Saturday, March 31, 2018
Friday, March 30, 2018
Probiotics detoxify Your Body
7 Ways Probiotics DETOXIFY Your Body
Posted on: Friday, March 30th 2018 at 6:00 am
Written By: Sayer Ji, Founder
This article is copyrighted by GreenMedInfo LLC, 2018
Did you know that probiotic bacteria are capable of helping you detoxify the most noxious chemicals known to humankind?
You've probably heard the buzz already about the many health benefits of probiotics, a word which literally translates to: pro- "for" + biotics "life" -- FOR LIFE. But did you know that these remarkable commensal microorganisms, which outnumber our bodily cells by some estimates up to 10 to 1, and contribute over 99% of our body's total genetic information, also break down highly toxic manmade chemicals which your body is either incapable, or only partially capable, of defending itself from?
Learn about some of the amazing ways in which 'good bacteria' help to detoxify chemicals within our body:
- Bisphenol A: This ubiquitous toxicant -- linked to over 40 diseases -- found in anything from thermal printer receipts, paper money, canned food liners, dental composites, and of course plastics, is a powerful endocrine disrupter now found in everyone's bodies. Remarkably, two common probiotic strains, Bifidobacterium breve and Lactobacillus casei, have been found in animal research to help the body detoxify it by reducing the intestinal absorption of bisphenol A through facilitating increased excretion.[i] The animals receiving probiotic treatment were found to have 2.4 times higher excretion of Bisphenol A in their feces, suggesting probiotic supplementation could be of significant benefit to humans as well.
- Pesticides: Probiotic strains from the traditional Korean fermented cabbage dish known as kimchi have been identified to degrade a variety of organophosphorous pesticides such as chlorpyrifos, coumaphos, diazinon, methylparathion, and parathion.[ii] These nifty organisms actually use these exceedingly hard to break down chemicals as sources of carbon and phosphorous – 'food'! – and were found to break down the pesticide 83.3% after 3 days and degraded it completely by day 9.[iii] While this test tube study likely does not reflect exactly what happens in our gut when we ingest both chlorpyrifos and Kimchi, it is provocative, and may indicate there is some protective effects in the gut, and certainly cabbage tainted with organophosphorous pesticide which is subsequently fermented as an ingredient in Kimchi would certainly reduce the burden of this chemical in the diet.
- Heavy Metals: Lactobacillus bacteria found in food have been looked at as a potential adjunct agent for reducing metal toxicity in humans. According to one study, "This is because they have resistance mechanisms which are effective in preventing damage to their cells and they can bind and sequester heavy metals to their cell surfaces, thus removing them through subsequent defecation." [iv] The study differentiates between detoxification and detoxication, the former of which is described as "the ability to remove drugs, mutagens, and other harmful agents from the body," and the latter of which is the mechanism through which 'good bacteria' prevent "of damaging compounds into the body." Because there is a large body of research on probiotics preventing and/or healing up intestinal permeability, this may be another way in which toxic stomach contents are preventing from doing harm to the body as a whole.
- Cancerous Food Preservatives: Another imchi study found it contained a strain of bacteria capable of breaking down sodium nitrate, a naturally and artificially occurring chemical (used from anything to rocket fuel and gunpowder) linked to a variety of chronic degenerative diseases, including cancer.[v] The study found a depletion of sodium nitrate by up to 90.0% after 5 days. Sodium nitrate becomes toxic when it is converted in food products, and even our intestines via microbiota, to N-nitrosodimethylamine. A recent study found that four lactobacillus strains where capable of breaking this toxic byproduct down by up to 50%.[vi]
- Perchlorate – perchlorate is an ingredient in jet fuel and fireworks that widely contaminates the environment and our food. Sadly, even organic food has been found concentrate high levels of this toxicant, making it exceedingly difficult to avoid exposure. It is now found in disturbing concentrations in breast milk and urine, and is a well-known endocrine disrupter capable of blocking the iodine receptor in the thyroid, resulting in hypothyroidism and concomitant neurological dysfunction. A recent study found that the beneficial bacterial strain known as Bifidobacterium Bifidum is capable of degrading perchlorate, and that breast fed infants appear to have lower levels than infant formula fed babies due to the breast milk bacteria's ability to degrade perchlorate through the perchlorate reductase pathway.[vii]
- Heterocylic Amines: Heterocyclic aromatic amines (HCA) are compounds formed when meat is cooked at high temperatures of 150-300 degrees C, and are extremely mutagenic (damage the DNA). Lactobacillus strains have been identified that significantly reduce the genotoxicity of theses compounds.[viii]
- Toxic Foods: While not normally considered a 'toxin,' wheat contains a series of proteins that we do not have the genomic capability to produce enzymes to degrade. When these undigested proteins – and there are over 23,000 that have been identified in the wheat proteome – enter into the blood, they can wreak havoc on our health. Recent research has found that our body has dozens of strains of bacteria that are capable of breaking down glutinous proteins and therefore reduce its antigenicity and toxicity.
While the role of probiotics in degrading gluten proteins sounds great, a word of caution is in order. Since modern wheat is not a biologically compatible food for our species – having been introduced only recently in biological time, and having been hybridized to contain far more protein that our ancient ancestors were ever exposed to – it would be best to remove it entirely from the diet. Also, the aforementioned research showing bacteria in the human gut are capable of breaking some of these wheat proteins revealed that some of the species that were capable of doing this for us are intrinsically pathogenic, e.g. Clostidium botulinum and Klebsiella. So, relying on the help of bacteria to do the job of digesting a 'food' we are not capable of utilizing on our own, is a double-edged sword. Again, the best move is to remove it entirely from the diet as a precuationary step.
What Probiotic Should I Take?
While plenty of probiotic pills and liquids exist on the market, and many of which have significant health benefits, it is important to choose one that is either shelf stable, or has been refrigerated from the place of manufacture all the way to the place you are purchasing it from. Moreover, many probiotics are centrifugally extracted or filtered, leaving the nourishing food medium within which it was cultured behind. This is a problem in two ways: 1) without sustenance, the probiotics are in 'suspended animation' and may either die or not properly 'root' into your gastrointestinal tract when you take them. 2) the 'food matrix' within probiotics are grown provides a protective medium of essential co-factors that help them survive the difficult journey down your gastointestinal tract.
With that said, another option is to consume a traditionally fermented, living probiotic food like sauerkraut, kimchi, or yogurt (focusing on non-cow's milk varieties, unless you are lucky enough to find a source that has the beta-casein A2 producing cows). There is always goat's milk which is relatively hypoallergenic.
Finally, the reality is that the probiotics in our bodies and in cultured foods ultimately derive from the soil, where an unimaginably vast reservoir of 'good bacteria' reside – assuming your soil is natural and not saturated with petrochemical inputs and other environmental toxicants. And really fresh, organically produced – preferably biodynamically grown – raw food is an excellent way to continually replenish your probiotic stores. Food is always going to be the best way to support your health, probiotic health included.
References
[i] Kenji Oishi, Tadashi Sato, Wakae Yokoi, Yasuto Yoshida, Masahiko Ito, Haruji Sawada. Effect of probiotics, Bifidobacterium breve and Lactobacillus casei, on bisphenol A exposure in rats. Biosci Biotechnol Biochem. 2008 Jun;72(6):1409-15. Epub 2008 Jun 7. PMID: 18540113
[ii] Shah Md Asraful Islam, Renukaradhya K Math, Kye Man Cho, Woo Jin Lim, Su Young Hong, Jong Min Kim, Myoung Geun Yun, Ji Joong Cho, Han Dae Yun. Organophosphorus hydrolase (OpdB) of Lactobacillus brevis WCP902 from kimchi is able to degrade organophosphorus pesticides. J Agric Food Chem. 2010 May 12;58(9):5380-6. PMID: 20405842
[iii] Kye Man Cho, Reukaradhya K Math, Shah Md Asraful Islam, Woo Jin Lim, Su Young Hong, Jong Min Kim, Myoung Geun Yun, Ji Joong Cho, Han Dae Yun. Biodegradation of chlorpyrifos by lactic acid bacteria during kimchi fermentation. J Agric Food Chem. 2009 Mar 11;57(5):1882-9. PMID: 19199784
[iv] Marc Monachese, Jeremy P Burton, Gregor Reid. Bioremediation and tolerance of humans to heavy metals through microbial processes: a potential role for probiotics? Appl Environ Microbiol. 2012 Sep ;78(18):6397-404. Epub 2012 Jul 13. PMID: 22798364
[v] Chang-Kyung Oh, Myung-Chul Oh, Soo-Hyun Kim. The depletion of sodium nitrite by lactic acid bacteria isolated from kimchi. J Med Food. 2004;7(1):38-44. PMID: 15117551
[vi] Adriana Nowak, Sławomir Kuberski, Zdzisława Libudzisz. Probiotic lactic acid bacteria detoxify N-nitrosodimethylamine. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2014 Jul 10. Epub 2014 Jul 10. PMID: 25010287
[vii] C Phillip Shelor, Andrea B Kirk, Purnendu K Dasgupta, Martina Kroll, Catrina A Campbell, Pankaj K Choudhary. Breastfed infants metabolize perchlorate. Environ Sci Technol. 2012 May 1 ;46(9):5151-9. Epub 2012 Apr 20. PMID: 22497505
[viii] Adriana Nowak, Zdzislawa Libudzisz. Ability of probiotic Lactobacillus casei DN 114001 to bind or/and metabolise heterocyclic aromatic amines in vitro. Eur J Nutr. 2009 Oct ;48(7):419-27. Epub 2009 May 16. PMID: 19448966
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.
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Thursday, March 29, 2018
Wednesday, March 28, 2018
5 types of Diabetes
Breaking down diabetes: Researchers have identified FIVE types of diabetes that should each be treated differently
Wednesday, March 28, 2018 by: Frances Bloomfield
Tags: diabetes, diabetes research, diabetes subtypes, medical science, Mild age-related diabetes, Mild obesity-related diabetes, Misdiagnosis, Severe autoimmune diabetes, Severe insulin-deficient diabetes, Severe insulin-resistant diabetes, type 1 diabetes, Type 2 Diabetes
Tags: diabetes, diabetes research, diabetes subtypes, medical science, Mild age-related diabetes, Mild obesity-related diabetes, Misdiagnosis, Severe autoimmune diabetes, Severe insulin-deficient diabetes, Severe insulin-resistant diabetes, type 1 diabetes, Type 2 Diabetes
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(Natural News) For the longest time, diabetes has been divided into two classifications: Type 1 diabetes and Type 2 diabetes. Yet, as a new study has demonstrated, it may not be as simple as that. The study, which was published in The Lancet Diabetes & Endocrinology, suggests that diabetes comprised five clusters, with Type 2 diabetes comprising four different subtypes.
Beginning 2008, the researchers behind the study kept track of 13,720 patients in southern Sweden. All of the patients, whose ages ranged from 18 to 97, had been newly diagnosed with diabetes. They were able to come up with six variables based on their health data analyses: Age, body mass index (BMI), beta-cell antibodies, metabolic control levels, beta-cell function, and insulin resistance.
From here, the researchers identified five clusters of diabetes:
- Severe autoimmune diabetes (SAID): Type 1 diabetes and latent autoimmune diabetes in adults (LADA) fall under this category. The characteristics of this cluster include the onset of diabetes at a young age, reduced insulin production, low metabolic control, and the appearance of glutamic acid decarboxylase autoantibodies (GADA).
- Severe insulin-deficient diabetes (SIDD): People in this group are distinguished by their elevated glycated haemoglobin (HbA1C), moderate insulin resistance, poor insulin secretion, and the highest occurrence of retinopathy out of the other clusters.
- Severe insulin-resistant diabetes (SIRD): Obesity and severe insulin resistance are the defining characteristics of this subtype. Those considered part of this group were notable for having the greatest incidence of kidney damage.
- Mild obesity-related diabetes (MOD): This subtype is comprised mostly of obese patients diagnosed with diabetes during their early years.
- Mild age-related diabetes (MARD): Nearly 40 percent of the patients were grouped into this category, making the largest of the five subtypes. According to the researchers, almost all of the patients with MARD were of older age.
They repeated their analyses three more times. One of the following studies, which was carried out using Finnish patients, yielded slightly different results but were still noted as positive. “The outcome exceeded our expectations and highly corresponded with the analysis from [All New Diabetics In Scania]. The only difference was that Group 5 was larger in Finland than in Skåne. The disease progression was remarkably similar in both groups,” said Leif Groop, study author and principal investigator at Diabetes and Endocrinology at Lund University.
Though the study has so far been limited in scope (having focused exclusively on Scandinavians), Groop and his colleagues have stated that they intend to broaden future studies to include other ethnic groups. As is, their findings hold immense potential for the tens of millions of people struggling with diabetes.
“The longer the study is running, the more and better data we’ll get,” said study co-author and Lund University assistant researcher Emma Ahlqvist. “This will give us even better opportunities to tailor the treatment to each individual.”
The biggest problem that comes with treating diabetes is that, many times, a doctor may give an incorrect diagnosis. This could then lead to a patient being forced to undergo treatments that may not have been needed in the first place. Diabetic patients falling under SIRD have the most to gain from the new subtypes since, as per Groop, they’re the ones who tend to be the “most incorrectly treated.” (Related: Are Your Prescriptions Killing You? 5 Juices Recipe That Reverse Type 2 Diabetes.)
However, if and when these new subtypes become the norm, the chances of misdiagnosis may be slim to none.
Visit DiabtesScienceNews.com to remain updated on any future developments about this story.
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Tetanus Shot: How Do We Know It Works?
Tetanus Shot: How Do We Know That It Works?
Posted on: Thursday, October 16th 2014 at 4:00 pm
Written By: Tetyana Obukhanych, PhD
This article is copyrighted by GreenMedInfo LLC, 2018
Do we know how tetanus shots work? The medical establishment holds a view that a tetanus shot prevents tetanus, but how do we know this view is correct?
The cure for tetanus, a life-threatening and often deadly disease, has been sought from the very inception of the modern field of Immunology. The original horse anti-serum treatment of tetanus was developed in the late 19th century and introduced into clinical practice at the time when a bio-statistical concept of a randomized placebo-controlled trial (RCT) did not yet exist. The therapy was infamous for generating a serious adverse reaction called "serum sickness" attributed to the intolerance of humans to horse-derived serum. To make this tetanus therapy usable, it was imperative to substitute the animal origin of anti-serum with the human origin. But injecting a lethal toxin into human volunteers as substitutes for horses would have been unthinkable.
A practical solution was found in 1924: pre-treating the tetanus toxin with formaldehyde (a fixative chemical) made the toxin lose its ability to cause clinical tetanus symptoms. The formaldehyde-treated tetanus toxin is called the toxoid. The tetanus toxoid can be injected into human volunteers to produce a commercial human therapeutic product from their sera called tetanus immunoglobulin (TIG), a modern substitute of the original horse anti-serum. The tetanus toxoid has also become the vaccine against clinical tetanus.
The tetanus toxin, called tetanospasmin, is produced by numerous C. tetani bacterial strains. C. tetani normally live in animal intestines, notably in horses, without causing tetanus to their intestinal carriers. These bacteria require anaerobic (no oxygen) conditions to be active, whereas in the presence of oxygen they turn into resilient but inactive spores, which do not produce the toxin. It has been recognized that inactive tetanus spores are ubiquitous in the soil. Tetanus can result from the exposure to C. tetani via poorly managed tetanus-prone wounds or cuts, but not from oral ingestion of tetanus spores. Quite to the contrary, oral exposure to C. tetani has been found to build resistance to tetanus without carrying the risk of disease, as described in the section on "Natural Resistance to Tetanus."
Once secreted by C. tetani germinating in a contaminated wound, tetanospasmin diffuses through the tissue's interstitial fluids or bloodstream. Upon reaching nerve endings, it is adsorbed by the cell membrane of neurons and transported through nerve trunks into the central nervous system, where it inhibits the release of a neurotransmitter gamma-aminobutyric acid (GABA). This inhibition can result in various degrees of clinical tetanus symptoms: rigid muscular spasms, such as lockjaw, sardonic smile, and severe convulsions that frequently lead to bone fractures and death due to respiratory compromise.
Curative effects of the anti-serum therapy as well as the preventative effects of the tetanus vaccination are deemed to rely upon an antibody molecule called antitoxin. But the assumption that such antitoxin was the sole "active" ingredient in the original horse anti-serum has not been borne out experimentally. Since horses are natural carriers of tetanus spores, their bloodstream could have contained other unrecognized components, which got harnessed in the therapeutic anti-serum. "Natural Resistance to Tetanus" discusses other serum entities detected in research animals carrying C. tetani, which better correlated with their protection from clinical tetanus than did serum antitoxin levels. Nevertheless, the main research effort in the tetanus field remained narrowly focused on antitoxin.
Antitoxin molecules are thought to inactivate the corresponding toxin molecules by virtue of their toxin-binding capacity. This implies that to accomplish its protective effect, antitoxin must come into close physical proximity with the toxin and combine with it in a way that would prevent or preempt the toxin from binding to nerve endings. Early research on the properties of a newly discovered antitoxin was done in small-sized research animals, such as guinea pigs. The tetanus toxin was pre-incubated in a test tube with the animal's serum containing antitoxin before being injected into another (antitoxin-free) animal, susceptible to tetanus. Such pre-incubation made the toxin lose its ability to cause tetanus in otherwise susceptible animals — i.e. the toxin was neutralized.
Nevertheless, researchers in the late 19th and early 20th centuries were baffled by a peculiar observation. Research animals, whose serum contained enough antitoxin to inactivate a certain amount of the toxin in a test tube, would succumb to tetanus when they were injected with the same amount of the toxin. Furthermore, it was noted that the mode of the toxin injection had a different effect on the ability of serum antitoxin to protect the animal. The presence of antitoxin in the serum of animals afforded some degree of protection against the toxin injected directly into the bloodstream (intravenously). However, when the toxin was injected into the skin it would be as lethal to animals containing substantial levels of serum antitoxin as to animals virtually free of serum antitoxin.[1]
The observed difference in serum antitoxin's protective "behavior" was attributed to the toxin's propensity to bind faster to nerve cells than to serum antitoxin. The pre-incubation of the toxin with antitoxin in a test tube, or the injection of the toxin directly into the bloodstream, where serum antitoxin is found, gives antitoxin a head start in combining with and neutralizing the toxin. However, a skin or muscle injection of the toxin does not give serum antitoxin such a head start.
Researchers in the 21st century have developed an advanced fluorescent labeling technique to track the uptake of the injected tetanus toxin into neurons. Using this technique, researchers examined the effect of serum antitoxin, which was induced by vaccinating mice with the tetanus toxoid vaccine ahead of time (the same one currently used in humans), on blocking the neuronal uptake and transport of the tetanus toxin fragment C (TTC) to the brain from the site of intramuscular injection. Vaccinated and non-vaccinated animals showed similar levels of TTC uptake into the brain. The authors of the study concluded that the "uptake of TTC by nerve terminals from an intramuscular depot is an avid and rapid process and is not blocked by vaccination."[2] They have further commented that their results appear to be surprising in view of protective effects of immunization with the tetanus toxoid. Indeed, the medical establishment holds a view that a tetanus shot prevents tetanus, but how do we know this view is correct?
Neonatal Tetanus
Neonatal tetanus is common in tropical under-developed countries but is extremely rare in developed countries. This form of tetanus results from unhygienic obstetric practices, when cutting the umbilical cord is performed with unsterilized devices, potentially contaminating it with tetanus spores. Adhering to proper obstetric practices removes the risk of neonatal tetanus, but this has not been the standard of birth practices for some indigenous and rural people in the past or even present.
The authors of a neonatal tetanus study performed in the 1960s in New Guinea describe the typical conditions of childbirth among the locals:
"The mother cuts the cord 1 inch (2.5 cm) or less from the abdominal wall; it is never tied. In the past she would always use a sliver of sago bark, but now she uses a steel trade-knife or an old razor blade. These are not cleaned or sterilized in any way and no dressing is put of the cord. The child lies after birth on a dirty piece of soft bark, and the cut cord can easily become contaminated by dust from the floor of the hut or my mother's feces expressed during childbirth, as well as by the knife and her finger."[3]
Not surprisingly, New Guinea had a high rate of neonatal tetanus. Because improving birth practices seemed to be unachievable in places like New Guinea, subjecting pregnant women to tetanus vaccination was contemplated by public health authorities as a possible solution to neonatal tetanus.
A randomized controlled trial (RCT) assessing the effectiveness of the tetanus vaccine in preventing neonatal tetanus via maternal vaccination was conducted in the 1960s in rural Colombia in a community with high rates of neonatal tetanus.[4] The design of this trial has been recently reviewed by the Cochrane Collaboration for potential biases and limitations and, with minor comments, has been considered of good quality for the purposes of vaccine effectiveness (but not safety) determination.[5] The trial established that a single dose of the tetanus vaccine given before or during pregnancy had a partial effect on preventing neonatal tetanus in the offspring: 43% reduction was observed in the tetanus vaccine group compared to the control group, which instead of the tetanus shot received a flu shot. A series of two or three tetanus booster shots, given six or more weeks apart before or during pregnancy, reduced neonatal tetanus by 98% in the tetanus vaccine group compared to the flu shot control group. The duration of the follow up in this trial was less than five years.
In addition to testing the effects of vaccination, this study has also documented a clear relationship between the incidence of neonatal tetanus and the manner in which childbirth was conducted. No babies delivered in a hospital, by a doctor or a nurse, contracted neonatal tetanus regardless of the mother's vaccination status. On the other hand, babies delivered at home by amateur midwives had the highest rate of neonatal tetanus.
Hygienic childbirth appears to be highly effective in preventing neonatal tetanus and makes tetanus vaccination regimen during pregnancy unnecessary for women who give birth under hygienic conditions. Furthermore, it was estimated in 1989 in Tanzania that 40% of neonatal tetanus cases still occurred in infants born to mothers who were vaccinated during pregnancy,[6] stressing the importance of hygienic birth practices regardless of maternal vaccination status.
Tetanus In Adults
Based on the protective effect of maternal vaccination in neonatal tetanus, demonstrated by an RCT and discussed above, we might be tempted to infer that the same vaccine also protects from tetanus acquired by stepping on rusty nails or incurring other tetanus-prone injuries, when administered to children or adults, either routinely or as an emergency measure. However, due to potential biologic differences in how tetanus is acquired by newborns versus by older children or adults, we should be cautious about reaching such conclusions without first having direct evidence for the vaccine effectiveness in preventing non-neonatal tetanus.
It is generally assumed that the tetanus toxin must first leach into the blood (where it would be intercepted by antitoxin, if it is already there due to timely vaccination) before it reaches nerve endings. This scenario is plausible in neonatal tetanus, as it appears that the umbilical cord does not have its own nerves.[7] On the other hand, the secretion of the toxin by C. tetani germinating in untended skin cuts or in muscle injuries is more relevant to how children or adults might succumb to tetanus. In such cases, there could be nerve endings near germinating C. tetani, and the toxin could potentially reach such nerve endings without first going through the blood to be intercepted by vaccine-induced serum antitoxin. This scenario is consistent with the outcomes of the early experiments in mice, discussed in the beginning.
Although a major disease in tropical under-developed countries, tetanus in the USA has been very rare. In the past, tetanus occurred primarily in poor segments of the population in southern states and in Mexican migrants in California. It was swiftly diminishing with each decade prior to the 1950s (in the pre-vaccination era), as inferred from tetanus mortality records and similar case-fatality ratios (about 67-70%) in the early 20th century[8] versus the mid-20th century).[9] The tetanus vaccine was introduced in the USA in 1947 without performing any placebo-controlled clinical trials in the segment of the population (children or adults), where it is now routinely used.
The rationale for introducing the tetanus vaccine into the U.S. population, at low overall risk for tetanus anyway, was simply based on its use in the U.S. military personnel during World War II. According to a post-war report:[10]
- the U.S. military personnel received a series of three injections of the tetanus toxoid, routine stimulating injection was administered one year after the initial series, and an emergency stimulating dose was given on the incurrence of wounds, severe burns, or other injuries that might result in tetanus;
- throughout the entire WWII period, 12 cases of tetanus have been documented in the U.S. Army;
- in World War I there were 70 cases of tetanus among approximately half a million admissions for wounds and injuries, an incidence of 13.4 per 100,000 wounds. In World War II there were almost three million admissions for wounds and injuries, with a tetanus case rate of 0.44 per 100,000 wounds.
The report leads us to conclude that vaccination has played a role in tetanus reduction in wounded U.S. soldiers during WWII compared to WWI, and that this reduction vouches for the tetanus vaccine effectiveness. However, there are other factors (e.g. differences in wound care protocols, including the use of antibiotics, higher likelihood of wound contamination with horse manure rich in already active C. tetani in earlier wars, when horses were used by the cavalry, etc.), which should preclude us from uncritically assigning tetanus reduction during WWII to the effects of vaccination.
Severe and even deadly tetanus is known to occur in recently vaccinated people with high levels of serum antitoxin.[11] Although the skeptic might say that no vaccine is effective 100% of the time, the situation with the tetanus vaccine is quite different. In these cases of vaccine-unpreventable tetanus, vaccination was actually very effective in inducing serum antitoxin, but serum antitoxin did not appear to have helped preventing tetanus in these unfortunate individuals.
The occurrence of tetanus despite the presence of antitoxin in the serum should have raised a red flag regarding the rationale of the tetanus vaccination program. But such reports were invariably interpreted as an indication that higher than previously thought levels of serum antitoxin must be maintained to protect from tetanus, hence the need for more frequent, if not incessant, boosters. Then how much higher "than previously thought" do serum levels of antitoxin need to be to ensure protection from tetanus?
Crone & Reder (1992) have documented a curious case of severe tetanus in a 29-year old man with no pre-existing conditions and no history of drug abuse, typical among modern-day tetanus victims in the USA. In addition to the regular series of tetanus immunization and boosters ten years earlier during his military service, this patient had been hyper-immunized (immunized with the tetanus toxoid to have extremely high serum antitoxin) as a volunteer for the purposes of the commercial TIG production. He was monitored for the levels of antitoxin in his serum and, as expected, developed extremely high levels of antitoxin after the hyper-immunization procedure. Nevertheless, he incurred severe tetanus 51 days after the procedure despite clearly documented presence of serum antitoxin prior to the disease. In fact, upon hospital admission for tetanus treatment his serum antitoxin levels measured about 2,500 times higher than the level deemed protective. His tetanus was severe and required more than five weeks of hospitalization with life-saving measures. This case demonstrated that serum antitoxin has failed to prevent severe tetanus even in the amounts 2,500 times higher than what is considered sufficient for tetanus prevention in adults.
The medical establishment chooses to turn a blind eye to the lack of solid scientific evidence to substantiate our faith in the tetanus shot. It also chooses to ignore the available experimental and clinical evidence that contradicts the assumed but unproven ability of vaccine-induced serum antitoxin to reduce the risk of tetanus in anyone other than maternally-vaccinated neonates, who do not even need this vaccination measure when their umbilical cords are dealt with using sterile techniques.
Ascorbic Acid In Tetanus Treatment
Anti-serum is not the only therapeutic measure tried in tetanus treatment. Ascorbic acid (Vitamin C) has also been tried. Early research on ascorbic acid has demonstrated that it too could neutralize the tetanus toxin.[12]
In a clinical study of tetanus treatment conducted in Bangladesh in 1984, the administration of conventional procedures, including the anti-tetanus serum, to patients who contracted tetanus left 74% of them dead in the 1-12 age group and 68% dead in the 13-30 age group. In contrast, daily co-administration of one gram of ascorbic acid intravenously had cut down this high mortality to 0% in the 1-12 age group, and to 37% in the 13-30 age group.[13] The older patients were treated with the same amount of ascorbic acid without adjustments for their body weight.
Although this was a controlled clinical trial, it is not clear from the description of the trial in the publication by Jahan et al. whether or not the assignment of patients into the ascorbic acid treatment group versus the placebo-control group was randomized and blinded, which are crucial bio-statistical requirements for avoiding various biases. A more definitive study is deemed necessary before intravenous ascorbic acid can be recommended as the standard of care in tetanus treatment.[14] It is odd that no properly documented RCT on ascorbic acid in tetanus treatment has been attempted since 1984 for the benefit of developing countries, where tetanus has been one of the major deadly diseases. This is in stark contrast to the millions of philanthropic dollars being poured into sponsoring the tetanus vaccine implementation in the Third world.
Natural Resistance To Tetanus
In the early 20th century, investigators Drs. Carl Tenbroeck and Johannes Bauer pursued a line of laboratory research, which was much closer to addressing natural resistance to tetanus than the typical laboratory research on antitoxin in their days. Omitted from immunologic textbooks and the history of immunologic research, their tetanus protection experiments in guinea pigs, together with relevant serological and bacteriological data in humans, nevertheless provide a good explanation for tetanus being a rather rare disease in many countries around the world, except under the conditions of past wars.
In the experience of these tetanus researchers, the injection of dormant tetanus spores could never by itself induce tetanus in research animals. To induce tetanus experimentally by means of tetanus spores (as opposed to by injecting a ready-made toxin, which never happens under natural circumstances anyway), spores had to be premixed with irritating substances that could prevent rapid healing of the site of spore injection, thereby creating conditions conducive to spore germination. In the past, researchers used wood splinters, saponin, calcium chloride, or aleuronat (flour made with aleurone) to accomplish this task.
In 1926, already being aware that oral exposure to tetanus spores does not lead to clinical tetanus, Drs. Tenbroeck and Bauer set out to determine whether feeding research animals with tetanus spores could provide protection from tetanus induced by an appropriate laboratory method of spore injection. In their experiment, several groups of guinea pigs were given food containing distinct strains of C. tetani. A separate group of animals were used as controls—their diet was free of any C. tetani. After six months, all groups were injected under the skin with spores premixed with aleuronat. The groups that were previously exposed to spores orally did not develop any symptoms of tetanus upon such tetanus-prone spore injection, whereas the control group did. The observed protection was strain-specific, as animals still got tetanus if injected with spores from a mismatched strain—a strain they were not fed with. But when fed multiple strains, they developed protection from all of them.
Quite striking, the protection from tetanus established via spore feeding did not have anything to do with the levels of antitoxin in the serum of these animals. Instead, the protection correlated with the presence of another type of antibody called agglutinin—so named due to its ability to agglutinate (clump together) C. tetani spores in a test tube. Just like the observed protection was strain-specific, agglutinins were also strain-specific. These data are consistent with the role of strain-specific agglutinins, not of antitoxin, in natural protection from tetanus. The mechanism thereby strain-specific agglutinins have caused, or correlated with, tetanus protection in these animals has remained unexplored.
In the spore-feeding experiment, it was still possible to induce tetanus by overwhelming this natural protection in research animals. But to accomplish this task, a rather brute force procedure was required. A large number of purified C. tetani spores were sealed in a glass capsule; the capsule was injected under the skin of research animals and then crushed. Broken glass pieces were purposefully left under the skin of the poor creatures so that the gory mess was prevented from healing for a long time. Researchers could succeed in overwhelming natural tetanus defenses with this excessively harsh method, perhaps mimicking a scenario of untended war-inflicted wounds.
How do these experimental data in research animals relate to humans? In the early 20th century, not only animals but also humans were found to be intestinal carriers of C. tetani without developing tetanus. About 33% of tested human subjects living around Beijing, China were found to be C. tetani carriers without any prior or current history of tetanus disease.[15] Bauer & Meyer (1926) cite other studies, which have reported around 25% of tested humans being healthy C. tetani carriers in other regions of China, 40% in Germany, 16% in England, and on average 25% in the USA, highest in central California and lowest on the southern coast. Based on the California study, age, gender, or occupation denoting the proximity to horses did not appear to play a role in the distribution of human C. tetani carriers.
Another study was performed back in the 1920s in San Francisco, CA.[16] About 80% of the examined subjects had various levels of agglutinins to as many as five C. tetani strains at a time, although no antitoxin could be detected in the serum of these subjects. C. tetani organisms could not be identified in the stool of these subjects either. It is likely that tetanus spores were in their gut transiently in the past, leaving serological evidence of oral exposure, without germinating into toxin-producing organisms. It would be important to know the extent of naturally acquired C. tetani spore agglutinins in humans in various parts of the world now, instead of relying on the old data, but similar studies are not likely to be performed anymore.
Regrettably, further research on naturally acquired agglutinins and on exactly how they are involved in the protection from clinical tetanus appears to have been abandoned in favor of more lucrative research on antitoxin and vaccines. If such research continued, it would have given us clear understanding of natural tetanus defenses we may already have by virtue of our oral exposure to ubiquitous inactive C. tetani spores.
Since the extent of our natural resistance to clinical tetanus is unknown due to the lack of modern studies, all we can be certain of is that preventing dormant tetanus spores from germinating into toxin-producing microorganisms is an extremely important measure in the management of potentially contaminated skin cuts and wounds. If this crucial stage of control—at the level of preventing spore germination—is missed and the toxin production ensues, the toxin must be neutralized before it manages to reach nerve endings.
Both antitoxin and ascorbic acid exhibit toxin-neutralizing properties in a test tube. In the body, however, vaccine-induced antitoxin is located in the blood, whereas the toxin might be focally produced in the skin or muscle injury. This creates an obvious physical impediment for toxin neutralization to happen effectively, if at all, by means of vaccine-induced serum antitoxin. Furthermore, no placebo-controlled trials have ever been performed to rule out the concern about such an impediment by providing clear empirical evidence for the effectiveness of tetanus shots in children and adults. Nevertheless, the medical establishment relies upon induction of serum antitoxin and withholds ascorbic acid in tetanus prevention and treatment.
When an old medical procedure of unknown effectiveness, such as the tetanus shot, has been the standard of medical care for a long time, finalizing its effectiveness via a modern rigorous placebo-controlled trial is deemed unethical in human research. Therefore, our only hope for the advancement of tetanus care is that further investigation of the ascorbic acid therapy is performed and that this therapy becomes available to tetanus patients around the world, if confirmed effective by rigorous bio-statistical standards.
Until then, may the blind faith in the tetanus shot help us!
About The Author
Tetyana Obukhanych earned her Ph.D. in Immunology at the Rockefeller University in New York, NY with her research dissertation focused on understanding immunologic memory, perceived by the mainstream biomedical establishment to be key to vaccination and immunity. She was subsequently involved in laboratory research as a postdoctoral research fellow within leading biomedical institutions, such as Harvard Medical School and Stanford University School of Medicine.
Having had several childhood diseases despite being properly vaccinated against them, Dr. Obukhanych has undertaken a thorough investigation of scientific findings regarding vaccination and immunity. Based on her analysis, Dr. Obukhanych has articulated a view that challenges mainstream assumptions and theories on vaccination in her e-book Vaccine Illusion.
Dr. Obukhanych continues her independent in-depth analysis of peer-reviewed scientific findings related to vaccination and natural requirements of the immune system function. Her goal is to bring a scientifically-substantiated and dogma-free perspective on vaccination and natural immunity to parents and health care practitioners. Visit www.naturalimmunityfundamentals.com for more information.
[1] Tenbroeck, C. & Bauer, J.H. The immunity produced by the growth of tetanus bacilli in the digestive tract. J Exp Med 43, 361-377 (1926).
[2] Fishman, P.S., Matthews, C.C., Parks, D.A., Box, M. & Fairweather, N.F. Immunization does not interfere with uptake and transport by motor neurons of the binding fragment of tetanus toxin. J Neurosci Res 83, 1540-1543 (2006).
[3] Schofield, F.D., Tucker, V.M. & Westbrook, G.R. Neonatal tetanus in New Guinea. Effect of active immunization in pregnancy. Br Med J 2, 785-789 (1961).
[4] Newell, K.W., Dueñas Lehmann, A., LeBlanc, D.R. & Garces Osorio, N. The use of toxoid for the prevention of tetanus neonatorum. Final report of a double-blind controlled field trial. Bull World Health Organ 35, 863-871 (1966).
[5] Demicheli, V., Barale, A. & Rivetti, A. Vaccines for women to prevent neonatal tetanus. Cochrane Database Syst Rev 5:CD002959 (2013).
[6] Maselle, S.Y., Matre, R., Mbise, R. & Hofstad, T. Neonatal tetanus despite protective serum antitoxin concentration. FEMS Microbiol Immunol 3, 171-175 (1991).
[7] Fox, S.B. & Khong, T.Y. Lack of innervation of human umbilical cord. An immunohistological and histochemical study. Placenta 11, 59-62 (1990).
[8] Bauer, J.H. & Meyer, K.F. Human intestinal carriers of tetanus spores in California. J Infect Dis 38, 295-305 (1926).
[9] LaForce, F.M., Young, L.S. & Bennett, J.V. Tetanus in the United States (1965-1966): epidemiologic and clinical features. N Engl J Med 280, 569-574 (1969).
[10] Editorial: Tetanus in the United States Army in World War II. N Engl J Med 237, 411-413 (1947).
[11] Abrahamian, F.M., Pollack, C.V., Jr., LoVecchio, F., Nanda, R. & Carlson, R.W. Fatal tetanus in a drug abuser with "protective" antitetanus antibodies. J Emerg Med 18, 189-193 (2000).
Beltran, A. et al. A case of clinical tetanus in a patient with protective antitetanus antibody level. South Med J 100, 83 (2007).
Berger, S.A., Cherubin, C.E., Nelson, S. & Levine, L. Tetanus despite preexisting antitetanus antibody. JAMA 240, 769-770 (1978).
Crone, N.E. & Reder, A.T. Severe tetanus in immunized patients with high anti-tetanus titers. Neurology 42, 761-764 (1992).
Passen, E.L. & Andersen, B.R. Clinical tetanus despite a protective level of toxin-neutralizing antibody. JAMA 255, 1171-1173 (1986).
Pryor, T., Onarecker, C. & Coniglione, T. Elevated antitoxin titers in a man with generalized tetanus. J Fam Pract 44, 299-303 (1997).
[12] Jungeblut, C.W. Inactivation of tetanus toxin by crystalline vitamin C (L-ascorbic acid). J Immunol 33, 203-214 (1937).
[13] Jahan, K., Ahmad, K. & Ali, M.A. Effect of ascorbic acid in the treatment of tetanus. Bangladesh Med Res Counc Bull 10, 24-28 (1984).
[14] Hemilä, H. & Koivula, T. Vitamin C for preventing and treating tetanus. Cochrane Database Syst Rev 2:CD006665 (2008).
[15] Tenbroeck, C. & Bauer, J.H. The tetanus bacillus as an intestinal saprophyte in man. J Exp Med 36, 261-271 (1922).
[16] Coleman, G.E. & Meyer, K.F. Study of tetanus agglutinins and antitoxin in human serums. J Infect Dis 39, 332-336 (1926).
Tetyana Obukhanych earned her Ph.D. in Immunology at the Rockefeller University in New York, NY with her research dissertation focused on understanding immunologic memory, perceived by the mainstream biomedical establishment to be crucial to vaccination and immunity. During her subsequent involvement in laboratory research as a postdoctoral fellow within leading biomedical institutions, such as Harvard Medical School and Stanford University School of Medicine, Dr. Obukhanych realized the flaws and limitations of current immunologic paradigms. Learn more about her work on her website.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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Tuesday, March 27, 2018
Beet Juice helps heart Failure patients
Beet juice helps heart failure patients improve quality of life
Posted by: Lori Alton, staff writer in Food News March 26, 2018 0 Comments
(Naturalhealth365) New research is highlighting a remarkable array of beet juice benefits – among them, the ability to enhance exercise capability and overall performance in people with heart failure issues.
Heart failure – characterized by the heart’s inability to pump enough oxygen-rich blood to meet the body’s needs – is one of the most common complications of heart disease. Currently affecting over 5.7 million Americans, heart failure can severely limit patients’ ability to be physical active – thereby leading to decreased mobility, reduced independence, and a dramatically lower quality of life.
But, an ordinary root vegetable may have the potential to help alleviate this cycle of ill health.
Beet juice to the rescue: Nitric oxide is the key to better cardiovascular health
Unsurprisingly, researchers have found that skeletal muscle strength, velocity and power can be dramatically reduced in patients with heart failure.
The reason: failing cardiac muscle produces increased amounts of reactive oxygen species, thereby decreasing the availability of a valuable substance, nitric oxide. This, in turn, affects the ability of the heart muscle to contract.
In fact, roughly 50 percent of all heart failure patients have a decreased “ejection fraction,” a measure of the heart’s ability to circulate nutrient-rich blood throughout the body. Labored breathing, ‘unexplained’ swelling in the hands or feet, fatigue, constipation, diminished peak oxygen uptake and exercise difficulty can all be signs of a lowered ejection fraction.
Of course, it almost goes without saying, these symptoms carry serious health implications and should not be ignored.
Among patients with heart failure, research has shown that decreases in peak oxygen uptake are indicative of a higher chance of premature death. But, a new study involving dietary nitrate from beets showed that beet extracts can impart some extraordinary benefits to heart failure patients.
Beetroot juice NEWS: What did the latest study reveal?
In a double-blind, placebo-controlled study conducted at Indiana University and published in Journal of Cardiac Failure, researchers wanted to find out if ingestion of dietary nitrate from beet juice could improve muscle function in patients with heart failure.
(Earlier studies had strongly supported the ability of beetroot juice to enhance the athletic performances of healthy runners and cyclists. This study, however, was the first to examine the effects of beet supplementation on patients with heart failure).
The patients – all of whom had ejection fractions of 45 percent or lower – were divided into two groups, with one group given beet juice containing 11.2 millimoles of nitrate and the other group given a placebo.
Two hours later, the participants’ muscle function was assessed, along with their nitric oxide levels.
The team found that the dietary nitrates caused a marked increase in nitric oxide levels, which was reflected in increases in breath nitric oxide ranging from 35 to 50 percent.
Beetroot juice, the researchers noted, “enhanced exercise capacity” and caused significant improvements in exercise duration, peak power and peak oxygen uptake. The nitrate group also experienced “considerable” improvements in peak knee extensor power and velocity (a sign of leg strength) – all without any adverse effects.
The researchers concluded that “supplementation with beetroot extracts could be a valuable addition to treatment for exercise intolerance among heart failure patients with reduced ejection fraction” – and called for further study to fully explore the implications.
How does beetroot promote the bioavailability of nitric oxide and help the heart?
Dietary nitrate – which is found in abundant quantities in beets and other vegetables – is reduced to nitrite when ingested, courtesy of anaerobic bacteria in the mouth. Next, acidic conditions in the stomach or other tissues further reduce the nitrite to desirable nitric oxide – which relaxes and dilates blood vessels, lowering blood pressure and improving muscle contractile function.
But aren’t nitrates “bad?”
The short answer is: no, not under these circumstances. Nitrates are only potentially harmful when exposed to high heat in the presence of amino acids. They can then form nitrosamines – many of which are potent carcinogens.
Although nitrates found in processed lunch meats have been linked to cancer, the dietary nitrates in beets pose no danger.
Beets are storehouses of disease-fighting antioxidants, vitamins and minerals
The brilliant ruby-red coloration of beets is an eye-catching tip-off that this root vegetable is loaded with carotenes and betalains, natural antioxidant pigments that fight oxidative damage and promote health.
Beets and beet juice are also high in vitamin C, vitamin E, and folate, along with the minerals potassium and manganese. Plus, in its liquid form, this is an easy-to-absorb source of great nutrition.
The healthy dietary fiber in beets gives them cancer-fighting effects, while also slowing the absorption of glucose. (Studies have even shown that beets can improve insulin sensitivity and lower blood sugar in diabetics).
Beets are also packed with glutathione, a powerful natural antioxidant and detoxifier that helps to boost the immune system and neutralize heavy metals and carcinogens.
When eating beets, it is best to enjoy them uncooked or juiced, as the heat from cooking can deplete some of their nutrients. For those looking to enhance their athletic performance, many natural health experts recommend 70 milliliters of beet juice, taken two hours before exercise or any competitive event.
Of course, whenever possible, opt for organic beets for maximum benefit.
Beet juice nutrients are also available in powdered and liquid extracts.
(Note: you may experience a pinkish or reddish urine after consuming beets. Not to worry – this startling effect is harmless).
Of course, before supplementing with beets, you should check first with your integrative healthcare provider – especially if you have heart disease, heart failure, kidney disease or any other medical condition.
In reality, throughout the ages, natural healers and herbalists have employed beets to treat digestive and cardiovascular conditions. Now, modern biochemical research is confirming the power of this ‘ancient remedy’ – and the ability of beets to improve exercise capacity and quality of life for those with heart failure.
Sources for this article include: