pathway system as a sentinel ensemble in toxicological screening. Toxicological Science, 111, 202-225.


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.

the Harmful Effects of Electromagnetic Fields Explained

The Harmful Effects of Electromagnetic Fields Explained

  • 1.5K 
  • September 03, 2017 • 74,826 views














An error occurred.

Try watching this video on www.youtube.com, or enable JavaScript if it is disabled in your browser.
To see full interview, Click Here or
Story at-a-glance
  • Exposure to microwave EMFs, like cellphones, causes massive mitochondrial dysfunction due to damage done by free radicals from peroxynitrite that also cause single and double stranded breaks in your DNA
  • Excessive free radicals triggered by low-frequency microwave exposure from cellphones and Wi-Fi networks have been linked to chronic diseases such as cardiac arrhythmias, anxiety, depression, autism, Alzheimer’s and infertility
  • Excessive calcium signaling produced by EMF exposures also has important roles in producing pathophysiological effects of EMFs including each of the effects listed above
  • Strategies that may help reduce the harmful effects of EMFs include optimizing your magnesium level, certain Nrf2-boosting foods, exercise, calorie restriction and strategies that boost nitric oxide signaling (which acts, in turn, by raising Nrf2)


By Dr. Mercola
I’ve often noted that electromagnetic fields (EMFs) are a pernicious, hidden health risk. But exactly how does this kind of microwave radiation damage your health? Martin Pall, Ph.D., has identified and published research describing the likely molecular mechanisms of how EMFs from cellphones and wireless technologies damage plants, animals and humans.1,2 ,3,4
Pall has a bachelor’s in physics from Johns Hopkins and a Ph.D. in biochemistry and genetics from Caltech, and is uniquely qualified for this type of research. For the past 18 years, he’s been scouring the medical literature, integrating and drawing parallels between work done by others to answer this pressing question. Pall explains:
“There is a huge amount of information out here that nobody has the time to integrate, digest and make connections [between]. That’s what I’ve been doing … I was interested in EMFs before I could understand how they worked. Then I stumbled onto two papers that told me, ‘Well, this looks like the way they work,’ and then I dug out more and more papers …
What the [initial two] studies showed was that you could block or greatly lower the effects [of EMF] by using calcium channel blockers … That was the key observation …
Now [I have found] 26 [papers] … They all show that EMFs work by activating what are called voltage-gated calcium channels (VGCCs). These are channels in the outer membrane of the cell, the plasma membrane that surrounds all our cells. When they’re activated, they open up and allow calcium to flow into the cell. It’s the excess calcium in the cell which is responsible for most if not all of the [biological effects].”
EMFs and Intracellular Calcium










An error occurred.

Try watching this video on www.youtube.com, or enable JavaScript if it is disabled in your browser.
When you expose cells to EMFs, there’s increased intercellular calcium. You also get increases in calcium signaling, which is important as well, in terms of explaining the damage EMFs cause. For the past 25 years, the industry has claimed that non-ionizing radiation is harmless and that the only radiation worth worrying about is ionizing radiation. Pall’s research unequivocally proves that this assumption is false.
“It’s been very clear, going back all the way to 1971 and even before that, that this wasn’t true. But we didn’t know what the mechanism was. Now, we do. I think it’s very important, because the industry’s been trying to hoodwink everybody for decades. Now we know how it works. One of the other things that’s very important about this is that there is a wide variety of different health impacts that have been reported. Now we can explain how [these problems arise].”
How EMFs Damage Your Health
When your VGCCs are exposed to EMFs, they open up, allowing abnormally large volumes of calcium ions into the cells — about 1 million ions per second per channel. Each VGCC has a voltage sensor, a structure that detects electrical changes across the plasma membrane and opens the channel. EMFs work through the voltage sensor to activate the channel and radically increase intracellular levels into dangerous ranges.
“Because of the structure of the voltage sensor and its location in the plasma membrane, one can predict from basic physics that it’s extraordinarily sensitive to the electrical forces from EMFs,” Pall notes. On average, these forces are approximately 7.2 million times stronger on the voltage sensor than they are on singly charged electrical groups in the aqueous (watery) part of the cell. What this means is that current safety standards are off by a factor of about 7 million.
That’s how these very weak EMFs, which industry claims can’t possibly cause you any harm, are actually taking you out prematurely. They work by activating VGCCs. This turns out to be absolutely critical, because when there’s excess calcium in the cell, a number of things happen. Not only do you get excess calcium signaling, you also get increased nitric oxide (NO). While NO has many beneficial health effects, massively excessive NO reacts with superoxide.

Superoxide levels also rise in response to increased intercellular calcium. Together, they form peroxynitrite, which is an extremely potent oxidant stressor. While not a free radical, peroxynitrites break down to form reactive free radicals, both reactive nitrogen species and reactive oxygen species (ROS) including hydroxyl free radicals.
“You get both, because you get hydroxyl radicals and carbonate radicals and NO2 radicals,” Pall explains. All three do damage. According to Pall, most of the damage is likely done by excessive free radicals, but some damage is caused directly by the peroxynitrites. The end result is rather massive harm, as excessive oxidative stress and nitrosative stress are involved in nearly all chronic disease. Much of the pathophysiology also has to do with the excessive calcium signaling, independently of peroxynitrite.
NO Signaling Pathway Versus Peroxynitrite Pathway
It’s important to realize that not all oxidative stress is harmful. There’s a certain baseline of free radicals that’s biologically useful and necessary. NO, for example, is a free radical, yet it has many very beneficial effects. The problem is excessive oxidative stress. Interestingly, Pall notes that the NO signaling pathway and the peroxynitrite pathways inhibit each other, which I never previously knew. This provides support for the new nitric oxide dump exercise to decrease damage from EMFs.
Why You Cannot Depend on Industry Claims
Many are unaware that the telecommunications industry is perhaps more well-funded than the pharmaceutical industry, and just as powerful politically. Their lobbyists are very effective in disseminating and protecting the industry’s version of the truth. Needless to say, the industry will also actively discredit research that demonstrates harm and/or defund research projects that start to reveal problems.
In fact, the current head of the Federal Communications Commission was formerly the chief lobbyist for the telecommunications industry — one of the worst cases of the disgusting revolving door between industry and government and the fox guarding the hen house that I have seen in sometime.
“I know how they’ve attacked various people,” Pall says. “In the U.S. … the funding for the EMF research [by the Environmental Protection Agency] was cut off starting in 1986 … The U.S. Office of Naval Research had been funding a fair amount of research in this area [in the ‘70s]. They [also] … stopped funding new grants in 1986 …  And then the National Institutes of Health (NIH) a few years later followed the same path …
[I]t’s actually shocking to say there are only two countries in the world that are doing a lot of research in this, well beyond their normal scope … Turkey and Iran … they’re doing quite a bit of good research in both of those countries on EMFs … What I’ve been doing is I’ve been doing it on my own. I’ve been contributing my time to it and my efforts and, at least to a small extent, some money to it. But it doesn’t cost that much, so I can do it.
So, we have the fact that the money was cut off. One strongly suspects the industry had a role on that. The industry, with the 1996 Telecommunications Act, gave the regulation to the Federal Communications Commission (FCC), which has done nothing in terms of protecting the public.
In addition, they prevented the public from protecting their health with regard to their exposures from the cellphone towers. We cannot sue to prevent cellphone towers from being put near our workplace or homes. Basically, what the Congress did was to say our health makes no difference … So, we’re in extremely deep trouble,” Pall says.
Neuropsychiatric Effects of EMF Exposure
And this brings us to the crux of the problem, namely the physical locations where VGCCs are the densest, and the subsequent diseases you can expect from chronic excessive exposure to EMFs. The highest density of VGCCs are found in your nervous system and, indeed, studies dating back to the 1950s and ‘60s show the nervous system is the organ that is most sensitive to EMFs.
Some of these studies show massive changes in the structure of neurons, including cell death and synaptic dysfunction. When the VGCCs are activated in the brain they release neurotransmitters and neuroendocrine hormones. Hence, consequences of chronic EMF exposure to the brain include the following, which Pall details in a 2016 paper:5
In animals exposed to EMFs, there are massive, cumulative effects in the brain. Genetic polymorphism studies also show that elevated VGCC activity in certain parts of the brain produces a variety of neuropsychiatric effects.
“I reviewed a [large number] of studies on various kinds of EMF exposures, each of them showing neuropsychiatric effects. What you find is that these effects have been repeated many times in these epidemiological studies. It’s the same thing that everybody’s complaining about, ‘I’m tired all the time,’ ‘I can’t sleep,’ ‘I can’t concentrate,’ ‘I’m depressed,’ ‘I’m anxious all the time,’ ‘My memory doesn’t work well anymore.’ All the things everybody’s complaining about.
We know all those things are caused by EMF exposures. There’s no doubt about that. Because we know their effects on the brain, we know that the VGCCs’ excessive activity can produce various neuropsychiatric problems.
Here we’ve got all of these epidemiological data that confirms this is happening in humans who live near cellphone towers, who were exposed to Wi-Fi, who were exposed to broadcasting radiation, who use cellphones, tablets and so on. That’s very important. I think we should care about this.”
Cardiac Effects
Your heart is also very sensitive to EMFs, particularly the pacemaker cells of your heart, as they have the highest density of VGCCs. As a consequence of this, we find that EMFs tend to trigger the following conditions. If you have any of these conditions (or any of the ones discussed above and below), you need to know that EMF exposure is a major contributing factor and take immediate and aggressive steps to remediate your exposure.
  • Cardiac arrhythmias (associated with sudden cardiac death)
  • Atrial fibrillation / atrial flutter
  • Premature atrial contractions (PACs) and premature ventricular contractions (PVCs), also known as heart palpitations
  • Tachycardia (fast heartbeat) and brachycardia (slow heartbeat)
Reproductive Effects
A third area with densely populated VGCCs is the reproductive system, particularly the male testes. A consequence here is impaired or reduced fertility. There is evidence showing EMFs can cause both male and female infertility, but male infertility has been more studied. Pall describes a classic reproduction experiment published 19 years ago by Ioannis Magras and Thomas Xenos in Greece:
“They took young pairs of mice, one male and female. They put them in a little cage on the ground outside in an antenna park … The [radiation] levels at the ground were well within our current safety guidelines … They put them in two different locations, one with a higher level of exposure and one with a lower level of exposure.
What they found was that at the higher-level exposure, each pair produced one litter that was approximately normal sized, then a second litter that was clearly down in numbers and then complete infertility — not a single mouse born …
At lower level exposure, it was basically the same story, except it took twice as long. They produced four litters with decreasing numbers, and then complete infertility. We have now, in humans in many countries around the world, decreased male sperm count — down by over 50 percent in Western countries, and about half of that amount in other countries around the world. 6,7
The senior author in that paper is saying, ‘If this keeps going, we’re going to become extinct,’ just from the drop in male sperm count. We know that that occurs in humans — in people who carry their cellphones in their front pockets, men who use their laptops with the Wi-Fi on sitting on their lap. We know that occurs. But of course, industry denies everything.”
Indeed, studies have linked low-level electromagnetic radiation (EMR) exposure from cellphones to an 8 percent reduction in sperm motility and a 9 percent reduction in sperm viability.8,9 Wi-Fi equipped laptop computers have also been linked to decreased sperm motility and an increase in sperm DNA fragmentation after just four hours of use.10
EMFs and Cancer
Studies on cancer have also been blocked by the industry in a number of ways, including preventing researchers from obtaining real-world data on cellphone usage. Obviously, people who use their cellphones the most are at greatest risk. While not at the top of the list of concerns associated with EMF exposure, cancer is yet another potential consequence of mitochondrial damage.
Women who carry their cellphones in their bra, for example, risk cancer in the upper inner quadrant of the breast, which is very atypical and not the usual upper outer quadrant.
Brain cancer is another possibility from extended cellphone use if you keep the phone to your ear. That said, emphasizing the cancer risk is likely counterproductive, as most people use cellphones and those who develop brain cancer are few and far in between. The problem is brain cancer has a latency period of a decade or more. Arrhythmias, autism, anxiety and Alzheimer’s, on the other hand, are extremely prevalent these days, and we now have a mechanism that explains how EMF contributes to all of them.
So, even though two U.S. senators likely got brain cancer from cell phones (Ted Kennedy and John McCain), it’s important to understand that cellphone dangers are not just about brain cancer. It’s all these other problems as well, including infertility. “In my judgment, cancer is down around No.4 or No. 5 on the list of my concerns. It’s not that cancer is not important. It’s very important. We’re just looking right now at the early stages because of long latencies,” Pall says.
What Is More Dangerous, Cellphones or X-Rays?
If you are like most, the answer is obvious: X-rays. That is because you have been convinced by the deceptive lies of the telecommunications industry that have lobbied the government to reinforce this delusional myth. The reality is that there is compelling evidence showing cellphones are more dangerous than X-rays — by several orders of magnitude.
Some of the best evidence comes from a German study (headed by professor Franz Adlkofer), in which the effects of ionizing radiation equivalent to 1,600 chest X-rays were compared to 24 hours on a cellphone. Surprisingly, they found both produced roughly equivalent amounts of DNA breaks in in-vitro assays. According to Pall, this actually vastly underestimates the effects of cellphones, because they used a continuous wave EMF, not pulsed.
There’s extensive evidence showing pulsed EMFs are far more damaging than continuous wave EMFs. That’s important for a number of reasons, including the fact that all wireless communication devices communicate by pulsations. In another paper, the group showed that when you use pulsations designed to be similar to the pulsation from a real cellphone, damage occurred at far lower intensities.
“This raises the question, ‘How can this possibly happen?’ I think the answer comes from the kind of diagram I’ve published, which is how EMFs produce free radicals,” Pall says. “Both ionizing radiation and the microwave frequency EMFs produce DNA damage through free radicals. They’re similar in that way. Where you get the free radicals is through the peroxynitriate pathway.
It turns out that when you go from EMFs to the free radicals on that pathway, there are three steps that involve high levels of amplification. One of them is when you open up the channels, you get about a million calcium ions flowing in per second. The second is that you get increases in NO and superoxide.
Those, in effect, will be the calcium acting catalytically, because once it’s in the cell, as long as it’s elevated, you keep getting more and more [NO and superoxide]. And then those two react with each other to form peroxynitrite. The reaction rates are the product of the two concentrations. So you have three levels of amplification. If you have three levels of amplification, you get a hell of a response to a very small stressor.”
Ionizing Radiation and DNA Breaks
The industry says there’s not enough energy in microwave radiation to cause direct damage to covalent bonds in DNA. This is true. There isn’t. It’s the biological amplification resulting in excessive oxidative stress that causes the damage. Interestingly, even most of the damage caused by ionizing radiation is actually due to secondary free radical formation that breaks DNA. It’s not directly from the energy within the radiation. Pall explains:
“That was published by Arthur Compton. He got the Nobel Prize for it in 1927. The way in which ionizing radiation works, it basically gets molecules and atoms and knocks electrons out, and then you get pairs of free radicals generated. That’s called Compton scattering.
There is amplification from ionizing radiation, but it’s only at one level. One energetic photon can produce a chain of free radicals. You’ve got three levels of amplification with the microwave frequency EMFs. The amount of damage you get based on those studies is truly extraordinary. Of course, Adlkofer and [Pilger] Rudinger were severely attacked by the industry.”
Practical Strategies to Limit Your Exposure
Naturally, to reduce your risk of harm, you need to reduce your exposure to EMFs. Cellphone towers should be a major concern if you work or go to school within 300 meters (about 1,000 feet) of one. Even just driving around can expose you to substantial cellphone tower radiation.  
Your cellphone is a major source of exposure, as are cordless phones, Wi-Fi routers, Bluetooth headsets and other Bluetooth-equipped items, wireless mice, keyboards, smart thermostats, baby monitors, smart meters and the microwave in your kitchen. Ideally, address each source and determine how you can best limit their use.
A simple remedy is to turn off your Wi-Fi each night. That’s just unnecessary exposure. Not carrying your cellphone on your body, and not using your laptop directly on your lap are other simple measures.
You can get cellphone pouches that are shielded on one side, so putting that side toward your body gives you some protection. Use your cellphone with a headset or on speaker phone. Work toward hardwiring your devices so you don't have to be in a Wi-Fi field and don't get unnecessary radiation from cordless mice, keyboards and printers. It is also possible to put up shielding in your house or apartment to lower exposures. 
Once you know the mechanism of harm, you have a better idea of how to remediate the problem. In this case, since we now know the effects of EMFs are reduced by calcium-channel blockers, a natural solution would be to make sure you’re getting enough magnesium. Most people are deficient in magnesium, which will worsen the impact of EMFs. As noted by Pall:
“It is clear that when you’re deficient in magnesium, you get excessive activity of the VGCCs. You also get excessive calcium influx through the N-methyl-D-aspartate receptor, caused by magnesium deficiency, which is also problematic, so it’s important to allay that deficiency.
Now, I always tell people I’m a Ph.D. and not an M.D. None of these [suggestions] should be viewed as medical advice. But I think one approach to dealing with these things is to raise the level of nuclear factor erythroid-2-related factor 2 (Nrf2), which I published [a paper11] on.”
How to Activate Nrf2 to Reduce EMF Impact
I am in the process of writing a very comprehensive paper on Nrf2, which is a vitally important biological hormetic that upregulates superoxide dismutase, catalase and all the other beneficial intercellular antioxidants. It also:
  • Lowers inflammation
  • Improves mitochondrial function
  • Stimulates mitochondrial biogenesis
  • Helps detoxify the body from xenobiotics, carbon-containing toxicants and toxic metals
  • Activates the transcription of over 500 genes in the human genome, most of which have cytoprotective functions. This includes the three genes that encode enzymes required for synthesis of reduced glutathione, which is one of the most important antioxidants produced in your body

One simple way to activate Nrf2 is to consume Nrf2-boosting food compounds, such as sulforaphane from cruciferous vegetables, foods high in phenolic antioxidants, the long-chained omega-3 fats DHA and EPA, carotenoids (especially lycopene), sulfur compounds from allum vegetables, isothiocyanates from the cabbage group and terpenoid-rich foods.
Exercise, calorie restriction (such as intermittent fasting) and activating the NO signaling pathway (one way of doing that is the NO dump exercise) will also raise Nrf2. In his paper, Pall notes:
“The important detoxification roles of Nrf2 mean that raising Nrf2 activity is likely to be of particular importance to the hundreds of millions of people around the globe who are regularly exposed to toxic chemicals that cause diseases characterized by oxidative stress, inflammation and mitochondrial dysfunction, diseases which include most of the chronic diseases of 21st century life.”
“One of the things I argued in that paper is that the two most helpful diets known — the traditional Mediterranean diet and the traditional Okinawan diet — are both high in nutrients that raise Nrf2,” Pall adds.
Take-Home Message
I personally believe EMF exposure may be one of the most significant factors for the observed decrease in male sperm count, and the increased prevalence of anxiety, depression, autism and Alzheimer’s. It is also highly likely a contributing factor to cancer.
While not widely publicized, in May 2011, the cancer research arm of the World Health Organization, the International Agency for Research on Cancer, classified radiofrequency EMF — such as the radiation from cellphones — a class 2B carcinogen, meaning it is possibly carcinogenic to humans.12
Pall has made a significant contribution to public welfare with his discovery of how EMFs cause biological harm, and it would be wise to take notice. I personally believe he deserves a Nobel Prize for his contribution to the science.
Again, the damage is not done through heat or ionizing radiation; it’s done by activating your VGCCs, thereby triggering a chain-reaction that produces excessive amounts of ROS, peroxynitrites and hydroxyl free radicals — the most destructive free radicals known to man, as well as through excessive calcium signaling.
Hydroxyl free radicals decimate mitochondrial and nuclear DNA, their membranes and proteins. Too much calcium in the mitochondria can also impact their function. The end result is mitochondrial dysfunction, which we now know is at the heart of most chronic disease. Since your brain, the pacemaker in your heart and male testes have the highest densities of VGCCs, these areas are the most prone to damage when exposed to EMFs.

What this research tells us is that excessive microwave exposure can be a direct contributor to conditions such as Alzheimer’s, anxiety, depression, autism, cardiac arrhythmias and infertility.13 So, if you care about your heart, brain and reproductive health, avoid carrying your cellphone in your pocket or on your hip, avoid using portable computers and tablets on your lap, and take measures to limit or eliminate as many unnecessary EMF sources as you can, in your home and at work.

Saturday, September 2, 2017

In light of the gadolinium controversy: The impact of recent verdict by major regulators

In light of the gadolinium controversy: The impact of recent verdict by major regulators
Mak Wen Yao , 17 days ago



MRI contrasts agents are crucial for clearer imaging – but are now under scrutiny in view of the recent issues pertaining its safety and efficacy.

After a year-long review, the European Medicines Agency (EMA) finally suspended three contrast agents used in MRI scans on 21 July 2017. This was due to concerns that a potentially toxic metal in the agents, gadolinium can deposit in the brain tissue. The regulator did not find evidence of harm, but acted to “prevent any risks.” 

The contrast agents, collectively known as gadolinium chelates, have been long used as a contrast medium for magnetic resonance imaging (MRI) scans. These chemical agents function as a "dye" that enhances the MRI images for better quality scans and more accurate diagnosis of the underlying condition. 

The EMA’s decision means several intravenous linear products – gadodiamide, gadopentetic acid and gadoversetamide – would be suspended within the EU. The review was conducted by the Pharmacovigilance Risk Assessment Committee (PRAC), responsible to appraise post-marketing safety evidence of medicines for human use. 

Gadolinium retention in the body

The gadolinium-based contrast agents (GBCA), were thought to be safe and well-tolerated by patients when used according to recommendations. However, in recent years, there is a growing body of evidence that refuted the established safety of GBCA. 

More than a decade ago, the contrast agents were also the focus of regulatory reviews and lawsuits filed by patients, as due to existing kidney impairment, they have been placed at risk of developing potentially fatal kidney disease – their kidneys could not excrete gadolinium. 

When patients underwent MRI scans and were exposed to GBCA, substantial evidence indicated gadolinium would accumulate in various tissues including the brain, bone and kidneys. The retention of GBCA in these tissues was also cumulative in nature – further increasing the exposure led to increased concentrations in the body. 

Free forms of the gadolinium ion are known toxic heavy metals. However, when it is chelated to a carrier molecule, the resultant complex reveals to exhibit little toxicity while retaining the gadolinium contrast properties.

Conventional understanding of GBCA states that the bond between the gadolinium ion and the chelating agent was sufficiently strong – to allow the contrast agents to be removed from the human body as a whole. However, the PRAC review discovered that "linear agents have a structure more likely to release gadolinium, which can build up in the body tissues." 

EMA decision stirred controversy

EMA’s decision has received backlash from the vendors of these agents – with many requesting the agency to re-evaluate the evidence. GE Healthcare, which markets Gadodiamide (Omniscan) in Malaysia and Singapore, issued a statement that conveyed the company's disappointment with EMA's recommendation. Another linear contrast agent, Magnevist – marketed by Bayer (also available in Malaysia and Singapore) – further echoed GE’s concerns; but assured that they would delve into “whether there are any clinical implications.” 

Singapore’s Health Services Authority (HSA) has also warned against the use of Omniscan or Magnevist in patients with severe renal failure. All other GBCAs were also advised to be used “only when absolutely necessary”. 

Given the potential impact of gadolinium retention in the body, the US Food and Drug Administration (FDA) has also launched its investigation into the safety of GBCA. On 22 May 2017, the agency announced that it will maintain the existing recommendation on all GBCAs, including those that are associated with higher rate of retention in the brain. 

FDA did not take a parallel course of action with EMA, as no adverse health effect was identified. Although gadolinium was shown to retain within the brain tissue, bone and skin – this evidence was not sufficient to establish a causal relationship with any adverse clinical outcome. 

The agency assured to continue monitoring the use of these agents and urged both patients and healthcare professionals to report any side effects associated with the use of GBCA.

Reactions towards the decisions

The EMA’s decision to suspend the marketing authorisation for linear contrast agents has prompted patients and physicians to seek alternative imaging solutions

As the medical community becomes more aware of the potential for gadolinium bio-retention in the body, the safety of these agents will be put under intense scrutiny. In addition, regional pharmaceutical regulatory bodies are expected to clarify their respective position on this issue in near future – to provide guidance to local healthcare professionals to approach this issue.

However, establishing a direct causal relationship between GBCA and adverse health outcome is also not an easy feat. High-quality data may only become available after several years of investigations. Currently, the risk-adverse medical community is expected to lean towards what the EMA is recommending – and refrain from unnecessary, albeit insufficiently proven, risks to their patients. MIMS

Read more:

Sources: 
https://www.statnews.com/pharmalot/2017/08/02/ema-fda-mri-scans-dyes/
http://www.ema.europa.eu/docs/en_GB/document_library/Press_release/2017/07/WC500231829.pdf
https://www.ncbi.nlm.nih.gov/pubmed/27053146
http://www.ema.europa.eu/ema/index.jsp?curl=pages/news_and_events/news/2017/03/news_detail_002708.jsp&mid=WC0b01ac058004d5c1
https://www.fda.gov/Drugs/DrugSafety/ucm559007.htm
http://www.auntminnie.com/index.aspx?sec=ser&sub=def&pag=dis&ItemID=116837
http://www.hsa.gov.sg/content/hsa/en/Health_Products_Regulation/Safety_Information_and_Product_Recalls/Dear_Healthcare_Professional_Letters/2007/Important_safety_warnings_for_gadoliniumbased_contrast_agents_Omniscan_and_Magnevist.html
http://pubs.rsna.org/doi/pdf/10.1148/radiol.2015150805
https://www.linkedin.com/pulse/what-verdict-gadolinium-mri-contrast-agent-mri-scan-group




Friday, September 1, 2017

Former ‘Antifa’ Speaks Out

David Icke Shatters The Antifa Left Alt Right Paradigm

Researchers Seek to Catch Alzheimer's Early by Peeking into the Eyes

Researchers Seek to Catch Alzheimer's Early by Peeking into the Eyes 



"Inclusion bodies" of amyloid plaque are visible in a subject's retina in this scan published in Peter Snyder's 2016 paper. Photo: Snyder et al.
Mark Wolff wanted to know. To him, the thought of suffering through Alzheimer's disease the way his father did—without knowing, and without his family knowing, what he was up against until late in its progression— is worse than learning, even while he's still perfectly healthy, that a possible precursor of the disease has gained a toehold.
"I'm not a worrier by nature," Wolff said. "I just don't want to wind up like my dad. It was just a nightmare what happened to him. He didn't get the medical attention he needed and his quality of life could have been better."
So Wolff, a lighting company executive from Bristol, R.I., enrolled in a trial at Butler Hospital and found out through a positron emission tomography (PET) scan of his brain that he has early signs of amyloid plaque. The presence of plaque, a tangle of proteins that could eventually cause the neurodegeneration of Alzheimer's disease, is a risk factor—even so, Wolff might never develop the disease. Or if he does, it might not affect him for a decade or more.
The trial, being conducted at both Butler and Rhode Island Hospital, is led by Stephen Salloway, a professor of neurology at Brown University and director of Butler's Memory and Aging Program. It has two goals. One is to test whether the drug solanezumab will prevent or delay memory loss and slow amyloid plaque buildup in people at increased risk for Alzheimer's. The other, via a sub-study launched at Butler Hospital, is to test whether a retinal scan can monitor that progress as well as the much more expensive PET scans. Salloway is working on the larger trial with Brian Ott, a Brown professor of neurology and director of the Alzheimer's Disease and Memory Disorders Center at Rhode Island Hospital.
As part of the research, Wolff returned to Butler on a warm summer afternoon for what unfolded like an eye doctor's appointment. Nurse practitioner Brittany Dawson dilated Wolff's eyes with drops. From there, he stared into the same optical coherence tomography (OCT) scanner that an ophthalmologist or optometrist would use to look for macular degeneration or glaucoma. For about 20 minutes, while postdoctoral researcher Dr. Jessica Alber operated the machine and guided him through the experiment, Wolff posed his retinas for multiple close-ups that will be independently inspected for the presence of amyloid plaques.
Inspired in large part by research led by colleague Peter Snyder, a professor of neurology and ophthalmology at Brown and senior vice president and chief research officer at Lifespan, Salloway and Ott believe that the retina may provide a reliable reflection of early but significant Alzheimer's disease risk in the brain. If so, that could vastly expand the number of people around the world who receive an early risk assessment and could save tremendous amounts of money compared to $5,000 PET scans, Snyder said.
The best chance for treating Alzheimer's, Snyder said, will be to identify and treat the disease long before symptoms arise, because by then too much damage may be done. Meanwhile, the need is so widespread that it must be done inexpensively and with non-invasive equipment as common as an OCT eye scanner. PET is both too costly and not widely available enough to be the first-line screening tool.
"We have to identify markers that are accessible to point-of-care clinicians," Snyder said. "The number of people with Alzheimer's disease is going to triple over the next 50 years. We have to change the impact of this disease. If we don't get this right, the burden on society is going to be devastating."
Snyder expects that doctors will need to combine several biomarkers to produce an estimate of patients' eventual Alzheimer's risk: family history, genetics, and cognitive and memory tests will likely combine with multiple retinal indicators into a comprehensive algorithm. Those with especially high emerging risk might then go on to PET scans and early-stage treatments—perhaps solanezumab—as those are proven, he said.
The brain in the eyes
The retina is a part of the central nervous system that doctors can see by opening nothing more than an eyelid.
"Potentially, the eye could be the window to the brain in the fight against Alzheimer's," said Salloway, who along with Ott and Snyder is affiliated with the Brown Institute for Brain Science,
The retina has the same biochemistry and similar organization and cell types as the brain, Snyder said, so it makes sense that it, too, would be similarly susceptible to amyloid plaques. It's no surprise given that the retina forms out of the same tissue as the brain in just the first few weeks of an embryo's development.
In recent years, scientists have noticed that amyloid plaques built up in the retinas. In 2016 in the journal Alzheimer's and Dementia, Snyder and co-authors published a study of 63 cognitively normal adults with at least one parent with Alzheimer's (just like Wolff) that compared the results of OCT scans with PET scans in the same patients. Snyder's team found a significant relationship between amyloid levels in the cortex of the brain, as measured by PET, and the total surface area of what appear to be amyloid plaques visible in the retina.
"Our findings support the hypothesis that retinal biomarkers could be a useful screening tool to distinguish individuals at risk for developing Alzheimer's disease, and could be helpful in identifying ideal candidates for secondary prevention trials," he and his co-authors wrote.
That hypothesis is now being tested further in Salloway's sub-study.
In other recent work, Snyder's research group led by Alber showed that retinal scans can also indicate other potential precursors of closely related neurodegenerative disorders, such as cerebral amyloid angiopathy.
The group is also studying how OCT can image changes in the vasculature of the retina, because amyloid can attack and alter blood vessels as well as neurons. Finally, the researchers are measuring associations between the presence of amyloid plaque and the thickness of individual layers of the retina. In a recent presentation in London of a small study, the team reported that the retinal nerve fiber layer thins as amyloid plaque in the brain increases.
Pushing the technology further
As sensitive as conventional OCT has proven to be in measuring the retina, Snyder said, it could get even better through the work of Jonghwan Lee, an assistant professor of engineering at Brown.
In his work to improve neural imaging, Lee has developed sophisticated algorithms that amplify the signal of OCT and reduce the noise. These improvements have allowed him to produce stunningly high-resolution imaging of blood flow—red blood cell by red blood cell—in even the tiniest capillaries of neural tissue. That means he might be able to very precisely observe some of the small but early changes in vasculature that Snyder is interested in.
The two have begun to collaborate. Working in a mouse model of Alzheimer's and with healthy controls, Lee hopes to track down the earliest vascular, neural and behavioral changes associated with the disease as the mice age.
"Our first hypothesis is that maybe alterations in vasculature and blood flow will appear in the brain first, so we are imaging the animal brain every month," Lee said. "And at the same time we are testing the cognitive function of the animal and how it declines and we are looking at blood flow and vasculature in the retina."
"So we will make a bigger picture of which one is first, which one is earlier and how much it is earlier and significant," Lee said.
The goal would be to compile a predictive algorithm of the disease's progression in the mouse from its very earliest stage using a similar combination of biomarkers—physiology, cognition and genetics—that Snyder suspects will need to be compiled for people.
The study is very early stages, Lee said: "No one knows the exact answer yet."
'Better to know'
In the exam room at Butler, Betty Wolff, Mark's wife of 45 years, shared that it was initially hard for her to hear the results of the PET scan, but she agreed that it's better to know. If the infusions he'll begin later in the summer contain solanuzemab rather than the placebo and if the medication works, his enrollment in the trial might help to stop or slow the disease even before it even gets started. And at least if Wolff becomes symptomatic with Alzheimer's down the road, the family will have had ample warning and will be able to manage the condition as well as possible, right from the start.
None of those possibilities was available for Wolff's dad, which is why he's so eager to volunteer to advance this research. He's no stranger to volunteering, having been a blood donor and a Big Brother for decades. Volunteering for research is a way to help society get the upper hand on Alzheimer's disease, he said, and the huge suffering and costs that it brings.
"We're living longer and we understand what makes our bodies live longer," said Wolff, who turns 70 in September. "If this is something that they don't conquer, people are not going to have a quality of life at the end."

How to Grow and Enjoy Brussel Sprouts

How to Grow and Enjoy Brussels Sprouts






An error occurred.

Try watching this video on www.youtube.com, or enable JavaScript if it is disabled in your browser.
Story at-a-glance
  • Isothiocyanates, found in cruciferous vegetables such as Brussels sprouts, have potent anticancer activity. Men who ate 1.5 cups of Brussels sprouts daily for five weeks had a 28 percent decrease in DNA damage, thereby lowering their cancer risk
  • Brussels sprouts are among the hardiest of the cabbage family, and overnight frost will bring out their sweetness. Plan to plant them 80 to 100 days before your first frost date
  • The key to successful preparation of Brussels sprouts is to avoid overcooking, as this will affect flavor and diminish valuable nutrients. Tips for cooking, optimizing nutrition and proper preservation are given


By Dr. Mercola
Several studies have confirmed that plant compounds called isothiocyanates, found in cruciferous vegetables, have potent anticancer activity. One particular isothiocyanate compound called sulforaphane has been shown to inhibit growth of cultured human breast cancer cells, leading to cell death.
Broccoli and broccoli sprouts have garnered a reputation for being high in these beneficial compounds, but other cruciferous veggies have them as well, including Brussels sprouts, which have actually been shown to contain greater amounts of glucosinolates than broccoli.1 Glucoraphanin is a glucosinolate precursor of sulforaphane that influences carcinogenesis and mutagenesis.2,3 Compared to mature broccoli, broccoli sprouts can contain up to 20 times more glucoraphanin.
Health Benefits of Brussels Sprouts
In one study,4 men who ate about 1.5 cups of Brussels sprouts daily for five weeks had a 28 percent decrease in DNA damage, which the researchers concluded showed "that consumption of cruciferous vegetables [Brussels sprouts] may result in a decreased cancer risk.” As noted by World’s Healthiest Foods:5
“This connection between Brussels sprouts and cancer prevention should not be surprising since Brussels sprouts provide special nutrient support for three body systems that are closely connected with cancer development as well as cancer prevention.
These three systems are (1) the body's detox system, (2) its antioxidant system, and (3) its inflammatory/anti-inflammatory system. Chronic imbalances in any of these three systems can increase risk of cancer, and when imbalances in all three systems occur simultaneously, the risk of cancer increases significantly.” 
One cup of cooked Brussels sprouts also contains more than 240 percent of the recommended dietary allowance (RDA) for vitamin K1, and nearly 130 percent of the RDA for vitamin C. They’re also a good source of fiber, manganese, potassium (which helps control your blood pressure by balancing the rather high sodium), choline, B vitamins, antioxidants and other health-promoting phytochemicals.
Brussels Sprouts — A Hardy Winter Crop
Brussels sprouts are a valuable addition to your home garden,6,7 and while they require quite a bit of space, they are among the hardiest of the cabbage family. If you time your planting to coincide with fall frost, they’ll actually be tastier, as the overnight chill brings out their sweetness. While they rarely do well in hotter climates, some newer hybrid varieties allow for greater temperature variances.
Popular hybrid varieties8 include Bubbles, which has shorter maturation (82 days instead of 100), tolerates warmer weather and is resistant to rust, and Prince Marvel, which produces tighter, sweeter sprouts and has a maturation rate of about 90 days. Other recommended varieties include Jade Cross, Oliver, Royal Marvel and Valiant.
How to Grow Brussels Sprouts
A perfect cool weather crop, plan to transplant your Brussels sprout plants into your garden about 100 days before the first frost date. You can start your plants either indoors or out. If growing them directly in your garden, plant the seeds about one-half inch deep, and once they’ve reached a height of about 5 inches, thin them out so that they’re spaced about 2 feet apart. They’ll grow best in full sun but can handle partial shade.
Alternatively, start your seeds indoors in starter containers four to five weeks before transplanting. When transplanting them into your garden, plant them a little bit deeper than they originally grew. The lowest leaves should be just above ground. Mulching around them will help retain moisture. If you let them dry out, the crop will usually fail.
As for the soil, it should drain well, but need to be packed or pressed as excessively loose soil will encourage clubroot, a common disease affecting the cabbage family.9 In the featured video, they recommend tamping the soil down with your feet.
Once or twice a month, spray the leaves with compost tea or seaweed extract. They’re very nitrogen dependent, so be sure to use plenty of high nitrogen compost. Brussels sprouts also grow well next to bush peas and beans for this reason, as these plants deliver an extra shot of nitrogen to the soil. As the plant matures, remove yellowing leaves to allow the sprouts room to grow. Just be sure to leave several of the largest, healthiest leaves toward the top.
If you want or need the plant to mature faster, pinch off the top of the plant, but make sure you still have some healthy, fully expanded leaves remaining. Another growth-promoting tip is demonstrated in the MIgardener video above. You can promote maturation of the Brussels sprouts by snapping off most or all of the leaves, leaving only a healthy bunch at the crown. This will shock the plant into maturation and funnel energy toward the sprouts.
Harvest Guidelines
The Brussels sprouts are ready to harvest in 80 to 100 days (depending on the variety) or when they’re about 1 inch in diameter. You can let them grow larger, but the smaller ones are more tender and tend to have a more pleasant flavor. Harvest the sprouts from the bottom, up, by twisting them off the stem.
Should you expect a hard freeze, you can still salvage your crop. Dig out the plant, remove any remaining leaves, hang the plant upside-down in a cool place and harvest as the sprouts mature. Sprouts that fail to develop into firm heads, remaining loosely bound instead, is a sign of heat exposure. Essentially, the weather was too warm.
Flavor goes hand in hand with freshness, so avoid storing or refrigerating your Brussels sprouts for more than two days. Also avoid washing them before storing. Simply remove any damaged outer leaves and place them, unwashed, in the vegetable bin in your fridge. Wash them right before cooking if needed.
How to Properly Prepare and Cook Brussels Sprouts










An error occurred.

Try watching this video on www.youtube.com, or enable JavaScript if it is disabled in your browser.
The key to successful preparation of Brussels sprouts is to avoid overcooking. Brussels sprouts are very much like broccoli in this matter. Preparation is paramount in order to maximize their nutritional value. Here are some key considerations and helpful tips:
How to achieve more even cooking: The outer leaves cook faster than the core, so for more even cooking, carve an X into the bottom of each stem if cooking them whole. Larger sprouts will cook more evenly if cut in half. You can tell you’ve overcooked them by their color. They should remain bright green; a dull green or yellowing is an indication that valuable nutrients have been lost.
How to optimize sulforaphane content: As with broccoli (discussed in the video above),10 the sulforaphane content of Brussels sprouts is easily diminished by overcooking, as heat degrades the enzyme responsible for producing sulforaphane. To optimize retention, your best bet is to steam them for three to four minutes, until bright green.11
This will increase the available sulforaphane content by eliminating epithiospecifier protein — a heat-sensitive sulfur-grabbing protein that inactivates sulforaphane — while still retaining the enzyme myrosinase, which converts glucoraphanin to sulforaphane. Beyond the five-minute mark, you start losing valuable compounds.
How to maximize sulforaphane even further: To further boost sulforaphane content, pair your Brussels sprouts with a myrosinase-containing food12,13 such as mustard seed, daikon radishes, wasabi, arugula or coleslaw. Of these, mustard seed has been found to contain a particularly resilient form of myrosinase.14
For a recipe pairing Brussels sprouts with shallots and mustard seeds, see Epicurious.com.15 You could also try roasted Brussels sprouts with a mustard vinaigrette made with grainy mustard or mustard seed powder,16 or my balsamic drizzled Brussels sprouts recipe, to which you could simply add a dash of mustard seed powder.
How to Optimize Preservation
The best way to preserve your Brussels sprouts if you cannot eat them within a day or two of harvesting is to freeze them.17 But first, they need to be blanched. After picking off any damaged or coarse outer leaves, wash them and sort by size into small, medium and large.
Bring a gallon of water to a rolling boil over high heat. You can blanch 1 pound of sprouts per batch. Small heads should be blanched for three minutes; medium-sized sprouts for four minutes and large heads for five minutes. While blanching can rapidly destroy anticancer compounds like glucosinolate in broccoli, Brussels sprouts have been found to be less severely affected by the blanching process, retaining far more of their glucosinolate than broccoli when blanched.18

To stop the cooking process, immerse the Brussels sprouts in ice water for the same amount of time as the blanching. Drain the Brussels sprouts on a paper towel. Once dry, pack into a freezer container. They’ll keep for up to one year if frozen at or below zero degrees F.