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
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
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Friday, July 21, 2017

Thursday, July 20, 2017

Learn the Secrets of the Nakshatras, Punarvasu: Return of the Light

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 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:
  1. About 5% of the U.S. population will be affected by Hashimoto’s thyroiditis at some point in their life.
  2. 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.
  3. Postpartum thyroiditis occurs in about 10% of patients.
  4. 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.
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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?
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  • 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

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.

Tuesday, July 18, 2017

Learn the Secrets of the Nakshatras: Ardra the star of Tragedy

THE FRIEND ZONE

K2 100 mcg a day helps Rheumatoid Arthritis

Vitamin K2 Effective in Rheumatoid Arthritis
Posted on: Friday, July 7th 2017 at 1:00 pm
Written By: Dr. Michael Murray

Originally published on DoctorMurray.com
Introduction:
Just as there has been an explosion of positive science on the importance of vitamin D3, another nutrient, vitamin K2, is showing tremendous promise in the treatment and prevention of a wide range of health conditions. A new study, set to be published in the August issue of the European Journal of Pharmacology, indicates that this underutilized form of vitamin K might hold the key to one of the most debilitating inflammatory conditions known to humans – rheumatoid arthritis.
Background Data:
Rheumatoid arthritis (RA) is a chronic inflammatory condition that affects the entire body, but especially the joints. There is abundant evidence that RA is an autoimmune reaction, in which antibodies develop against components of joint tissues, but what exactly triggers this autoimmune reaction has centered on genetic factors, abnormal bowel permeability, lifestyle and nutritional factors, food allergies, and microorganisms. RA is a classic example of a multifactorial disease, wherein an assortment of genetic, dietary, and environmental factors contribute to this disease.
There are several forms of vitamin K. Phylloquinone is derived from plant sources and is referred to as K1, whereas menaquionines are derived primarily from bacteria and are referred to a K2. There are several different forms of menaquinones based upon the number of attached molecules known as isoprenoids. MK-7 is the most important commercial form of vitamin K2. It contains seven isoprenoid residues attached to menaquinone.
While the role that vitamin K plays in blood clotting is well known, it also functions in important roles for bone and joint health. Clinical studies have documented the long-term effect of 180 mcg of MK-7 in improving bone density and overall bone health.
Based upon pre-clinical studies showing another form of vitamin K2 (MK-4) blocked the development of arthritis in the experimental animal model of RA, it was suggested that MK-4 might offer benefit in human RA. Human studies following and it was shown MK-4 supplementation reduced RA disease activity associated with a marked decrease in clinical and biochemical markers. However, since MK-7 has greater bioavailability than MK-4 after oral administration, researchers were quite curious if even better results might be produced with this form.

New Data:
To clarify the therapeutic role of MK-7 added to normal therapeutic regimen of RA in patients with different stages of the disease, 84 RA patients (24 male, 60 female) (average age=47.2 years) were enrolled in a randomized clinical trial. The patients were divided into MK-7 treated group (n=42) and a control group (n=42). MK-7 capsules were administered in a dose of 100 mcg/day for three months in the first group without changing other medications.
To assess the benefits with MK-7, the clinical and biochemical markers on RA patients treated with MK-7 and the control group were assessed before and after three months. The results showed a statistically significant decrease in MK-7 treated group for the levels of the following markers of inflammation: erythrocyte sedimentation rate (ESR), RA disease activity score assessing 28 joints, C-reactive protein (CRP) and matrix metalloproteinase (MMP-3). In addition, MK-7 also increased the level of the active form of osteocalcin, an important marker of bone health. The benefits noted with MK-7 were directly related to increased levels of MK-7 in the blood.
The authors’ conclusion was, “MK-7 represents a new promising agent for RA in combination therapy with other disease modifying antirheumatic drugs.”
Commentary:
In the treatment of RA, standard medical therapy is limited by its over-reliance on drugs designed to suppress the disease process and its symptoms, while failing to address the complex underlying causes of this disease. These drugs include powerful chemotherapy agents like methotrexate used in combination with newer biological agents like Enbrel. Unfortunately, while there have been some improvements in outcomes with these newer regimens, drug-free remission is still very rarely achieved and most patients experience higher disease activity upon discontinuation of therapy. They often have to quit treatment because of the serious side effects these drugs cause.
The natural treatment of RA can be quite successful. Diet alone can be used to produce a complete remission in some patients and there are many key supplements that can help. For a complete discussion on the natural approach to RA, please consult the 3rd Edition of the Encyclopedia of Natural Medicine.

Reference:
Abdel-Rahman MS, Alkady EA, Ahmed S. Menaquinone-7 as a novel pharmacological therapy in the treatment of rheumatoid arthritis: A clinical study. Eur J Pharmacol. 2015 Jun 11;761:273-278.

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.

To comment:

Vitain K2 Effective in Rheumatoid Arthritis

Vitamin K2 effective in Rheumatoid Arthritis
By Erin Elizabeth - July 17, 2017
0

(Note from the Editor: I would encourage you ALL to watch the video below.)
Introduction:
Just as there has been an explosion of positive science on the importance of vitamin D3, another nutrient, vitamin K2, is showing tremendous promise in the treatment and prevention of a wide range of health conditions. A new study, set to be published in the August issue of the European Journal of Pharmacology, indicates that this underutilized form of vitamin K might hold the key to one of the most debilitating inflammatory conditions known to humans – rheumatoid arthritis.
RELATED ARTICLE:










An error occurred.

Try watching this video on www.youtube.com, or enable JavaScript if it is disabled in your browser.
Background Data:
Rheumatoid arthritis (RA) is a chronic inflammatory condition that affects the entire body, but especially the joints. There is abundant evidence that RA is an autoimmune reaction, in which antibodies develop against components of joint tissues, but what exactly triggers this autoimmune reaction has centered on genetic factors, abnormal bowel permeability, lifestyle and nutritional factors, food allergies, and microorganisms. RA is a classic example of a multifactorial disease, wherein an assortment of genetic, dietary, and environmental factors contribute to this disease.
There are several forms of vitamin K. Phylloquinone is derived from plant sources and is referred to as K1, whereas menaquionines are derived primarily from bacteria and are referred to a K2. There are several different forms of menaquinones based upon the number of attached molecules known as isoprenoids. MK-7 is the most important commercial form of vitamin K2. It contains seven isoprenoid residues attached to menaquinone.
While the role that vitamin K plays in blood clotting is well known, it also functions in important roles for bone and joint health. Clinical studies have documented the long-term effect of 180 mcg of MK-7 in improving bone density and overall bone health.
Based upon pre-clinical studies showing another form of vitamin K2 (MK-4) blocked the development of arthritis in the experimental animal model of RA, it was suggested that MK-4 might offer benefit in human RA. Human studies following and it was shown MK-4 supplementation reduced RA disease activity associated with a marked decrease in clinical and biochemical markers. However, since MK-7 has greater bioavailability than MK-4 after oral administration, researchers were quite curious if even better results might be produced with this form.
New Data:
To clarify the therapeutic role of MK-7 added to normal therapeutic regimen of RA in patients with different stages of the disease, 84 RA patients (24 male, 60 female) (average age=47.2 years) were enrolled in a randomized clinical trial. The patients were divided into MK-7 treated group (n=42) and a control group (n=42). MK-7 capsules were administered in a dose of 100 mcg/day for three months in the first group without changing other medications.
RELATED ARTICLES:
To assess the benefits with MK-7, the clinical and biochemical markers on RA patients treated with MK-7 and the control group were assessed before and after three months. The results showed a statistically significant decrease in MK-7 treated group for the levels of the following markers of inflammation: erythrocyte sedimentation rate (ESR), RA disease activity score assessing 28 joints, C-reactive protein (CRP) and matrix metalloproteinase (MMP-3). In addition, MK-7 also increased the level of the active form of osteocalcin, an important marker of bone health. The benefits noted with MK-7 were directly related to increased levels of MK-7 in the blood.
The authors’ conclusion was, “MK-7 represents a new promising agent for RA in combination therapy with other disease modifying antirheumatic drugs.”
Commentary:
In the treatment of RA, standard medical therapy is limited by its over-reliance on drugs designed to suppress the disease process and its symptoms, while failing to address the complex underlying causes of this disease. These drugs include powerful chemotherapy agents like methotrexate used in combination with newer biological agents like Enbrel. Unfortunately, while there have been some improvements in outcomes with these newer regimens, drug-free remission is still very rarely achieved and most patients experience higher disease activity upon discontinuation of therapy. They often have to quit treatment because of the serious side effects these drugs cause.
The natural treatment of RA can be quite successful. Diet alone can be used to produce a complete remission in some patients and there are many key supplements that can help. For a complete discussion on the natural approach to RA, please consult the 3rd Edition of the Encyclopedia of Natural Medicine.

Reference:
Abdel-Rahman MS, Alkady EA, Ahmed S. Menaquinone-7 as a novel pharmacological therapy in the treatment of rheumatoid arthritis: A clinical study. Eur J Pharmacol. 2015 Jun 11;761:273-278.

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.


*Article originally appeared at Green Med Info.

Monday, July 17, 2017

Where Does the Arsenic in Chicken Come From?

Vegetables rate by nitrate

Foods for Heart Health

Which Foods Are Best for Your Heart Health?

  • 1K 



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Story at-a-glance
  • Many vegetables contain naturally occurring nitrates, which your body transforms into nitric oxide (NO), a soluble gas continually produced from the amino acid L-arginine inside your cells
  • NO supports healthy endothelial function and protects your mitochondria. Acting as a potent vasodilator, NO also relaxes and widens your blood vessels, improving blood flow and reducing blood pressure
  • Red beets are well-known for their high nitrate content, but leafy greens contain even more nitrates per serving; arugula contains the highest amounts, followed by rhubarb


By Dr. Mercola
Your diet is an important, if not crucial, factor for the maintenance of a healthy heart well into old age. Healthy dietary fats top the list of heart-healthy foods, of course, but aside from that, a nitrate-rich diet can go a long way toward protecting your heart.
Nitrates should not be confused with nitrites, found in bacon, hot dogs, ham and other less-than-healthy cured meats. Nitrites can convert into potentially dangerous nitrosamines, especially if heated, which is why processed meats are best avoided. In fact, after examining over 7,000 clinical studies, the World Cancer Research Fund concluded there’s no safe lower limit for processed meats.1 They should be avoided altogether.
On the other hand, many vegetables contain naturally occurring nitrates. When consumed, the bacteria in your mouth convert these nitrates to nitrites, but since vegetables are also rich in antioxidants, these nitrites do not pose a health hazard. More importantly, your body transforms the nitrates in vegetables into nitric oxide (NO),2 a soluble gas continually produced from the amino acid L-arginine inside your cells.
Nitrate-Rich Foods Boost Nitric Oxide Production
NO is a gas and free radical that is an important biological signaling molecule that supports normal endothelial function and protects the little powerhouses inside your cells, your mitochondria. Acting as a potent vasodilator, NO also helps relax and widen the diameter of your blood vessels, allowing a greater volume of blood to flow through.
Healthy blood flow helps your body function at its best, as your blood carries oxygen and nutrients to your heart, brain and other organs. It nourishes and oxygenizes your immune system and muscles, and helps keep your heart beating. It also carries away waste material and carbon dioxide.
As noted in research3 presented by Dr. Michael Greger above, a diet high in nitrate is a natural strategy recommended for the treatment of prehypertension and hypertension (high blood pressure), “and to protect individuals at risk of adverse vascular events,” i.e., heart attacks. Indeed, raw beets — which are high in nitrates — have been shown to lower blood pressure by an average of four to five points within a matter of hours.4
Some studies have shown a glass of beet juice can lower systolic blood pressure by more than eight points5 — far more than most blood pressure medications. In conventional medicine, nitrates are used to treat angina and congestive heart failure, and research shows a glass of beetroot juice has the same effect as prescription nitrates.6
NO Promotes Healthy Heart and Brain Function
In one recent study,7,8,9,10 patients diagnosed with high blood pressure who drank beet juice an hour before exercise, three times a week for six weeks, experienced increased tissue oxygenation and blood flow. It also improved brain neuroplasticity by improving oxygenation of the somatomotor cortex (a brain area that is often affected in the early stages of dementia).
As noted by study co-author W. Jack Rejeski, a health and exercise science professor at Wake Forest University in North Carolina, NO is a vital biomolecule that “goes to the areas of the body which are hypoxic, or needing oxygen, and the brain is a heavy feeder of oxygen in your body.”11,12 Your heart, too, requires NO and oxygen for optimal function. As noted by cardiologist Dr. Stephen Sinatra:13
“Adequate NO production is the first step in a chain reaction that promotes healthy cardiovascular function, while insufficient NO triggers a cascade of destruction that eventually results in heart disease… NO promotes healthy dilation of the veins and arteries so blood can move throughout your body. Plus, it prevents red blood cells from sticking together to create dangerous clots and blockages.”
Which Foods Contain the Most Nitrates?
As noted by Greger in the featured video, leafy greens top the list of nitrate-rich foods. Beets, which are a root vegetable, are well-known for their high nitrate content, but leafy greens contain even more nitrates per serving. In fact, beets barely made it onto the top 10 list, which is as follows:
1. Arugula, 480 mg of nitrates per 100 grams
2. Rhubarb, 281 mg
3. Cilantro, 247 mg
4. Butter leaf lettuce, 200 mg
5. Spring greens like mesclun mix, 188 mg
6. Basil, 183 mg
7. Beet greens, 177 mg
8. Oak leaf lettuce, 155 mg
9. Swiss chard, 151 mg
10. Red beets, 110 mg
Arugula, in the No. 1 spot, contains more nitrates than any other vegetable, and by a wide margin too —  480 mg per 100 grams. The second-highest source, rhubarb, contains about 280 mg per 100 grams, which is about the same amount found in a 100-gram serving of beet root juice, whereas 100 grams of whole red beets provide a mere 110 mg of nitrates.
Other foods high in nitrates include the following.14,15,16 (While garlic is low in nitrates, it helps boost NO production by increasing NOS, which converts L-arginine to NO in the presence of cofactors such as vitamins B-2 and B-3.17)
Source
Mg of nitrates per 100 grams
Bok choy
70 to 95 mg
Carrots
92 to 195 mg
Mustard greens
70 to 95 mg
Spinach
24 to 387 mg
Chinese cabbage
43 to 161 mg
Winter melon
16 to 136 mg
Eggplant
25 to 42 mg
Parsley
100 to 250 mg
Leeks
100 to 250 mg
Turnips
50 to 100 mg
Cauliflower
20 to 50 mg
Broccoli
20 to 50 mg
Artichoke
Less than 20 mg
Garlic
Less than 20 mg
Onion
Less than 20 mg
Nitrate-Rich Foods Protect Against Heart Disease
Previous research has shown that the more vegetables and fresh fruits you eat, the lower your risk of heart disease, with leafy greens being the most protective. As noted by Greger, the reason for this is likely their NO-boosting nitrates. This was confirmed in a May 2017 study published in The American Journal of Clinical Nutrition.18
In this study, nearly 1,230 Australian seniors without atherosclerotic vascular disease (ASVD) or diabetes were followed for 15 years. A food-frequency questionnaire was used to evaluate food intake, while nitrate intake was calculated using a comprehensive food database. As expected, the higher an individual’s vegetable nitrate intake, the lower their risk for both ASVD and all-cause mortality. According to the authors:
“Nitrate intake from vegetables was inversely associated with ASVD mortality independent of lifestyle and cardiovascular disease risk factors in this population of older adult women without prevalent ASVD or diabetes. These results support the concept that nitrate-rich vegetables may reduce the risk of age-related ASVD mortality.”
Leafy Greens and Sports Performance
Most competitive athletes understand the value of NO, and the wise ones take advantage of Mother Nature’s bounty. While research19,20 has shown nitrate supplements can boost sports performance and enhance fast-twitch muscle fibers, you can get the same results using whole foods. For example, research shows raw beets can increase exercise stamina by as much as 16 percent,21 an effect attributed to increased NO.
In another study,22 nine patients diagnosed with heart failure who experienced loss of muscle strength and reduced ability to exercise were found to benefit from beet juice. The patients were given 140 milliliters (mL) — about two-thirds of a cup — of concentrated beet juice, followed by testing, which found an almost instantaneous increase in their muscle capacity by an average of 13 percent.
There’s one important caveat though: Avoid using mouthwashes or chewing gum, as this actually prevents the NO conversion from occurring.23 The reason for this is because the nitrate is converted into nitrite in your saliva by friendly bacteria. That nitrite is then converted into NO in other places in your body.
More Information About NO
NO24 — not to be confused with nitrous oxide, commonly known as laughing gas, a chemical compound with the formula N2O25 — serves as a signaling or messenger molecule in every cell of your body. Hence, it’s involved in a wide variety of physiological and pathological processes. As mentioned, it causes arteries and bronchioles to expand, but it’s also needed for communication between brain cells, and causes immune cells to kill bacteria and cancer cells.
Now, your body loses about 10 percent of its ability to make NO for every decade of life, which is why eating a nitrate-rich diet is so important. NO is further synthesized by nitric oxide synthase (NOS). There are three isoforms of the NOS enzyme:
  • Endothelial (eNOS): a calcium-dependent signaling molecule that produces low levels of gas as a cell signaling molecule
  • Neuronal (nNOS): a calcium-dependent signaling molecule that produces low levels of gas as a cell signaling molecule
  • Inducible (immune system) (iNOS): calcium independent; produces large amounts of gas, which can be cytotoxic
Problematically, when fluoride is present (such as when you’re drinking fluoridated water), the fluoride converts NO into the toxic and destructive nitric acid. As noted in “Pharmacology for Anesthetists 3,”26 “[NO] will react with fluorine, chlorine and bromine to form the XNO species, known as the nitrosyl halides, such as nitrosyl chloride.” Hence, avoiding fluoridated water and other halide sources, such as brominated flour, is important to optimize your health and avoid damaging interactions.
Exercise Also Boosts NO Production










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Aside from eating a nitrate-rich diet, one efficient way to increase NO production is a series of callisthenic exercises. I’m using a modified version of a routine originally developed by Dr. Zach Bush. You’ll find a quick demonstration of my “Nitric Oxide Dump” routine in the video above. This routine takes about three to four minutes and is ideally done three times a day, at least two hours apart.