Monday, July 31, 2017
Sunday, July 30, 2017
Friday, July 28, 2017
Chlorine in Swimming Pools transforms sunscreens in toxic chemicals
Science SHOCK: Chlorine in swimming pools transforms sunscreen into cancer-causing toxic chemical right on your skin
Tuesday, July 11, 2017 by: Isabelle Z.
Tags: avobenzone, cancer risk, chlorine, sunscreen, swimming pools, toxins
Tags: avobenzone, cancer risk, chlorine, sunscreen, swimming pools, toxins
|
|
|
|
|
|
|
|
27K
VIEWS
(Natural News) If you think you’re doing something good by slathering sunscreen on yourself and your kids before hitting the pool, you might want to think again. A new study places sunscreen firmly on the list of products that can do more harm than good as Russian scientists discover the destructive effects of chlorine in swimming pools on sunscreen.
Researchers from Lomonosov Moscow State University have discovered that the world’s most popular active sunscreen ingredient, avobenzone, breaks down into something far more sinister in chlorinated water. Two of the chemicals it produces upon mixing with the water, phenols and acetyl benzenes, are of particular concern because of their toxicity. This reaction takes place on your wet skin when the sunscreen reacts to UV radiation and chlorinated water, and the chemicals have been linked to problems like immune system damage, infertility, and cancer.
In swimming pools that use copper salts to make the water look blue, this reaction is even worse. In that case, the sunscreen can break down into bromoform, a substance that has been linked to nervous system disorders, liver problems, and kidney problems.
In addition to sunscreen, avobenzone is often used in moisturizers, creams and lipsticks that offer SPF.
Should you avoid avobenzone?
While there are still some unanswered questions about how far-reaching the effects of this reaction are, it is enough to warrant concern.
University of Kansas Health System Dermatologist Daniel Aires told the Kansas City Star: “It can degrade into some very harmful compounds, some of which are known carcinogens. What isn’t known is how much is absorbed into the skin, or if it’s to a level that can cause, or potentially increase, the risk of cancer. But this is certainly alarming.”
He added that people should be particularly cautious when it comes to using this type of sunscreen on young children, who might absentmindedly ingest the chemicals, for example, by licking their arms after swimming.
The scientists are now looking into how avobenzone breaks down in freshwater and sea water to see if similar dangers exist.
Safer sun protection
If you’re concerned about having safe sun protection, a physical sunblock like zinc oxide is a much safer bet. The Environmental Working Group has a comprehensive searchable database of sunscreens on their website. You can find out which ingredients are in many popular sunscreens and view assessments of the dangers they pose to help you find a sunscreen that won’t put your health at risk.
You might also consider foregoing sunscreen if you’ll just be outside for a short time. Spending 15 to 20 minutes outdoors is all it takes to help most people’s bodies produce an adequate amount of Vitamin D, which can help protect against many types of cancer. It can also help to reverse vitamin D deficiency, which affects a disproportionate number of Americans and has been linked to diabetes, cancer, kidney disease, heart disease, obesity, and depression. Sunscreen actually blocks your skin’s production of vitamin D, making deficiencies worse. If you’ll be outdoors for a long time, you should still protect your skin, but you might want to first allow yourself some unprotected exposure so you can boost your Vitamin D production.
You can also turn to your diet to help build up your body’s natural sun resistance. Eating natural antioxidants has been shown to help your skin resist sunburn, so stock up on berries and other antioxidant-rich foods.
It’s a bit disconcerting to learn that something that is supposed to protect you can actually have the opposite effect, but it’s important to be aware of these situations so you do not have a false sense of security. Many sunscreens contain toxic chemicals, and now it appears that swimming pools can make them even more toxic.
Sources include:
Powerful Aspirin Alterative
The Powerful Aspirin Alternative Your Doctor Never Told You About
7Posted on: Sunday, July 23rd 2017 at 3:15 pm
Written By: Sayer Ji, Founder
This article is copyrighted by GreenMedInfo LLC, 2017
Aspirin's long held promises are increasingly falling flat. A natural, safer and more effective alternative to this synthetic drug has been known about for at least 15 years!
In a previous article titled "The Evidence Against Aspirin and For Natural Alternatives," we discussed the clear and present danger linked with the use of aspirin as well as several clinically proven alternatives that feature significant side benefits as opposed to aspirin's many known side effects.
Since writing this article, even more evidence has accumulated indicating that aspirin's risks outweigh its benefits. Most notably, a 15-year Dutch study published in the journal Heart found that among 27,939 healthy female health professionals (average age 54) randomized to receive either 100 mg of aspirin every day or a placebo the risk of gastrointestinal bleeding outweighed the benefit of the intervention for colorectal cancer and cardiovascular disease prevention in those under 65 years of age.
Of course, aspirin is not alone as far as dangerous side effects are concerned. The entire non-steroidal anti-inflammatory (NSAID) category of prescription and over-the-counter drugs is fraught with serious danger. Ibuprofen, for instance, is known to kill thousands each year, and is believed no less dangerous than Merck's COX-2 inhibitor NSAID drug Vioxx which caused between 88,000-140,000 cases of serious heart disease in the five years it was on the market (1999-2004). Tylenol is so profoundly toxic to the liver that contributing writer Dr. Michael Murray recently asked in his Op-Ed piece, "Is it Time for the FDA to Remove Tylenol From the Market?"
Given the dire state of affairs associated with pharmaceutical intervention for chronic pain issues, what can folks do who don't want to kill themselves along with their pain?
Pine Bark Extract (Pycnogenol) Puts Aspirin To Shame
When it comes to aspirin alternatives, one promising contender is pycnogenol, a powerful antioxidant extracted from French maritime pine back, backed by over 40 years of research, the most compelling of which we have aggregated on GreenMedInfo.com here: Pycnogenol Research. Amazingly, you will find research indexed there showing it may have value for over 80 health conditions.
In 1999, a remarkable study published in the journal Thrombotic Research found that pycnogenol was superior (i.e. effective at a lower dosage) to aspirin at inhibiting smoking-induced clotting, without the significant (and potentially life-threatening) increase in bleeding time associated with aspirin use. The abstract is well worth reading in its entirety:
"The effects of a bioflavonoid mixture, Pycnogenol, were assessed on platelet function in humans. Cigarette smoking increased heart rate and blood pressure. These increases were not influenced by oral consumption of Pycnogenol or Aspirin just before smoking. However, increased platelet reactivity yielding aggregation 2 hours after smoking was prevented by 500 mg Aspirin or 100 mg Pycnogenol in 22 German heavy smokers. In a group of 16 American smokers, blood pressure increased after smoking. It was unchanged after intake of 500 mg Aspirin or 125 mg Pycnogenol. In another group of 19 American smokers, increased platelet aggregation was more significantly reduced by 200 than either 150 mg or 100 mg Pycnogenol supplementation. This study showed that a single, high dose, 200 mg Pycnogenol, remained effective for over 6 days against smoking-induced platelet aggregation. Smoking increased platelet aggregation that was prevented after administration of 500 mg Aspirin and 125 mg Pycnogenol. Thus, smoking-induced enhanced platelet aggregation was inhibited by 500 mg Aspirin as well as by a lower range of 100-125 mg Pycnogenol. Aspirin significantly (p<0 .001="" 167="" 236="" b="" bleeding="" did="" from="" increased="" not.="" pycnogenol="" seconds="" time="" to="" while=""> These observations suggest an advantageous risk-benefit ratio for Pycnogenol." [emphasis added]"
As emphasized in bold above, pycnogenol unlike aspirin did not significantly increase bleeding time. This has profound implications, as aspirin's potent anti-platelet/'blood thinning' properties can also cause life-threatening hemorrhagic events. If this study is accurate and pycnogenol is more effective at decreasing pathologic platelet aggregation at a lower dose without causing the increased bleeding linked to aspirin, then it is clearly a superior natural alternative worthy of far more attention by the conventional medical establishment and research community than it presently receives.
Not Just A Drug Alternative
Pycnogenol, like so many other natural interventions, has a wide range of side benefits that may confer significant advantage when it comes to reducing cardiovascular disease risk. For instance, pycnogenol is also:
- Blood Pressure Reducing/Endothelial Function Enhancer: A number of clinical studies indicate that pycnogenol is therapeutic for those suffering with hypertension. Pycnogenol actually addresses a root cause of hypertension and cardiovascular disease in general, namely, endothelial dysfunction (the inability of the inner lining of the blood vessels to function correctly, e.g. fully dilate).[1] It has been shown to prevent damage in microcirculation in hypertensive patients, as well as reducing the dose of blood pressure drugs in hypertensive patients,[2] including hypertensive diabetic patients.[3] It has even been found to reduce intraocular hypertension found in glaucoma patients.[4]
- Anti-Inflammatory Effects: There is a growing appreciation among the medical community that inflammation contributes to cardiovascular disease. Several markers, including C-reactive protein are now being fore grounded as being at least as important in determining cardiovascular disease risk as various blood lipids and/or their ratios, such as low-density lipoprotein (LDL). Pycnogenol has been found to reduce C-reactive protein in hypertensive patients.[5] Pycnogenol has been found to rapidly modulate downward (inhibit) both Cox-1 and Cox-2 enzyme activity in human subjects, resulting in reduced expression of these inflammation-promoting enzymes within 30 minutes post-ingestion.[6] Another observed anti-inflammatory effect of pycnogenol is its ability to down-regulate the class of inflammatory enzymes known as matrix metalloproteinases (MMPs).[7] Pycnogenol has also been found to significantly inhibit NF-kappaB activation, a key body-wide regulator of inflammation levels whose overexpression and/or dysregulation may result in pathologic cardiovascular manifestations.[8] Finally, pycnogenol has been found to reduce fibrinogen levels, a glycoprotein that contributes to the formation of blood clots; fibrinogen has been identified as an independent risk factor for cardiovascular disease.[9]
- The Ideal Air Travel Companion: In a previous article entitled, "How Pine Bark Extract Could Save Air Travelers Lives," we delve into a compelling body of research that indicates pycnogenol may be the perfect preventive remedy for preventing flight-associated thrombosis, edema, and concens related to radiotoxicity and immune suppression.
Given the evidence for pycnogenol's pleotrophic cardioprotective properties, we hope that pycnogenol will become more commonly recommended by health care practitioners as the medical paradigm continues to evolve past its reliance on synthetic chemicals, eventually (we hope) returning to natural, increasingly evidence-based interventions. However, it is important that we don't fall prey to the one-disease-one-pill model, convincing ourselves to focus on popping pills – this time natural ones – as simply countermeasures or 'insurance' against the well known harms associated with the standard American diet, lack of exercise, and uncontrolled stress. The ultimate goal is to remove the need for pills altogether, focusing on preventing cardiovascular disease from the ground up and inside out, e.g. letting high quality food, clean water and air, and a healthy attitude nourish and sustain your health and well-being.
References
[1] Ximing Liu, Junping Wei, Fengsen Tan, Shengming Zhou, Gudrun Würthwein, Peter Rohdewald. Pycnogenol, French maritime pine bark extract, improves endothelial function of hypertensive patients. Life Sci. 2004 Jan 2;74(7):855-62. PMID: 14659974
[2] Gianni Belcaro, Maria Rosaria Cesarone, Andrea Ricci, Umberto Cornelli, Peter Rodhewald, Andrea Ledda, Andrea Di Renzo, Stefano Stuard, Marisa Cacchio, Giulia Vinciguerra, Giuseppe Gizzi, Luciano Pellegrini, Mark Dugall, Filiberto Fano. Control of edema in hypertensive subjects treated with calcium antagonist (nifedipine) or angiotensin-converting enzyme inhibitors with Pycnogenol. Clin Appl Thromb Hemost. 2006 Oct;12(4):440-4. PMID: 17000888
[3] Sherma Zibadi, Peter J Rohdewald, Danna Park, Ronald Ross Watson. Reduction of cardiovascular risk factors in subjects with type 2 diabetes by Pycnogenol supplementation. Nutr Res. 2008 May;28(5):315-20. PMID: 19083426
[4] Robert D Steigerwalt, Belcaro Gianni, Morazzoni Paolo, Ezio Bombardelli, Carolina Burki, Frank Schönlau. Effects of Mirtogenol on ocular blood flow and intraocular hypertension in asymptomatic subjects. Mol Vis. 2008;14:1288-92. Epub 2008 Jul 10. PMID: 18618008
[5] Maria Rosaria Cesarone, Gianni Belcaro, Stefano Stuard, Frank Schönlau, Andrea Di Renzo, Maria Giovanna Grossi, Mark Dugall, Umberto Cornelli, Marisa Cacchio, Giuseppe Gizzi, Luciano Pellegrini. Kidney flow and function in hypertension: protective effects of pycnogenol in hypertensive participants--a controlled study. J Cardiovasc Pharmacol Ther. 2010 Mar;15(1):41-6. Epub 2010 Jan 22. PMID: 20097689
[6] Angelika Schäfer, Zuzana Chovanová, Jana Muchová, Katarína Sumegová, Anna Liptáková, Zdenka Duracková, Petra Högger. Inhibition of COX-1 and COX-2 activity by plasma of human volunteers after ingestion of French maritime pine bark extract (Pycnogenol). Biomed Pharmacother. 2006 Jan;60(1):5-9. Epub 2005 Oct 26. PMID: 16330178
[7] Tanja Grimm, Angelika Schäfer, Petra Högger. Antioxidant activity and inhibition of matrix metalloproteinases by metabolites of maritime pine bark extract (pycnogenol). Wei Sheng Yan Jiu. 2011 Jan;40(1):103-6. PMID: 14990359
[8] Tanja Grimm, Zuzana Chovanová, Jana Muchová, Katarína Sumegová, Anna Liptáková, Zdenka Duracková, Petra Högger. Inhibition of NF-kappaB activation and MMP-9 secretion by plasma of human volunteers after ingestion of maritime pine bark extract (Pycnogenol). J Inflamm (Lond). 2006;3:1. Epub 2006 Jan 27. PMID: 16441890
[9] G Belcaro, M R Cesarone, S Errichi, C Zulli, B M Errichi, G Vinciguerra, A Ledda, A Di Renzo, S Stuard, M Dugall, L Pellegrini, G Gizzi, E Ippolito, A Ricci, M Cacchio, G Cipollone, I Ruffini, F Fano, M Hosoi, P Rohdewald. Variations in C-reactive protein, plasma free radicals and fibrinogen values in patients with osteoarthritis treated with Pycnogenol. Redox Rep. 2008;13(6):271-6. PMID: 19017467
Sayer Ji is founder of Greenmedinfo.com, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.
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:
Recommended Related Articles
184,816 views
380,700 views
168,123 views
416,392 views
1,270,244 views
Thursday, July 27, 2017
Heart Disease the silent pet killer that you can now avoid
Heart Disease: The Silent Pet Killer That You Can Now Avoid
|
|
An error occurred.
In this informative video, Dr. Karen Becker discusses a wonderful new tool for early detection of heart disease in dogs and cats.
|
Dr. Becker's Comments:
|
|
Heart disease in companion animals is too often a silent killer.
By the time your dog or cat shows the classic signs of heart disease like lethargy, wheezing, croupy coughing (a liquid-sounding cough, as though there’s fluid in the lungs) or exercise intolerance, it’s very often too late to save your beloved pet.
To make matters worse, an enlarged heart can’t be detected with a stethoscope. Significant heart disease can be present and undiagnosed by your veterinarian long before your pet shows clinical symptoms of illness.
Too many pet owners too often find themselves in this heartbreaking situation.
Two Types of Heart Disease
Both dogs and cats are at risk for heart disease, and both can develop either type:
- Heart muscle disease
- Valvular disease
Cardiomyopathy is the scientific term for an enlarged heart muscle.
Some breeds of dogs are predisposed to the condition, including New Foundlands, Great Danes and Dobermans.
Cardiomyopathy can also be caused by a dietary deficiency. The amino acids taurine and carnitine are critical for normal heart development and performance. If your dog’s or cat’s diet is lacking in these amino acids, heart muscle damage can result.
Poor valve health can also lead to heart disease. A leaky valve makes your pet’s heart work harder, and the harder it works, the bigger it gets. Valve disease leads to congestive heart failure in both dogs and cats.
Heart murmurs (which are usually present when there are valve problems) are ranked on a scale from 1 to 6, where 1 is considered mild and 6 is the worst case.
Leaky valves or heart murmurs are frequently seen in predisposed breeds like the Cavalier King Charles Spaniel.
Leaky valves are also found in aging pets and animals with some metabolic conditions like feline hyperthyroidism.
Diagnosing Heart Disease in Your Pet
If your veterinarian suspects a heart problem -- usually by hearing a murmur through a stethoscope, by doing a physical examination, and/or by considering symptoms your dog or cat is experiencing -- diagnostic tests will be required to confirm presence of disease.
These tests, usually x-rays, EKG or cardiac ultrasound, can cost several hundred dollars.
For many pet owners who want to be proactive in detecting heart disease in a dog or cat, the expense of these tests is prohibitive.
It’s a terrible situation to be in. If you’ve lost a dog or cat to heart disease, you’re bound to be fearful it could happen again to another pet. You want to take proactive steps to help your current dearly loved dog or cat avoid the problem, but you can’t afford the tests that will tell you whether or not you need to do more to insure the health of your companion animal.
It feels as if you have no choice but to wait to see if heart disease sneaks up silently to claim another four-legged member of your family.
That is, until now.
A Blood Test for Early Detection of Heart Disease in Pets
This is wonderful news!
At long last, veterinary medicine has developed a blood test that can identify which dogs and cats are at greatest risk for heart disease and heart failure.
The test is called a proBNP test. BNP = B-type Natriuretic Peptide.
The proBNP is a blood test that measures how much peptide hormone, released by the heart, is in circulation in your pet’s body. This hormone is only released when the heart is pushed beyond its capacity.
Very early in the disease process, small amounts of the hormone will be released into your dog’s or cat’s bloodstream, and it’s presence is a signal that steps must be taken in order to preserve your pet’s heart health.
If heart pathology continues to progress, the blood value of the peptide hormone will continue to rise.
How to Proactively Protect Your Pet’s Heart Health
- Ask your veterinarian for the proBNP blood test if you’re concerned about your pet’s heart for any reason.
The proBNP blood test can give you peace of mind that your pet has no early signs of heart disease.
It can also help you and your veterinarian differentiate between, for example, a respiratory condition like feline asthma and an underlying heart condition.
The proBNP is a simple blood test with a fast turn-around time that can provide the information you need to proactively manage your dog’s or cat’s heart health. You can have the test repeated as often as necessary to chart your progress in meeting your pet’s cardiovascular health needs throughout his life. - Make sure you’re meeting your pet’s CoQ10 requirement . CoQ10 is a naturally occurring coenzyme that young dogs and cats have in plentiful supply. But as she ages, your pet’s ability to produce CoQ10 decreases.
I recommend you supplement your pet’s amino-acid-rich diet with Coenzyme Q10, especially if you have an animal that is predisposed to cardiovascular disease. Supplying your pet with extra CoQ10 can insure she has the quantity her body needs to maintain a healthy heart muscle.
CoQ10 supplements come in two forms: Ubiquinone and Ubiquinol. Ubiquinol is a reduced form of CoQ10 and is the supplement I recommend for my dog and cat patients. A good heart-healthy maintenance dose is: - 50 mg per day for cats and small dogs
- 100 mg per day for medium sized dogs
- 100 mg twice per day for large dogs
Wednesday, July 26, 2017
Ginger Effective for Migraines
Ginger as Effective as Synthetic Drug in Migraine, but Without the Side Effects
Posted on: Monday, July 17th 2017 at 11:00 am
Written By: Dr. Michael Murray
Originally published on doctormurray.com.
The healing effects of ginger are well-documented, and now new data shows the efficacy of ginger on migraine headaches.
Introduction:
Migraine headaches are estimated to affect over 28 million Americans. These headaches are caused by excessive dilation of blood vessels in the head and are characterized by a throbbing or pounding sharp pain.
The standard medical approach is the use of over-the-counter (OTC) and prescription (Rx) drugs. The OTC options are pain relievers alone or in combination such as the combination of acetaminophen, aspirin and caffeine. OTC choices are usually of limited benefit, especially in more severe cases.
The most popular Rx drugs are the triptans. These drugs work by constricting blood vessels as well as blocking pain pathways in the brain. Sumatriptan (Imitrex) is regarded as the gold standard of these drugs as it has the longest track record and is the most studied. It brings about almost immediate relief for many patients, but headache recurs in almost 40% of people within 24 hours after taking the drug. Minor side effects of triptans include nausea, dizziness, drowsiness and muscle weakness. But, these medications can also cause more serious side effects such as coronary artery spasms, heart attacks, stroke, abnormal heart beats, and seizures.
There are a number of dietary and supplement strategies that have been shown to be effective alternative treatments in migraine with success rates often superior to standard therapy. In particular, a new study compared ginger powder head-to-head with Sumatriptan. Ginger showed equal effectiveness, but a better safety profile.
Background Data:
Historically, the majority of complaints for which ginger was used concerned the gastrointestinal system. Ginger is generally regarded as an excellent carminative (a substance that promotes the elimination of intestinal gas) and intestinal spasmolytic (a substance that relaxes and soothes the intestinal tract). Several double-blind studies have shown ginger to yield positive results in a variety of gastrointestinal issues, especially those related to nausea and vomiting.
Ginger was also used historically in pain and inflammation. Some, but not all clinical studies have supported this use with positive results in various forms of arthritis, chronic low back pain, painful menstruation, and muscle pain. The active compounds of ginger are the volatile, aromatic compounds like gingerol.
Ginger has also been shown to exert a number of very interesting anti-inflammatory effects in experimental studies. Early studies in the treatment of migraine headaches were promising, but most were conducted with a combination product containing ginger extract and feverfew.
New Data:
In a study conducted in Iran, a team of neurologists compared ginger and sumatriptan in 100 men and women who had suffered migraines for an average of seven years. The patients were randomly assigned to either the ginger group or the sumatriptan group. They were given a box of 5 caplets containing their test medication (250 mg caplet of dried ginger powder or an identically looking caplet containing 50 mg of sumatriptan in a double-blind fashion. Neither the participants nor the observers knew which caplets the patient was taking until the study was completed. Patients were instructed to take a caplet as soon as a migraine started.
For each headache that occurred during that month, participants recorded the time the headache began, headache severity before taking the medication and degree of pain relief at 30, 60, 90 and 120 minutes as well as 24 hours after taking it.
Results showed that ginger was equally as effective as sumatriptan achieving 90% relief within two hours after ingestion. While ginger had a very small percentage (4%) experiencing minor digestive symptoms, 20% of patients taking sumatriptan reported dizziness, drowsiness, or heartburn.
Commentary:
The dosage of ginger used in this study was very low (250 mg dried ginger root). Higher dosages more than likely would have produced even better results. Most clinical studies have used a dosage of 1g powdered ginger daily. My feeling is that fresh ginger at an equivalent dosage would yield even better results because it contains active enzymes and higher levels of other more active constituents as well. This equivalent dosage would be about 10g or one-third ounce fresh ginger, roughly a quarter-inch slice. The best method to take advantage of fresh ginger is to juice it. Ginger is a great addition to virtually every fresh fruit and vegetable juice. You can also juice or grate fresh ginger and add it to sparkling mineral water for some real ginger ale.
Fresh ginger can now be purchased in the produce section at most supermarkets. It is a phenomenal, easy available super natural medicine. When buying fresh ginger, the bronze root should be fresh looking, with no signs of decay like soft spots, mildew, or a dry, wrinkled skin. Store fresh ginger in the refrigerator.
Reference:
Maghbooli M, Golipour F, Moghimi Esfandabadi A, Yousefi M. Comparison between the efficacy of ginger and sumatriptan in the ablative treatment of the common migraine. Phytother Res. 2014 Mar;28(3):412-5.
Dr. Murray is one of the world’s leading authorities on natural medicine. He has published over 40 books featuring natural approaches to health. His research into the health benefits of proper nutrition is the foundation for a best-selling line of dietary supplements from Natural Factors, where he is Director of Product Development. He is a graduate, former faculty member, and serves on the Board of Regents of Bastyr University in Seattle, Washington. Please Click Here to receive a Free 5 Interview Collection from Dr Murray's Natural Medicine Summit with the Top Leaders in the Field of Natural
Medicine. Sign up for his newsletter and receive a free copy of his book on Stress, Anxiety and Insomnia.
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.
Monday, July 24, 2017
Sunday, July 23, 2017
Are Micro RNA's from Plants the Future of Healing with Food?
Are MicroRNAs from Plants the Future of Healing with Food?
Posted on: Monday, July 17th 2017 at 9:45 am
Written By: Dr. Michael Murray
Originally published on doctormurray.com.
New research is exploding into scientific journals detailing exciting ways in which foods interact with the expression of our genes. In fact, there is a whole new field of study known as “nutrigenomics” researching the effects of foods and food constituents on gene expression.
Recently, there have been major development in nutrigenomics that opens the possibility that successfully preventing and treating many diseases may be as simple as administering vegetables and medicinal herbs to deliver specific factors known as microRNAs.
Background Data:
The first step in transferring the genetic code of DNA occurs via a process called transcription. During transcription, the double-helix strand of DNA is split and then transcribed into a parallel single stranded RNA molecule. One form of RNA is called messenger RNA because it is “translated” by various cell components to assemble a specific protein or perform another specific vital task in cell function. Another type of RNA is composed of small fragments called microRNAs. It is now well-accepted that microRNA play a huge role in turning up and down the levels of key regulatory proteins within cells.
MicroRNAs are used by cells to modify many processes, including how cells grow and die, as well as restore balance in cell function. Many researchers feel that delivering the right microRNAs offer tremendous potential in the treatment of virtually every human disease.
Until recently scientists thought microRNAs were only made by our own cells, but new research shows that microRNAs from plants are absorbed from the diet and affect cell function just like the microRNAs transcribed from our own DNA. In other words, the microRNAs that we ingest from plants can influence the expression of our genetic code and cell function. Since microRNAs affect the expression of up to 30% of our genes, these results are extremely thought-provoking and provide another avenue that plant foods may be influencing our health and reducing our risk for certain diseases.
New Data:
To investigate the therapeutic potential of plant microRNAs in treating infectious diseases, researchers in China used an old herbal remedy for colds and influenza, Chinese honeysuckle (Lonicera japonica). Previous work had shown that this plant contains a high amount of a microRNA identified as miR2911. The study showed that miR2911 is taken up by the GI tract upon ingestion of honeysuckle tea, and travels via the bloodstream to the lungs, where it directly targets influenza A virus replication. In other words, the honeysuckle microRNA is delivered to the area of infection and effectively prevents the virus from reproducing. The authors suggested that that honeysuckle has medicinal properties not only because it possesses miR2911, but also because ingestion of the plant enhances dietary uptake of other microRNAs.
Commentary:
The discovery of plant microRNAs influencing human cell expression as well as in the case of the study reviewed here, viral genetic expression will ultimately revolutionize medicine. The possibilities are endless and the research is accumulating rapidly on a global basis.
Results from the Human Genome Project (HGP) taught researchers that our genetic code is important, but even more important are factors that influence how the genetic code is expressed. Chief among these other factors is diet and food components. An analogy would be that DNA is like a computer (hardware) while our diet, lifestyle, and attitude is like complex software. The hardware is important, for sure, but it is the software that actually tells the DNA what to do. The bottom line is that food definitely effects how our genetic code is expressed giving us the power to change our genetic predispositions to various health issues including cancer, heart disease, diabetes, and Alzheimer’s disease.
Additional Reading related to mRNAs
- Why The Only Thing Influenza May Kill Is Germ Theory
- No Sex Required: Body Cells Transfer Genetic Info To Germline Cells
- Why Food is Actually INFORMATION
- Amazing Food Science Discovery: Edible Plants 'Talk To Your Body
- Genetic Dark Matter, Return of the Goddess
- The GMO Agenda Takes a Menacing Leap Forward
Reference:
Zhou Z, Li X, Liu J, et al. Honeysuckle-encoded atypical microRNA2911 directly targets influenza A viruses. Cell Res. 2015 Jan;25(1):39-49.
Dr. Murray is one of the world’s leading authorities on natural medicine. He has published over 40 books featuring natural approaches to health. His research into the health benefits of proper nutrition is the foundation for a best-selling line of dietary supplements from Natural Factors, where he is Director of Product Development. He is a graduate, former faculty member, and serves on the Board of Regents of Bastyr University in Seattle, Washington. Please Click Here to receive a Free 5 Interview Collection from Dr Murray's Natural Medicine Summit with the Top Leaders in the Field of Natural
Medicine. Sign up for his newsletter and receive a free copy of his book on Stress, Anxiety and Insomnia.
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.
Saturday, July 22, 2017
Friday, July 21, 2017
Thursday, July 20, 2017
Black Seed May Treat Hypothyroidism (Hashimoto's Disease ) Clinical Trial Reveals
Black Seed May Treat Hypothyroidism (Hashimoto's Disease), Clinical Trial Reveals
Posted on: Sunday, March 12th 2017 at 5:45 am
Written By: Sayer Ji, Founder
This article is copyrighted by GreenMedInfo LLC, 2017
A recent clinical trial indicates that the most common cause of hypothyrodism (Hashimoto's disease) may be improved with the addition of only two grams of powdered black seed daily.
A powerful new randomized clinical trial reveals that the ancient healing food known as nigella sativa (aka “black seed”), once known as the “remedy for everything but death,” may provide an ideal treatment for the autoimmune thyroid condition known as Hashimoto’s disease, which is the most common cause of hypothyroidism.
The new study, published in the journal BMC Complementary and Alternative Medicine, evaluated the effects of nigella sativa on thyroid function, serum Vascular Endothelial Growth Factor (VEGF) - 1, Nesfatin -1 and anthropometric features in patients with Hashimoto’s thyroiditis.
The study took 40 patients with Hashimoto's thyroiditis, aged between 22 and 50 years old, and randomized them into one group receiving two grams of powdered encapsulated Nigella sativa and the other 2 grams starch placebo daily for 8 weeks.. Changes in anthropometric variables, dietary intakes, thyroid status, serum VEGF and Nesfatin-1 concentrations were measured.
The positive results were reported as follows:
"Treatment with Nigella sativa significantly reduced body weight and body mass index (BMI). Serum concentrations of thyroid stimulating hormone (TSH) and anti-thyroid peroxidase (anti-TPO) antibodies decreased while serum T3 concentrations increased in Nigella sativa-treated group after 8 weeks. There was a significant reduction in serum VEGF concentrations in intervention group. None of these changes had been observed in placebo treated group. In stepwise multiple regression model, changes in waist to hip ratio (WHR) and thyroid hormones were significant predictors of changes in serum VEGF and Nesgfatin-1 values in Nigella sativa treated group (P < 0.05)."
The researchers concluded:
"Our data showed a potent beneficial effect of powdered Nigella sativa in improving thyroid status and anthropometric variables in patients with Hashimoto's thyroiditis. Moreover, Nigella sativa significantly reduced serum VEGF concentrations in these patients. Considering observed health- promoting effect of this medicinal plant in ameliorating the disease severity, it can be regarded as a useful therapeutic approach in management of Hashimoto's thyroiditis."
What is Hashimoto’s Disease and Why Does Synthetic T4 Fail To Improve Well-Being
Hashimoto’s disease can be a devastating condition, especially when treated with a conventional medical approach. Also known as chronic lymphocytic thyroiditis, it is a progressive autoimmune disease where, in the many cases, the thyroid gland is eventually destroyed. It is considered the most common cause of hypothyroidism in North America. Some additional salient facts are:
- About 5% of the U.S. population will be affected by Hashimoto’s thyroiditis at some point in their life.
- Hashimoto’s occurs up to 15 times more often in women than in men. The highest density of Hashimoto’s cases are between 30 and 60 years of age.
- Postpartum thyroiditis occurs in about 10% of patients.
- Hashimoto’s related hypothyroid is often under-diagnosed because the reference ranges were drawn from an unscreened population likely inclusive of those already suffering from suboptimal thyroid function or outright dysfunction.
The standard of care is to ‘manage,’ or artificially suppress, modulate, and/or replace hormone levels. Hypothyroidism caused by Hashimoto’s thyroiditis is most commonly treated with synthetic T4 in an attempt to reduce TSH levels under 5.0 U/ml. This often results in the appearance of TSH normalization, with downstream adverse effects, and without concomitant improvements in well-being. Dr. Kelly Brogan, MD, further elaborates:
“For those who do receive the label of hypothyroid, they remain obliquely objectified by their lab work as their doctors use synthetic T4 – Synthroid – to attempt to move their TSH within range, more often leaving them symptomatic but “treated” because of poor conversion to active thyroid hormone (T3) and suppression of natural T3 production because of their now lower TSH.”
It should be noted that while synthetic T4 is described by its manufacturer to be “identical to that produced in the human thyroid gland,” it is in actuality quite different. This has to do primarily with the fact that while the primary structure of amino acids in synthetic thyroxine produced from genetically modified yeast is virtually identical to that produced by the human thyroid gland, the secondary, tertiary and quaternary folding patterns of that protein may differ in significant ways. Known as the protein’s conformational state, a slight change in folding structure can alter function profoundly. This could account for widespread reports of dissatisfaction among those treated with synthetic thyroid versus natural forms extracted from the glands of pigs.
Even if the T4 produced synthetically were identical in structure and function to natural T4, the reality is that virtually all T4 found naturally in the human body is not found in its free state.
Moreover, T4 is found inextricably bound together with T3, T2, T1, and calcitron, in the extraordinarily complex Thyroxine Binding Globulin (TBG) protein. Clearly, therefore, pharmaceutical preparations of isolated T4 can not be considered identical to whole-food complexed thyroid hormones derived from natural extracts.
In a post titled, “Natural Desiccated Thyroid and Synthetic are NOT the Same,” from thyroid-s.com, this point is driven home powerfully:
"To graphically illustrate the huge differences between Natural Desiccated Thyroid as compared to T4 Only Synthetics, please consider this graphic. It attempts to show the tiny T4, T3, T2, T1 and Calcitonin hormones tightly bound to the very large thyroglobulin molecules as found in Natural Desiccated Thyroid. Remember that the Thyroglobulin molecule is approximately 1,000 TIMES BIGGER than the T4 molecule. Then it also shows the tiny T4 molecules as found in synthetic T4 only products. The pharmaceutical companies would have us believe these are bio-identical. We will let you decide.”
Moreover, research published in 2010 in the Archives of Pharmaceutical Research shows that levothyroxine preparations are widely contaminated with a "mirror image" stereoismer called dextro-thyroxine at a level as high as 1-6% by dry weight. D-thyroxine violates the left-handed ‘chirality’ of natural thyroxine and is a powerful, cardiotoxic endocrine disruptor.
The process by which levothyroxine sodium is produced today is highly synthetic and involves the use of a wide range of chemicals. One patent describes the dizzyingly complex process as follows:
"The process for preparation of Levothyroxine sodium comprises the steps, wherein compound obtained from steps a-g is prepared by conventional methods, a. nitrating L-tyrosine to give 3,5- dinitro-L-tyrosine, b. acetylating 3,5- dinitro-L-tyrosine to give 3,5- dinitro-N-acetyl L-tyrosine, c. esterifying the compound obtained from step (b) to give 3,5- diπitro-N-acetyl L-tyrosine ethyl ester, d. reacting the compound obtained from step (c) with p-TsCI in presence of pyridine to give corresponding tosylate salt, which is further reacting with 4-methoxy phenol to give 3,5- DinKro-4-p-methoxy phenoxy-N-acetyl-L-phenyl alanine ethyl ester, e. the compound obtained from step (d) is hydrogenated to give 3,5-diamino-4-p-methoxy phenoxy-N-acetyl-L-phenyl alanine ethyl ester, f. the compound obtained from step (e) is tetrazotized and iodized to give 3,5-Diiodo-4-p- methoxy phenoxy-N-acetyl-L-phenyl alanine ethyl ester, g. the compound obtained from step (f) is O-demethylated, N-deacetylated, and deesterified using aqueous HI in acetic acid to give 3,5-Diiodo-4-p-hydroxy phenoxy-L-pheπyl alanine followed by preparing hydrochloride salt of same and isolating, drying it h. lodinating 3,5-Diiodo-4-p-hydroxy pheπoxy-L-phenyl alanine HCI salt using methyl amine,"
Clearly, synthetic T4 treatments, even if effective at suppressing TSH, may not produce clinical outcomes that translate into improvement in well-being. Nor do they address or resolve the root causes of Hashimoto’s, which include selenium deficiency, wheat intolerance, and vitamin D/sunlight deficiency [view studies on these links on our Hashimoto’s research dashboard], along with a wide range of still yet unknown environmental, dietary, lifestyle, and mind-body factors. Perhaps this latest study on black seed provides a new avenue for mitigating and correcting the metabolic and endocrine factors that are disturbed in Hashimoto’s disease, or at least complementing conventional treatment with a food-based approach that can improve both the subjective and objective aspects of the disease.
For more information on natural and integrative approaches to thyroid disease visit the following resource pageson GreenMedInfo.com:
To learn more about the powerful health benefits of black seed visit our research dashboard on the subject: Nigella Sativa (aka Black Seed)
Sayer Ji is founder of Greenmedinfo.com, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.
Wednesday, July 19, 2017
the five top pesticide soaked Fruits and Vegetables to avoid at all costs
The Top Five Pesticide Soaked Fruits and Vegetables
With such a striking level of pesticides on each of these “conventional” produce items, it would be wise to avoid them entirely (even though most people buy them non-organic without a second thought).
- Strawberries – Topping the list for the first time are strawberries, which may seem healthy at first glance but can actually be loaded with synthetic, toxic pesticides according to the EWG’s research.
Pesticides with negative effects on the brain and nervous system have been found in spades on strawberries, with 45 total pesticide residues found by the U.S. Department of Agriculture’s Pesticide Data Program (PDP) in 2009.
/29693840/HHL_In_Content_Ad_3_336x280_Mobile OLD /29693840/hhl_article_mobile_bb3
Organic strawberries are especially pricier but well worth the investment; buy them in season and freeze to save big money.
- Apples – Perhaps the most notable inclusion on this list is the apple, considering its reputation as a health food, and the lack of organic apple orchards for that matter. The vast majority of apple orchards remain “conventional,” and yet American apples were banned in Europe by regulators.
Over 47 pesticide residues were found in conventional apples by the USDA’s pesticide data program in 2010. Doesn’t exactly make for a healthy cup of apple juice now, does it?
Apples are one of the highest pesticide residue fruits out there. Will you think twice about that next apple orchard trip?
/29693840/hhl_article_mobile_bb4
- Nectarines- Similar to peaches with their soft, round shape and orange color, nectarines soak up pesticides like a sponge, making it important to always buy them organic or at the very least to limit consumption.
According to the 2012 EWG report, nectarines actually had the most overall weight of pesticides of any fruit or vegetable, meaning that you’re probably consuming these dangerous carcinogens in every bite and taxing the health of your liver.
- Peaches- The soft skin of peaches combined with a number of chemicals they’re treated with could spell serious trouble for your health.
A 2008 study by the PDP found 62 different pesticide residues on conventional peaches; several are considered as neurotoxins and/or known carcinogens. While you can wash some of the residues off, much of it remains in the soft flesh and skin of the peach.
- Celery- According to USDA data, non-organic celery may contain as many as 64 different pesticide residues, including as many as 16 that are considered toxic to honeybees.
This toxic onslaught has landed the otherwise healthy vegetable on the top 5 of the ‘Dirty Dozen’ in 2016, and underscores yet again the importance of buying organic.
Not only is organic celery far less contaminated by these and other pesticides (see the data here), but it also tastes quite a bit better (without the not-so-pleasant aftertaste in my humble opinion).
Final Thoughts:
You can easily find most of these top five most pesticide-laden fruits and vegetables in just about everyone’s kitchen, and that’s what makes them so dangerous to our health.
Don’t forget to share this information with your friends who still consider these pesticide-soaked fruits and vegetables to be “health foods.”
Article originally published on AltHealthwks.com republished with permission
Source
Van Hoesen, S. (2016, April 12). EWG’s 2016 Dirty Dozen™ List of Pesticides on Produce: Strawberries Most Contaminated, Apples Drop to Second. Retrieved from
Iodine Fuel to the Fire in Hashimoto's
Iodine: Fuel to the Fire in Hashimoto’s
Posted on: Saturday, July 15th 2017 at 8:30 am
Written By: Ali Le Vere, B.S., B.S.
Iodine is a hot topic of debate in the thyroid conversation. Here are the facts behind the iodine/thyroid connection.
Bring up the relationship between iodine and thyroid disorders, and people inevitably put the gloves on and get scrappy---not just an intellectual back and forth banter, supported by exchange of peer-reviewed scientific studies and empirically validated literature---but a throw-down, knock-out fight, where claims are made on the basis of anecdotal evidence based on what so-and-so blogger said, without a single primary or secondary source citation. This, I cannot endorse.
Despite clear trends in the scientific literature, there is rampant misinformation in the integrative medical community when it comes to iodine supplementation for Hashimoto’s thyroiditis in particular. I have heard many high profile functional medicine leaders advocate consumption of iodine-rich seaweed or high dose iodine supplementation for those of us with Hashimoto's...without a single evidence-based resource to substantiate their recommendation. Because one autoimmune condition can beget another, it is reckless and irresponsible to give recommendations to autoimmune cohorts without so much as a literature search. Thus, a disimpassioned examination of the science is warranted.
Iodine, the heaviest of the halogens, is required in proper quantities as an essential precursor to thyroid hormone synthesis. The thyroid gland converts the amino acid tyrosine into thyroglobulin, and attaches one to four iodine atoms to create T4 (thyroxine), the inactive storage hormone, T3 (triidothyronine), or metabolically active thyroid hormone, and two thyroid hormones whose clinical significance is less known, T2 and T1.
Mandatory salt iodization programs, to which 70% of the world's population are subject, have by and large eliminated iodine deficiency in most industrialized countries (1). For instance, after the development of the universal salt iodization initiative in China, median urinary iodine escalated from 164.8 μg/L in 1995 to 238.6 μg/L in 2011, well beyond the 100.0 to 199.0 μg/L levels recommended by the World Health Organization (WHO) from prevention of iodine deficiency disorders (IDD) (2). Meanwhile, however, “The spectrum of thyroid diseases has undergone a significant change ranging from simple goiter to toxic nodular goiter, Hashimoto’s thyroiditis, and thyroid cancer accompanied by the increase in iodine intake, especially for thyroid cancer with an annual increase of 14.51% in China” (3).
The Epidemic of Thyroid Cancer
While increased incidence of Hashimoto’s thyroiditis, the autoimmune disease responsible for the majority of cases of hypothyroidism, is part of a larger epidemic of autoimmune disorders, the skyrocketing rates of thyroid cancer are likely a consequence of over-diagnosis due to an unprecedented increase in thyroid imaging. Most of these thyroid cancers are being re-classified as benign morphological variations, or papillary lesions of indolent course (PLICs), “which do not evolve to cause metastatic disease or death” (4). According to Brito and colleagues (2014), the majority of these growths constitute the most indolent type of thyroid cancer, called small papillary cancers, with a mortality of less than 1% after 20 years of post-surgical follow-up (4). The researchers elucidate, “Now new risk factors, but one, can completely explain the surge of these lesions: the exponential increase in the use of diagnostic imaging” (4, p.1).
Volmer (2014) concluded similarly that, “The results of this study support the notion that many thyroid cancers are part of a reservoir of nonfatal tumors that are increasingly being overdetected and overdiagnosed” (5, p. 128). Devastatingly, standard of care for patients with these conditions is thyroidectomy—surgical removal of one of the most essential glands in the body—followed by carcinogenic radiation, lifelong synthetic thyroid hormone replacement, and surveillance for ‘cancer’ recurrence. Brito and colleagues (2014) state that, as evidenced by autopsies, many of us harbor these thyroid ‘cancers’ in our thyroid glands (4). In fact, studies suggest that if all thyroids were subjected to biopsy, pathologists would find these microscopic thyroid ‘cancers' to be ubiquitous in the population (6). The authors of these post-mortem studies state that these occult papillary carcinomas (OPCs), which arise from normal follicular cells, should be “regarded as a normal finding which should not be treated when incidentally found” (6, p. 531). Researchers further state that, “The great majority of the tumors remain small and circumscribed and even from those few tumors that grow larger and become invasive OPCs only a minimal proportion will ever become a clinical carcinoma” (6, p. 531).
Iodine and the Epidemic of Hashimoto’s Thyroiditis
On the other hand, iodine may be one of the potential culprits in the dramatic surge in diagnoses of Hashimoto’s thyroiditis, also known as autoimmune thyroiditis or chronic lymphocytic thyroiditis, which has occurred in recent years.
With respect to certain constructs, the natural medicine community often adopts a group-think mentality and becomes an echo chamber of reverberating ideas, a choir with one unanimous voice and little substantive discourse. However, as Benjamin Franklin stated, “If everyone is thinking alike, then no one is thinking”. Thus, the assertion that is frequently cited in alternative medical communities that we are in the midst of a massive iodine deficiency due to inundation with chlorinated, fluoridated, and brominated compounds, which displace iodine in the thyroid gland, is worthy of examination.
While these halogens are indisputably cause for concern, this theoretical iodine deficiency in Western nations does not materialize in the literature. According to a 2013 study, 10 countries have iodine excess, 111 countries have sufficient iodine intake, 9 countries are moderately deficient, 21 are mildly deficient, and none are considered severely deficient, as defined by a median urinary iodine concentration of 100-299 μg/L in school-aged children (1). According to studies, approximately 71% to 74% or more of the world’s population is now iodine sufficient, illuminating that the risk of iodine deficiency is overstated (1, 7). The most recent Food and Drug Administration's Total Diet Study also revealed that the U.S. population has adequate dietary iodine, with estimated average daily iodine intake ranging from 138 to 353 micrograms per person (8). Canada and Mexico are likewise iodine sufficient (1).
Importantly, iodine is a narrow therapeutic index or "Goldilocks" nutrient. It exhibits a biphasic U-shaped dose-response curve, where too much and too little is problematic for the thyroid. Iodine deficiency can create endemic goiter, growth retardation, neonatal hypothyroidism, intellectual impairments, cretinism, pregnancy loss, and infant mortality (9). On the other hand, excess iodine can induce hypothyroidism in euthyroid patients who have had previous episodes of subacute thyroiditis, in patients with a history of postpartum thyroiditis, in euthyroid patients with Hashimoto’s thyroiditis, and in some patients with chronic, systemic diseases (10). The Jod-Basedow phenomenon, also known as iodine-induced hyperthyroidism or thyrotoxicosis, can also occur in those with a history of autonomous multinodular or non-toxic goiter (1).
Evidence that Iodine Can Induce Hashimoto’s thyroiditis
Although iodine prophylaxis programs may decrease goiter prevalence, epidemiological research in China and Denmark has elucidated that excess iodine increases incidence of Hashimoto’s thyroiditis and hypothyroidism (11). Slovenia likewise showed an increase in Hashimoto’s thyroiditis incidence in the ten years after it became an iodine-replete country (12). Similarly, salt iodization was associated with increased frequency of thyroid autoantibodies and hypothyroidism in Great Britain, Denmark, and Iceland (13, 14, 30). Another study demonstrated an increased incidence of Hashimoto’s and positive thyroid autoantibodies when Italy improved its low iodine intake between 1995 and 2010 (15). Hypothyroidism and increases in serum thyroid autoantibodies also occurred with the introduction of iodine prophylaxis in Pescopagano (15). Furthermore, mean thyroid stimulating hormone (TSH), a biomarker for hypothyroidism, escalated significantly after a mandatory salt iodization program was implemented in a longitudinal DanThyr study (16). Astonishingly, in one study, 42.8% of subjects tested positive for thyroid autoantibodies after just three and six months of treatment with iodized oil (17).
In individuals with anti-thyroid peroxidase (TPO) or anti-thyroglobulin (TG) antibodies, the incidence of elevated TSH increased with greater levels of iodine intake (18). In addition, TG antibodies have been found more frequently in users of iodized salt (19). Zhao et al. (2014) found a significant correlation between excess iodine intake and thyroid disease incidence (3). Thyroid autoantibodies, specifically TG and TPO, were statistically higher in those with greater iodine intake (3). Researchers concluded that excess iodine intake can induce production of TPO and TG antibodies, both of which have positive predictive value for Hashimoto’s thyroiditis (3). In fact, positive anti-thyroid antibodies equate to an odds ratio of 8 for women and 25 for men for development of clinical hypothyroidism (13).
Lastly, the effect of iodine in Hashimoto’s is most dramatically demonstrated by a study by Yoon and colleagues (2003), where 78.3% of patients with Hashimoto’s regained euthyroid status (reversing their Hashimoto's thyroiditis) after three months of restricting iodine to less than 100 micrograms/day (versus 45.5% who recovered in an iodine non-restriction group) (24).
Molecular Mechanisms For Iodine-Induced Hashimoto’s
At a mechanistic level, thyroid autoimmunity induced by iodine is associated with synthesis of TG antibodies and the unmasking of a cryptic epitope of thyroglobulin, which is normally sequestered and unavailable to the immune system (19). According to Fiore, Latrofa, and Vitti (2015), “Thyroglobulin (TG) is an important target in iodine-induced autoimmune response due to post-translational modifications of iodinated TG,” as thyroglobulin is the only self-antigen subject to post-translational alterations resulting from exogenous iodine supply (9, p. 26). Enhanced iodination of TG alters its antigenicity and up-regulates presentation of its cryptic peptide to antigen-presenting cells (20; 21). Iodinated thyroglobulin is more antigenic because T cells that pass thymic selection, the process whereby self-reactive T cells are deleted, only recognize non-iodinated thyroglobulin motifs as belonging to self (22). Animal models strongly support this pathophysiological mechanism whereby iodine induces thyroid autoimmunity, as, “Excessive iodine intake can precipitate spontaneous thyroiditis in genetically predisposed animals, by increasing the immunogenicity of thyroglobulin (TG)” (19).
According to Topliss (2016), “Iodine supplementation is believed to increase the prevalence of circulating anti-TPO. The underlying mechanism is yet to be elucidated; however, more highly iodinated TG is more antigenic in experimental autoimmune thyroiditis” (11, p. 494). Experimental models of autoimmune thyroiditis have underscored that loss of B-cell self-tolerance occurs first for thyroglobulin and then secondarily for thyroid peroxidase, in line with these observations (23). Moreover, at a biochemical level, iodine may inhibit thyroid hormone synthesis and secretion, which is known as the Wolff-Chaikoff effect (10). According to Markou and colleagues (2001), “It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones” (10, p. 501).
The authors clarify that, “The acute Wolff-Chaikoff effect lasts for a few days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns” (10, p. 501). However, in euthyroid patients with Hashimoto’s thyroiditis, this escape phenomenon from the inhibitory effect of iodine is impaired, resulting in subclinical or clinical hypothyroidism (10).
Another potential mechanism through which iodine exacerbates or induces Hashimoto’s is by up-regulating Th17 cells, the immune cell subset responsible for tissue destruction in autoimmune disease, and by suppressing development of regulatory T cells, the population that invokes oral tolerance to arrest autoimmune responses (31). Duntas (2015) articulates, “In susceptible individuals, iodine excess increases intra-thyroid infiltrating Th17 cells and inhibits T regulatory (Treg) cells development, while it triggers an abnormal expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in thyrocytes, thus inducing apoptosis and parenchymal destruction” (31, p. 721). Also relevant to this phenomenon is the ratio of iodine to selenium, since selenoproteins mediate antioxidant, anti-inflammatory, and redox-related processes (31). “Selenostasis”, which is found to be compromised in Hashimoto’s thyroiditis and Graves’ disease, is critical to counterbalance iodine, because “Selenium enhances CD4+/CD25 FOXP3 and T regulatory cells activity while suppressing cytokine secretion, thus preventing apoptosis of the follicular cells and providing protection from thyroiditis” (31, p. 721).
Caveats for Iodine Supplementation
Based on a review of the literature, the only people who should be supplementing with iodine are those with lab-validated iodine deficiency. 90% of ingested iodine is excreted via renal pathways, such that median spot urinary iodine concentrations (UIC) will serve as a biomarker for recent dietary iodine intake (1). Iodine sufficiency is defined as median UIC of 100-299 micrograms per liter in school-aged children and greater than or equal to 140 micrograms per liter in pregnant women (32). However, some authors maintain that these tests are sufficient only at the population level and should not be applied to individuals due to the large day-to-day variation in iodized salt intake (1).
According to Konig and colleagues, (2011), "~10 repeat spot urine collections are needed to estimate individual iodine intakes with acceptable precision" (29, p. 524). On the other hand, the World Health Organization recommends urine iodine concentration (UIC) to monitor an individual’s iodine status (2). Because a single measurements serves only as an isolated snapshot in time, and may not be reflective of total body iodine status, repeat testing may be necessary before conclusions about iodine deficiency can be drawn.
Moreover, because thyroid hormone is critical for fetal and infant neurodevelopment in utero and post-partum, and since iodine deficiency can result in neurological and psychological deficits, using a multivitamin containing iodine may be indicated during pregnancy and breastfeeding. Although Prete, Paragliola, and Corsello (2015) caution against use of iodine in Hashimoto's thyroiditis at levels above 100 micrograms per day, they note that one exception is use of iodine supplementation during pregnancy to avoid damage to the newborn (25). Topliss (2016) also mentions, “Discouraging iodine mega-supplementation may not preclude appropriate physiological supplementation in pregnancy to a total intake of 250 µg/day” (11, p. 495). The post-partum period is a high-risk time for the development of thyroid autoimmunity due to Th1 dominance; however, researchers discuss that the risk of developmental retardation and intellectual deficits outweighs the risk of Hashimoto's onset.
Conclusions Regarding Iodine Supplementation in Hashimoto’s
When it comes to iodine, I have no dog in the fight. If the literature demonstrates that any natural food or nutraceutical helps Hashimoto's, I'm all for it, having the condition myself—but this is just not the case with iodine. Barring any lab-validated iodine deficiency, restriction of iodine seems to be warranted in Hashimoto’s thyroiditis, and use of iodized salts and supplements containing high doses of iodine would appear to be contraindicated. Thus, if your functional medicine practitioner, nutritionist, naturopathic doctor, or alternative medicine provider recommends that you supplement with supra-physiological doses of iodine—or that you incorporate massive sea vegetables into your diet to boost thyroid function—ask them for the peer-reviewed study supporting this practice. My bet is that they will come up empty.
So, why are people so invested in iodine? According to the Thyroid Pharmacist, Dr. Isabella Wentz, people may experience a short-term artificial increase in energy after beginning an iodine supplement (26). Dr. Wentz fleshes out a probable mechanism, whereby their newfound energy is derived from iodine-induced thyroid tissue destruction and the liberation of thyroid hormone into the circulation (26).
In summary, an across-the-board recommendation for iodine supplementation in people with Hashimoto’s thyroiditis is not evidence-based. Studies have rather supported the contrary notion, that, “high iodine intake [is] likely to lead to occurrence of thyroid diseases, such as Hashimoto’s thyroiditis, nodular goiter, and hyperthyroidism, through a long-term mechanism” (3). In fact, groups with the aforementioned thyroid diseases, as well as individuals with positive TG or TPO antibodies, have been demonstrated to exhibit significantly higher levels of urinary iodine, the main indicator of iodine nutritional status, compared to healthy controls (3).
What’s more, individuals with a family history of Hashimoto’s thyroiditis should be especially cautious about iodine intake, since the autoimmune reaction induced by iodine is particularly likely in genetically susceptible individuals. Besides promoting immunogenicity of the thyroglobulin molecule, dietary iodine can enhance levels of reactive oxygen species (ROS), which lead to expression of cell adhesion molecules (ICAM-1) that are crucial to the early phases of thyroid follicular inflammatory responses (3). Lastly, excessive iodine can generate high levels of hydrogen peroxide (H2O2), which damages thyrocytes and perpetuates thyroid autoimmunity (27).
The role of iodine in triggering Hashimoto’s thyroiditis should not be taken lightly, as an increased prevalence of thyroid autoantibodies was discovered even after cautious iodization programs were implemented (14, 28). According to researchers, this data cumulatively substantiates the notion that even small increases in supplemental iodine may increase risk for thyroid autoimmunity (9).
Caution should therefore be heeded before adding supplemental iodine to the regimen of any patient with thyroid autoimmunity, since, “Iodine intake modulates the pattern of thyroid diseases, even in cases of slight differences in intake and doses below 150 μg daily recommended for preventing IDD” (9).
References
1. Pearce, E.N., Andersson, M., & Zimmermann, M.B. (2013). Global iodine nutrition: Where do we stand in 2013? Thyroid, 23(5), 524-528.
2. WHO/UNICEF/ICCIDD. (2001). Assessment of the iodine deficiency disorders and monitoring their elimination: A Guide for Programme Managers. World Health Organization: Geneva.
3. Zhao, H. et al. (2014). Correlation between iodine intake and thyroid disorders: a cross-sectional study from the South of China. Biological Trace Elements Research, 162(1-3), 87-94. doi: 10.1007/s12011-014-0102-9.
4. Brito, J.P. et al. (2014). Papillary lesions of indolent course: reducing the overdiagnosis of indolent papillary thyroid cancer and unnecessary treatment. Future Medicine, 10(1), 1-4.
5. Volmer, R.T. (2014). Revisiting overdiagnosis and fatality in thyroid cancer. American Journal of Clinical Pathology, 141(1), 128-132. doi: 10.1309/AJCP9TBSMWZVYPRR.
6. Harach, H.R., Fransilla, K.O., & Wasenius, V.M. (1985). Occult papillary carcinoma of the thyroid: A 'normal' finding in Finland. A systematic autopsy study. Cancer, 56, 531-538.
7. Zimmermann, M.B. (2009). Iodine deficiency. Endocrinology Reviews, 30, 376-408.
8. Murray, C.W. et al. (2008). US Food and Drug Administration's Total Diet Study: dietary intake of perchlorate and iodine. Journal of Exposure Science and Environmental Epidemiology, 18, 571-580.
9. Fiore, E., Latrofa, F., & Vitti, P. (2015). Iodine, thyroid autoimmunity and cancer. European Thyroid Journal., 4(1), 26-35.
10. Markou, K. et al. (2001). Iodine-induced hypothyroidism. Thyroid, 11(5), 501-510.
11. Topliss, D.J. (2016). Clinical update in aspects of the management of autoimmune thyroid diseases. Endocrinology Metabolism (Seoul), 31(4), 493-499. doi: 10.3803/EnM.2016.31.4.493
12. Gaberšček, S., & Zaletel, K. (2016). Epidemiological trends of iodine-related thyroid disorders: an example from Slovenia. Arhiv Za Higijenu Rada I Toksikologiju, 67(2), 93-8. doi: 10.1515/aiht-2016-67-2725
13. Vanderpump, M.P.J. et al. (1995) The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickam Survey. Clinical Endocrinology, 43, 55–68.
14. Laurberg, P. et al. (2001). Environmental iodine intake affects the type of nonmalignant thyroid disease. Thyroid, 11, 457–469.
15. Lombardi, A. et al. (2013). The effect of voluntary iodine prophylaxis in a small rural community: the Pescopagano survey 15 years later. Journal of Clinical Endocrinology and Metabolism, 98(3), 1031-9. doi: 10.1210/jc.2012-2960
16. Bjergved, L. et al. (2012). Predictors of change in serum TSH after iodine fortification: an 11-year follow-up to the DanThyr study. Journal of Clinical Endocrinology and Metabolism, 97, 4022–4029.
17. Boukis, M.A. et al. (1983). Thyroid hormone and immunological studies in endemic goiter. Journal of Clinical Endocrinology & Metabolism, 57, 859–862.
18. Teng, W. et al. (2006). Effect of iodine intake on thyroid diseases in China. New England Journal of Medicine, 354, 2783–2793.
19. Latrofa, F. et al. (2013). Iodine contributes to thyroid autoimmunity in humans by unmasking a cryptic epitope on thyroglobulin. Journal of Clinical Endocrinology and Metabolism, 98, E1768-E1774.
20. Dai, Y.D., Rao, V.P., & Carayanniotis, G. (2002). Enhanced iodination of thyroglobulin facilitates processing and presentation of a cryptic pathogenic peptide. Journal of Immunology, 168, 5907-5911.
21. Saboori, A.M., Rose, N.R., & Burek, C.L. (1998). Iodination of human thyroglobulin (Tg) alters its immunoreactivity. II. Fine specificity of a monoclonal antibody that recognizes iodinated Tg. Clinical Experiments in Immunology, 113, 303-308.
22. Carayanniotis, G. (2007). Recognition of thyroglobulin by T cells: the role of iodine. Thyroid, 17, 963–973.
23. Chen, C.R., Hamidi, S., Braley-Mullen, H., Nagayama, Y., Bresee, C., Aliesky, H.A., Rapoport, B., & McLachlan, S.M. (2010). Antibodies to thyroid peroxidase arise spontaneously with age in NOD.H-2h4 mice and appear after thyroglobulin antibodies. Endocrinology, 151, 4583–4593.
24. Yoon, S.J., Choi, S.R., Kim, D.M., Kim, K.W., Ahn, C.W., Cha, B.S.,…Hun, K.B. (2003). The effect of iodine restriction on thyroid function in patients with hypothyroidism due to Hashimoto's thyroiditis. Yonsei Medical Journal, 44(2), 227-235. Retrieved from http://www.eymj.org/
25. Prete, A., Paragliola, R.M., & Corsello, S.M. (2015). Iodine supplementation: Usage “with a grain of salt”. International Journal of Endocrinology, 312305. doi: 10.1155/2015/312305
26. Wentz, I. (2017). Iodine and Hashimoto’s. Retrieved from https://thyroidpharmacist.com/articles/iodine-hashimotos/
27. Burek, C.L., & Rose, N.R. (2008). Autoimmune thyroiditis and ROS. Autoimmunity Reviews, 7, 530-537.
28. Pedersen, I.B., et al. (2011). A cautious iodization program bringing iodine intake to a low recommended level is associated with an increase in the prevalence of thyroid autoantibodies in the population. Clinical Endocrinology (Oxford), 75, 120–126.
29. Konig, F. et al. (2011). Ten repeat collections for urinary iodine from spot samples or 24-hour samples are needed to reliably estimate individual iodine status in women. Journal of Nutrition, 141, 2049-2054.
30. Laurberg, P. et al. (1998). Iodine intake and the pattern of thyroid disorders: a comparative epidemiological study of thyroid abnormalities in the elderly in Iceland and in Jutland, Denmark. Journal of Clinical Endocrinology and Metabolism, 8, 765–769.
31. Duntas, L. H. (2015). The role of iodine and selenium in autoimmune thyroiditis. Hormonal and Metabolic Research, 47(10), 721-726 DOI: 10.1055/s-0035-1559631
32. Zimmermann, M.B. et al. (2013). Thyroglobulin is a sensitive measure of both deficient and excess iodine intakes in children and indicates no adverse effects on thyroid function in the UIC range of 100-299 micrograms/L: a UNICEF/ICCIDD Study Group Report. Journal of Clinical Endocrinology and Metabolism, 98, 1271-1280.
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.
Subscribe to:
Posts (Atom)