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Wellness

Clinic Wellness Team. A key factor to spine or back pain conditions is staying healthy. Overall wellness involves a balanced diet, appropriate exercise, physical activity, restful sleep, and a healthy lifestyle. The term has been applied in many ways. But overall, the definition is as follows.

It is a conscious, self-directed, and evolving process of achieving full potential. It is multidimensional, bringing together lifestyles both mental/spiritual and the environment in which one lives. It is positive and affirms that what we do is, in fact, correct.

It is an active process where people become aware and make choices towards a more successful lifestyle. This includes how a person contributes to their environment/community. They aim to build healthier living spaces and social networks. It helps in creating a person’s belief systems, values, and a positive world perspective.

Along with this comes the benefits of regular exercise, a healthy diet, personal self-care, and knowing when to seek medical attention. Dr. Jimenez’s message is to work towards being fit, being healthy, and staying aware of our collection of articles, blogs, and videos.


Remedies For Joint Pain And Adrenal Fatigue

Remedies For Joint Pain And Adrenal Fatigue

Fatigue & Pain Of Unknown Origin (PUKO)

If you have fatigue and mysterious pain in your joints, muscles, and ligaments that seems to come out of nowhere, you are not alone: many people throughout the world face such issues, which are often disabling. Thousands of people per year visit their doctor in hopes of isolating the cause of such pain; most of them have tried traditional and over-the-counter remedies for joint pain to no avail.

Joint pain can be caused by a variety of accidents or existing conditions: it can be the consequence of a fall, structural issues, twisted ligaments, pulled muscles, or an underlying inflammatory condition, among other possibilities. These obvious causes are easily diagnosed by conventional methods. However, pain can also appear spontaneously, with no apparent cause and clean medical workup, making the etiology uncertain. Such pain can be associated with Adrenal Fatigue.

Migratory Pain

For those who suffer from Adrenal Fatigue, some of this pain might be migratory. Migratory pain is a type of pain that moves throughout the body with no discernible pattern. One day you may feel pain in the right side of your body, but the next day you may feel it in the left side. All too often, this type of mobile pain of unknown origin comes with underlying symptoms of Adrenal Fatigue and does not usually respond to typical remedies for joint pain, baffling doctors and many other medical practitioners.

After telling your doctor about the pain you are experiencing, he or she will likely perform a variety of tests, perhaps including an x-ray scan. More often than not, the results may seem perfectly normal, and yet the pain persists. Your doctor may decide that you have fibromyalgia, however, your pain may actually be due to Adrenal Fatigue. In those with Adrenal Fatigue Syndrome (AFS), the body is in a state of tiredness caused by advanced and chronic stress. This stress strains the adrenal glands and�disrupts the NeuroEndoMetabolic (NEM) stress response, which is the body�s main mechanism of dealing with stress.

NEM & Remedies For Joint Pain

lethargy-remedies-for-joint-pain-22589-2

The NEM stress response is a complex system in which organs and bodily systems work together to protect the body from excessive stress. The system includes six types of stress responses: inflammatory, neuro-active, cardiac, hormonal, metabolic, and detoxifying. Together, these responses work to restore the body�s normal function during times of heavy stress. It is important that remedies for joint pain do not disrupt this complex system.

The�adrenal glands are the main control�center for stress responses outside the nervous system. Your body has two adrenal glands, which are about the size of a walnut, located directly above the kidneys. They control your body�s responses by secreting cortisol, a hormone that helps your body cope with stress. Properly functioning adrenal glands are a keystone to overall health and wellbeing. Due to today�s high-stress society, however, this natural defense can easily become disrupted, allowing toxins to accumulate and do great damage to the body. Excessive and chronic stress can overburden the adrenal glands, inhibiting hormone output and causing the body�s natural coping mechanisms to fail.

As stress and fatigue advance, new symptoms and ailments associated with Adrenal Fatigue will emerge. Early stage symptoms include low blood pressure, insomnia, and lethargy; advanced stage symptoms include anxiety, panic disorders, heart palpitations, low libido, hypersensitivities to medication, and food sensitivities. All of these symptoms can negatively affect your daily life. Eventually, as the NEM stress response fails, even the smallest bodily stresses can seem unbearable because your body�s natural coping mechanisms have been slowed and overloaded.

The Detoxification & Inflammation Circuits

The liver is�the body�s primary detoxification organ, aided by the extracellular matrix. A buildup of toxins and metabolites will therefore occur when the liver slows down to conserve energy. This is the body�s way of conserving the nutritional reserves it has left. As your body slows down, your liver becomes more sluggish and levels of toxins and metabolites increase, often leading to inflammation. These toxins accumulate and are not eliminated efficiently. This accumulation causes many other problems because the blood circulates these metabolites throughout the body constantly and rapidly, with a one-minute cycle.

Some of these metabolites can be quite toxic to the body. These metabolites may trigger inflammation, which in turn can trigger pain. Upon reaching the joints, these metabolites may become �stuck,� meaning they are slow to move through the joints and muscles. If your joints or muscles are already inflamed, the toxins and metabolites will further irritate the muscles, causing additional inflammation.

The Inflammation Circuit consists of the gut, microbiome, and immune system.�The gastrointestinal tract and microbiome�play an important role in breaking down and absorbing metabolites. If you are constantly eating unhealthy foods that your body can�t handle, you may trigger inflammatory responses. If you are constipated, and food is rotting in your intestines for long periods of time, then you are at higher risk of inflammation. This inflammation causes pain in random places because of the buildup of metabolites in the bloodstream. This also slows the immune system, because it has to deal with the extra toxins, compounding the inflammation.

If you experience migrating pain, this is an important clue that the cause of the pain may be metabolic, rather than structural (such as the strain of a ligament or muscle, which is usually more confined to a certain area). If you experience a dull to slightly severe pain of unknown origin that seems to migrate throughout the body and no one can seem to give you a direct answer as to the cause, you may be suffering from Adrenal Fatigue Syndrome. Consider metabolites, examine your stress levels, and investigate your diet, including supplements. In rare cases, some medications and supplements�even those often used as a remedies for joint pain�can trigger inflammation that is fundamentally caused by Adrenal Fatigue.�Pain medications may help temporarily, but they tend to hide the underlying condition, and can cause collateral damage. Remember, pain is a sign of an underlying problem. Suppressing or ignoring pain can cause long-term damage if the cause is not addressed.

Remedies For Joint Pain: Conclusion

physiotherapy-remedies-for-joint-pain-22589-3Joint pain of unknown origin can cause a myriad of debilitating problems, including the additional stress of trying to find effective remedies for joint pain. It can be a scary and confusing time, especially when test results show no abnormalities and your doctor can�t figure out what�s wrong. It�s important to find and address the cause of the inflammation. If you experience other concurring symptoms similar to those of Adrenal Fatigue, find a practitioner who can support your NEM stress response. Proper restorative strategies will help your body cope with both the stress and the pain.

By:�Dr. Michael Lam, MD, MPH;�Justin Lam, ABAAHP, FMNM

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� Copyright 2016 Michael Lam, M.D. All Rights Reserved.

The Health Risks Of Genetically Modified (GM) Foods

The Health Risks Of Genetically Modified (GM) Foods

GMOs: We all know stories of tobacco, asbestos, and DDT. Originally declared safe, they caused widespread death and disease. Although their impact was vast, most of the population was spared. The same cannot be said for sweeping changes in the food supply. Everyone eats; everyone is affected. The increase in several diseases in North America may be due to the profound changes in our diet. The most radical change occurred a little over a decade ago when genetically modified (GM) crops were introduced. Their influence on health has been largely ignored, but recent studies show serious problems. Genetically modified organisms (GMOs) have been linked to thousands of toxic or allergic-type reactions, thousands of sick, sterile, and dead livestock, and damage to virtually every organ and system studied in lab animals.1 Nearly every independent animal feeding safety study shows adverse or unexplained effects.

GM foods were made possible by a technology developed in the 1970s whereby genes from one species are forced into the DNA of other species. Genes produce proteins, which in turn can generate characteristics or traits. The promised traits associated with GMOs have been sky high�vegetables growing in the desert, vitamin fortified grains, and highly productive crops feeding the starving millions. None of these are available. In fact, the only two traits that are found in nearly all commericialized GM plants are herbicide tolerance and/or pesticide production.

Herbicide tolerant soy, corn, cotton, and canola plants are engineered with bacterial genes that allow them to survive otherwise deadly doses of herbicides. This gives farmers more flexibility in weeding and gives the GM seed company lots more profit. When farmers buy GM seeds, they sign a contract to buy only that seed producer�s brand of herbicide. Herbicide tolerant crops comprise about 80% of all GM plants. The other 20% are corn and cotton varieties that produce a pesticide in every cell. This is accomplished due to a gene from a soil bacterium called Bacillus thuringiensis or Bt, which produces a natural insect-killing poison called Bt- toxin. In addition to these two traits, there are also disease resistant GM Hawaiian papaya, zucchini and crook neck squash, which comprise well under 1% of GMO acreage.

GMOs: The FDA’s “Non-Regulation” Of GM Foods

GMOs Bell peppersRhetoric from the United States government since the early 1990s proclaims that GM foods are no different from their natural counterparts that have existed for centuries. The Food and Drug Administration (FDA) has labeled them �Generally Recognized as Safe,� or GRAS. This status allows a product to be commercialized without any additional testing. According to US law, to be considered GRAS the substance must be the subject of a substantial amount of peer-reviewed published studies (or equivalent) and there must be overwhelming consensus among the scientific community that the product is safe. GM foods had neither. Nonetheless, in a precedent-setting move in 1992 that some experts contend was illegal, the FDA declared that GM crops are GRAS as long as their producers say they are. Thus, the FDA does not require any safety evaluations or labeling of GMOs. A company can even introduce a GM food to the market without telling the agency.

Such a lenient approach was largely the result of the influence of large agricultural corporations According to Henry Miller, who had a leading role in biotechnology issues at the FDA from 1979 to 1994, �In this area, the US government agencies have done exactly what big agribusiness has asked them to do and told them to do.�2 The Ag biotech company with the greatest influence was clearly Monsanto. According to the New York Times, �What Monsanto wished for from Washington, Monsanto and, by extension, the biotechnology industry got. . . . When the company abruptly decided that it needed to throw off the regulations and speed its foods to market, the White House quickly ushered through an unusually generous policy of self-policing.�3

This policy was heralded by Vice President Dan Quayle on May 26, 1992. He chaired the Council on Competitiveness, which had identified GM crops as an industry that could boost US exports. To take advantage, Quayle announced �reforms� to �speed up and simplify the process of bringing� GM products to market without �being hampered by unnecessary regulation.�4 Three days later, the FDA policy on non-regulation was unveiled.

The person who oversaw its development was the FDA�s Deputy Commissioner for Policy, Michael Taylor, whose position had been created especially for him in 1991. Prior to that, Taylor was an outside attorney for both Monsanto and the Food Biotechnology Council. After working at the FDA, he became Monsanto�s vice president. The Obama administration has put Talyor back into the FDA as the US Food Safety Czar.

The FDA Covers Up Health Risks

GMOs FDA press conferenceTaylor�s GMO policy needed to create the impression that unintended effects from GM crops were not an issue. Otherwise their GRAS status would be undermined and they would need the extensive testing and labels that are normally required for food additives. But internal memos made public from a lawsuit showed that the overwhelming consensus among the agency scientists was that GM crops can have unpredictable, hard-to-detect side effects. Various departments and experts spelled these out in detail, listing allergies, toxins, nutritional effects, and new diseases as potential dangers. They urged superiors to require long-term safety studies.5 In spite of the warnings, according to public interest attorney Steven Druker who studied the FDA�s internal files, �References to the unintended negative effects of bioengineering were progressively deleted from drafts of the policy statement (over the protests of agency scientists).�6

FDA microbiologist Louis Pribyl, PhD, wrote about the policy, �What has happened to the scientific elements of this document? Without a sound scientific base to rest on, this becomes a broad, general, �What do I have to do to avoid trouble�-type document. . . . It will look like and probably be just a political document. . . . It reads very pro-industry, especially in the area of unintended effects.�7

The scientists� concerns were not only ignored, their very existence was denied. The official FDA policy stated, �The agency is not aware of any information showing that foods derived by these new methods differ from other foods in any meaningful or uniform way.�8 In sharp contrast, an internal FDA report stated, �The processes of genetic engineering and traditional breeding are different and according to the technical experts in the agency, they lead to different risks.�9 The FDA�s deceptive notion of no difference was coined �substantial equivalence� and formed the basis of the US government position on GMOs.

Many scientists and organizations have criticized the US position. The National Academy of Sciences and even the pro-GM Royal Society of London10 describe the US system as inadequate and flawed. The editor of the prestigious journal Lancet said, �It is astounding that the US Food and Drug Administration has not changed their stance on genetically modified food adopted in 1992. . . . The policy is that genetically modified crops will receive the same consideration for potential health risks as any other new crop plant. This stance is taken despite good reasons to believe that specific risks may exist. . . . Governments should never have allowed these products into the food chain without insisting on rigorous testing for effects on health.�11 The Royal Society of Canada described substantial equivalence as �scientifically unjustifiable and inconsistent with precautionary regulation of the technology.� 12

GMOs Are Inherently Unsafe

safety signThere are several reasons why GM plants present unique dangers. The first is that the process of genetic engineering itself creates unpredicted alterations, irrespective of which gene is transferred. The gene insertion process, for example, is accomplished by either shooting genes from a �gene gun� into a plate of cells, or using bacteria to infect the cell with foreign DNA. Both create mutations in and around the insertion site and elsewhere.13 The �transformed� cell is then cloned into a plant through a process called tissue culture, which results in additional hundreds or thousands of mutations throughout the plants� genome. In the end, the GM plant�s DNA can be a staggering 2-4% different from its natural parent.14 Native genes can be mutated, deleted, or permanently turned on or off. In addition, the insertion process causes holistic and not-well-understood changes among large numbers of native genes. One study revealed that up to 5% of the natural genes altered their levels of protein expression as a result of a single insertion.

The Royal Society of Canada acknowledged that �the default prediction� for GM crops would include �a range of collateral changes in expression of other genes, changes in the pattern of proteins produced and/or changes in metabolic activities.�15 Although the FDA scientists evaluating GMOs in 1992 were unaware of the extent to which GM DNA is damaged or changed, they too described the potential consequences. They reported, �The possibility of unexpected, accidental changes in genetically engineered plants� might produce �unexpected high concentrations of plant toxicants.�16 GM crops, they said, might have �increased levels of known naturally occurring toxins,� and the �appearance of new, not previously identified� toxins.17 The same mechanism can also produce allergens, carcinogens, or substances that inhibit assimilation of nutrients.

Most of these problems would pass unnoticed through safety assessments on GM foods, which are largely designed on the false premise that genes are like Legos that cleanly snap into place. But even if we disregard unexpected changes in the DNA for the moment, a proper functioning inserted gene still carries significant risk. Its newly created GM protein, such as the Bt-toxin, may be dangerous for human health (see below). Moreover, even if that protein is safe in its natural organism, once it is transferred into a new species it may be processed differently. A harmless protein may be transformed into a dangerous or deadly version. This happened with at least one GM food crop under development, GM peas, which were destroyed before being commercialized.

FDA scientists were also quite concerned about the possibility of inserted genes spontaneously transferring into the DNA of bacteria inside our digestive tract. They were particularly alarmed at the possibility of antibiotic resistant marker (ARM) genes transferring. ARM genes are employed during gene insertion to help scientists identify which cells successfully integrated the foreign gene. These ARM genes, however, remain in the cell and are cloned into the DNA of all the GM plants produced from that cell. One FDA report wrote in all capital letters that ARM genes would be �A SERIOUS HEALTH HAZARD,� due to the possibility of that they might transfer to bacteria and create super diseases, untreatable with antibiotics.

Although the biotech industry confidently asserted that gene transfer from GM foods was not possible, the only human feeding study on GM foods later proved that it does take place. The genetic material in soybeans that make them herbicide tolerant transferred into the DNA of human gut bacteria and continued to function18. That means that long after we stop eating a GM crop, its foreign GM proteins may be produced inside our intestines. It is also possible that the foreign genes might end up inside our own DNA, within the cells of our own organs and tissues.

Another worry expressed by FDA scientists was that GM plants might gather �toxic substances from the environment� such as �pesticides or heavy metals,�19 or that toxic substances in GM animal feed might bioaccumulate into milk and meat products. While no studies have looked at the bioaccumulation issue, herbicide tolerant crops certainly have higher levels of herbicide residues. In fact, many countries had to increase their legally allowable levels�by up to 50 times�in order to accommodate the introduction of GM crops.

The overuse of the herbicides due to GM crops has resulted in the development of herbicide resistant weeds. USDA statistics show�that herbicide use is rapidly accelerating. Its use was up by 527 million pounds in the first 16 years of GM crops (1996-2011).�Glyphosate use per acre on Roundup Ready soybeans was up by 227% while use on non-GMO soy acreage decreased by 20% over�the same time period. The rate of application is accelerating due in large part to the emergence of herbicide tolerant weeds, now�found on millions of acres. According to a study by Charles Benbrook, the incremental increase per year was 1.5 million pounds in�1999, 18 million in 2003, 79 million in 2009, and about 90 million in 2011. And as Roundup becomes less effective, farmers are�now using more toxic herbicides, such as 2-4D.

The pesticide-producing Bt crops do reduce the amount of sprayed on insecticides, but the total amount produced by the crops is far�greater than the amount of displaced spray. For example, Bt corn that kills the corn rootworm produces one to two pounds of Bt�toxin per acre, but reduces sprayed insecticides by only about 0.19 pounds. SmartStax corn with eight genes produces 3.7 pounds of�Bt toxin per acre, but displaces only 0.3 pounds of sprayed insecticides. 20

All of the above risks associated with GM foods are magnified for high-risk groups, such as pregnant women, children, the sick, and the elderly. The following section highlights some of the problems that have been identified.

GM Diet Shows Toxic Reactions In The Digestive Tract

gmos digestive abdomenThe very first crop submitted to the FDA�s voluntary consultation process, the FlavrSavr tomato, showed evidence of toxins. Out of 20 female rats fed the GM tomato, 7 developed stomach lesions.21 The director of FDA�s Office of Special Research Skills wrote that the tomatoes did not demonstrate a �reasonable certainty of no harm,�22 which is their normal standard of safety. The Additives Evaluation Branch agreed that �unresolved questions still remain.�23 The political appointees, however, did not require that the tomato be withdrawn.1

According to Arpad Pusztai, PhD, one of the world�s leading experts in GM food safety assessments, the type of stomach lesions linked to the tomatoes �could lead to life-endangering hemorrhage, particularly in the elderly who use aspirin to prevent [blood clots].�24 Dr. Pusztai believes that the digestive tract, which is the first and largest point of contact with foods, can reveal various reactions to toxins and should be the first target of GM food risk assessment. He was alarmed, however, to discover that studies on the FlavrSavr never looked passed the stomach to the intestines. Other studies that did look found problems.

Mice fed potatoes engineered to produce the Bt-toxin developed abnormal and damaged cells, as well as proliferative cell growth in the lower part of their small intestines (ileum).25 Rats fed potatoes engineered to produce a different type of insecticide (GNA lectin from the snowdrop plant) also showed proliferative cell growth in both the stomach and intestinal walls (see photos).26 Although the guts of rats fed GM peas were not examined for cell growth, the intestines were mysteriously heavier; possibly as a result of such growth.27 Cell proliferation can be a precursor to cancer and is of special concern.

GMOs Rat GM Potato InfoGM Diets Cause Liver Damage

The state of the liver�a main detoxifier for the body�is another indicator of toxins.

  • Rats fed the GNA lectin potatoes described above had smaller and partially atrophied livers.28
  • Rats fed Monsanto�s Mon 863 corn, engineered to produce Bt-toxin, had liver lesions and other indications of toxicity.29
  • Rabbits fed GM soy showed altered enzyme production in their livers as well as higher metabolic activity.30
  • The livers of rats fed Roundup Ready canola were 12%�16% heavier, possibly due to liver disease or inflammation.31
  • Microscopic analysis of the livers of mice fed Roundup Ready soybeans revealed altered gene expression and structural and functional changes (see photos).32 Many of these changes reversed after the mice diet was switched to non-GM soy, indicating that GM soy was the culprit. The findings, according to molecular geneticist Michael Antoniou, PhD, �are not random and must reflect some �insult� on the liver by the GM soy.� Antoniou, who does human gene therapy research in King�s College London, said that although the long-term consequences of the GM soy diet are not known, it �could lead to liver damage and consequently general toxemia.�33
  • Rats fed Roundup Ready soybeans also showed structural changes in their livers. 34

GMOs Liver Cells Soy Fed Mice

GMOs Livers Soy Fed RatsGM Fed Animals Had Higher Death Rates & Organ Damage

In the FlavrSavr tomato study, a note in the appendix indicated that 7 of 40 rats died within two weeks and were replaced.35 In another study, chickens fed the herbicide tolerant �Liberty Link� corn died at twice the rate of those fed natural corn.36 But in these two industry-funded studies, the deaths were dismissed without adequate explanation or follow-up.

In addition, the cells in the pancreas of mice fed Roundup Ready soy had profound changes and produced significantly less digestive enzymes;37 in rats fed a GM potato, the pancreas was enlarged.38 In various analyses of kidneys, GM-fed animals showed lesions, toxicity, altered enzyme production or inflammation.39,40 Enzyme production in the hearts of rabbits was altered by GM soy.41 And GM potatoes caused slower growth in the brain of rats.42 A team of independent scientists re-analyzed the raw data in three Monsanto 90-day rat feeding studies and saw signs of toxicity in the liver and kidneys, as well as effects in the heart, adrenal glands, spleen, and blood.43 In one of the only long-term feeding studies, rats fed Roundup Ready corn for three years for 24 months (or even just low concentrations of Roundup in their drinking water) suffered significant damage to their kidneys, livers, and pituitary glands. They also died prematurely and had many massive tumors�as large as 25% of their body weight.44

Reproductive Failures & Infant Mortality

The testicles of both mice and rats fed Roundup Ready soybeans showed dramatic changes. In rats, the organs were dark blue instead of pink (see photos on next page).45 In mice, young sperm cells were altered.46 Embryos of GM soy-fed mice also showed temporary changes in their DNA function, compared to those whose parents were fed non-GM soy.47�Female rats fed GM soy showed changes in their uterus, ovaries, and hormonal balance.48 By the third generation, most hamsters fed GM soy were unable to have babies. The infant mortality was 4-5 times greater than controls, and many of the GMO-fed third generation had hair growing in their mouths.49

GMOs Testicles of Rats

An Austrian government study showed that mice fed GM corn (Bt and Roundup Ready) had fewer babies and smaller babies.50 More dramatic results were discovered by a leading scientist at the Russian National Academy of sciences. Female rats were fed GM soy, starting two weeks before they were mated.

  • Over a series of three experiments, 51.6 percent of the offspring from the GM-fed group died within the first three weeks, compared to 10 percent from the non-GM soy group, and 8.1 percent for non-soy controls.
  • �High pup mortality was characteristic of every litter from mothers fed the GM soy flour.�51
  • The average size and weight of the GM-fed offspring was quite a bit smaller (see photo on next page).52
  • In a preliminary study, the GM-fed offspring were unable to conceive.53After the three feeding trials, the supplier of rat food used at the Russian laboratory began using GM soy in their formulation. Since all the rats housed at the facility were now eating GM soy, no non-GM fed controls were available for subsequent GM feeding trials; follow-up studies were canceled. After two months on the GM soy diet, however, the infant mortality rate of rats throughout the facility had skyrocketed to 55.3 percent (99 of 179).54
GMOs 20 Day old rat 19 day old rat

Farmers Report Livestock Sterility & Deaths

gmos pigsAbout two dozen farmers reported that their pigs had reproductive problems when fed certain varieties of Bt corn. Pigs were sterile, had false pregnancies, or gave birth to bags of water. Cows and bulls also became sterile. Bt corn was also implicated by farmers in the deaths of cows, horses, water buffaloes, and chickens.55

When Indian shepherds let their sheep graze continuously on Bt cotton plants, within 5-7 days, one out of four sheep died. There was an estimated 10,000 sheep deaths in the region in 2006, with more reported in 2007. Post mortems on the sheep showed severe irritation and black patches in both intestines and liver (as well as enlarged bile ducts). Investigators said preliminary evidence �strongly suggests that the sheep mortality was due to a toxin. . . . most probably Bt-toxin.�56 In a small feeding study, 100% of sheep fed Bt cotton died within 30 days. Those fed natural plants had no symptoms.

Buffalo that grazed on natural cotton plants for years without incident react to the Bt variety. In one village in Andhra Pradesh, for example, 13 buffalo grazed on Bt cotton plants for a single day. All died within 3 days.57 Investigators in the state of Haryana, India, report that most buffalo that ate GM cottonseed had reproductive complications such as premature deliveries, abortions, infertility, and prolapsed uteruses. Many young calves and adult buffaloes died.

GM Crops Trigger Immune Reactions & May Cause Allergies

gmos cropsAllergic reactions occur when the immune system interprets something as foreign, different, and offensive, and reacts accordingly. All GM foods, by definition, have something foreign and different. And several studies show that they provoke reactions. Rats fed Monsanto�s GM corn, for example, had a significant increase in blood cells related to the immune system.58 GM potatoes caused the immune system of rats to respond more slowly.59 And GM peas provoked an inflammatory response in mice, suggesting that it might cause deadly allergic reactions in people.60

It might be difficult to identify whether GM foods were triggering allergic responses in the population, since very few countries conduct regular studies or keep careful records. One country that does have an annual evaluation is the UK. Soon after GM soy was introduced into the British diet, researchers at the York Laboratory reported that allergies to soy had skyrocketed by 50% in a single year.61 Although no follow-up studies were conducted to see if GM soy was the cause, there is evidence showing several ways in which it might have contributed to the rising incidence of allergies:

  • The only significant variety of GM soy is Monsanto�s �Roundup Ready� variety, planted in 89% of US soy acres. A foreign gene from bacteria (with parts of virus and petunia DNA) is inserted, which allows the plant to withstand Roundup herbicide. The protein produced by the bacterial gene has never been part of the human food supply. Because people aren�t usually allergic to a food until they have eaten it several times, it would be difficult to know in advance if the protein was an allergen. Without a surefire method to identify allergenic GM crops, the World Health Organization (WHO) and others recommend examining the properties of the protein to see if they share characteristics with known allergens. One method is to compare the amino acid sequence of the novel protein with a database of allergens. If there is a match, according to the WHO, the GM crop should either not be commercialized or additional testing should be done. Sections of the protein produced in GM soy are identical to shrimp and dust mite allergens,62 but the soybean was introduced before WHO criteria were established and the recommended additional tests were not conducted. If the protein does trigger reactions, the danger is compounded by the finding that the Roundup Ready gene transfers into the DNA of human gut bacteria and may continuously produce the protein from within our intestines.63
  • In addition to the herbicide tolerant protein, GM soybeans contain a unique, unexpected protein, which likely came about from the changes incurred during the genetic engineering process. Scientists found that this new protein was able to bind with IgE antibodies, suggesting that it may provoke dangerous allergic reactions. The same study revealed that one human subject showed a skin prick immune response only to GM soy, but not to natural soy.64 These results must be considered preliminary,�as the non-GM soy was a wild type and not necessarily comparable to the GM variety. Another study showed that the levels of one known soy allergen, called trypsin inhibitor, were as much as seven times higher in cooked GM soy compared to a non-GM control.65 This was Monsanto�s own study, and did use comparable controls.
  • GM soy also produces an unpredicted side effect in the pancreas of mice�the amount of digestive enzymes produced is dramatically reduced.66 If a shortage of enzymes caused food proteins to breakdown more slowly, then they have more time to trigger allergic reactions. Thus, digestive problems from GM soy might promote allergies to a wide range of proteins, not just soy.
  • The higher amount of Roundup herbicide residues on GM soy might create reactions in consumers. In fact, many of the symptoms identified in the UK soy allergy study are among those related to glyphosate exposure. [The allergy study identified irritable bowel syndrome, digestion problems, chronic fatigue, headaches, lethargy, and skin complaints, including acne and eczema, all related to soy consumption. Symptoms of glyphosate exposure include nausea, headaches, lethargy, skin rashes, and burning or itchy skin. It is also possible that glyphosate�s breakdown product aminomethylphosphonic acid (AMPA), which accumulates in GM soybeans after each spray, might contribute to allergies.]

It is interesting to note that in the five years immediately after GM soy was introduced, US peanut allergies doubled. It is known that a protein in natural soybeans cross-reacts with peanut allergies, i.e. soy may trigger reactions in some people who are allergic to peanuts.67 Given the startling increase in peanut allergies, scientists should investigate whether this cross-reactivity has been amplified in GM soy.

Roundup, tumors, etc.

BT-Toxin, Produced In GM Corn & Cotton, May Cause Allergies

gmos Bt-toxin-crystalsFor years, organic farmers and others have sprayed crops with solutions containing natural Bt bacteria as a method of insect control. The toxin creates holes in their stomach and kills them. Genetic engineers take the gene that produces the toxin in bacteria and insert it into the DNA of crops so that the plant does the work, not the farmer. The fact that we consume that toxic pesticide in every bite of Bt corn is hardly appetizing.

Biotech companies claim that Bt-toxin has a history of safe use, is quickly destroyed in our stomach, and wouldn�t react with humans or mammals in any event. Studies verify, however, that natural Bt-toxin is not fully destroyed during digestion and does react with mammals. Mice fed Bt-toxin, for example, showed an immune response as potent as cholera toxin, 68, became immune sensitive to formerly harmless compounds,69 and had damaged and altered cells in their small intestines.70 A 2008 Italian government study found that Bt corn provoked immune responses in mice.71 Moreover, when natural Bt was sprayed over areas around Vancouver and Washington State to fight gypsy moths, about 500 people reported reactions�mostly allergy or flu-like symptoms.72,73 Farm workers and others also report serious reactions7475767778 and authorities have long acknowledged that �people with compromised immune systems or preexisting allergies may be particularly susceptible to the effects of Bt.�79

The Bt-toxin produced in GM crops is �vastly different from the bacterial [Bt-toxins] used in organic and traditional farming and forestry.�80 The plant produced version is designed to be more toxic than natural varieties,81 and is about 3,000-5,000 times more concentrated than the spray form. And just like the GM soy protein, the Bt protein in GM corn varieties has a section of its amino acid sequence identical to a known allergen (egg yolk). The Bt protein also fails other allergen criteria recommended by the WHO, i.e. the protein is too resistant to break down during digestion and heat.

A 2011 study published in the Journal of Applied Toxicology showed that when Bt-toxin derived from Monsanto�s corn was exposed to human cells, the toxin disrupts the membrane in just 24 hours, causing certain fluid to leak through the cell walls. The authors specifically note, �This may be due to pore formation like in insect cells.� In other words, the toxin may be creating small holes in human cells in the same manner that it kills insects. The researchers �documented that modified Bt toxins [from GM plants] are not inert on human cells, but can exert toxicity.�82 A 2011 Canadian study conducted at Sherbrooke Hospital discovered that�93% of the pregnant women they tested had Bt-toxin from Monsanto�s corn in their blood. And so did 80% of their unborn�fetuses. 83

If Bt-toxin causes allergies, then gene transfer carries serious ramifications. If Bt genes relocate to human gut bacteria, our intestinal flora may be converted into living pesticide factories, possibly producing Bt-toxin inside of us year after year. The UK Joint Food Safety and Standards Group also described gene transfer from a different route. They warned that genes from inhaled pollen might transfer into the DNA of bacteria in the respiratory system.84 Although no study has looked into that possibility, pollen from a Bt cornfield appears to have been responsible for allergic-type reactions.

In 2003, during the time when an adjacent Bt cornfield was pollinating, virtually an entire Filipino village of about 100 people was stricken by mysterious skin, respiratory, and intestinal reactions.85 The symptoms started with those living closest to the field and spread to those further away. Blood samples from 39 individuals showed antibodies in response to Bt-toxin, supporting�but not proving�a link. When the same corn was planted in four other villages the following year, however, the symptoms returned in all four areas�only during the time of pollination.86

Bt-toxin might also trigger reactions by skin contact. In 2005, a medical team reported that hundreds of agricultural workers in India are developing allergic symptoms when exposed to Bt cotton, but not when
axposed to natural varieties.87 They say reactions come from picking the cotton, cleaning it in factories, loading it onto trucks, or even leaning against it. Their symptoms are virtually identical to those described by the 500 people in Vancouver and Washington who were sprayed with Bt.

Government Evaluations Miss Most Health Problems

gmos Example FDA Decision Making ProcessAlthough the number of safety studies on GM foods is quite small, it has validated the concerns expressed by FDA scientists and others. Unfortunately, government safety assessments worldwide are not competent to even identify most of the potential health problems described above, let alone protect its citizens from the effects.88

A 2000 review of approved GM crops in Canada by professor E. Ann Clark, PhD, for example, reveals that 70% (28 of 40) �of the currently available GM crops . . . have not been subjected to any actual lab or animal toxicity testing, either as refined oils for direct human consumption or indirectly as feedstuffs for livestock. The same finding pertains to all three GM tomato decisions, the only GM flax, and to five GM corn crops.� In the remaining 30% (12) of the other crops tested, animals were not fed the whole GM feed. They were given just the isolated GM protein that the plant was engineered to produce. But even this protein was not extracted from the actual GM plant. Rather, it was manufactured in genetically engineered bacteria. This method of testing would never identify problems associated with collateral damage to GM plant DNA, unpredicted changes in the GM protein, transfer of genes to bacteria or human cells, excessive herbicide residues, or accumulation of toxins in the food chain, among others. Clark asks, �Where are the trials showing lack of harm to fed livestock, or that meat and milk from livestock fed on GM feedstuffs are safe?�89

Epidemiologist and GM safety expert Judy Carman, PhD, MPH, shows that assessments by Food Safety Australia New Zealand (FSANZ) also overlook serious potential problems, including cancer, birth defects, or long-term effects of nutritional deficiencies. 90

�A review of twelve reports covering twenty-eight GM crops – four soy, three corn, ten potatoes, eight canola, one sugar beet and two cotton�revealed no feeding trials on people. In addition, one of the GM corn varieties had gone untested on animals. Some seventeen foods involved testing with only a single oral gavage (a type of forced-feeding), with observation for seven to fourteen days, and only of the substance that had been genetically engineered to appear [the GM protein], not the whole food. Such testing assumes that the only new substance that will appear in the food is the one genetically engineered to appear, that the GM plant- produced substance will act in the same manner as the tested substance that was obtained from another source [GM bacteria], and that the substance will create disease within a few days. All are untested hypotheses and make a mockery of GM proponents� claims that the risk assessment of GM foods is based on sound science. Furthermore, where the whole food was given to animals to eat,�sample sizes were often very low�for example, five to six cows per group for Roundup Ready soy�and they were fed for only four weeks.�91

Dr. Carman points out that GM �experiments used some very unusual animal models for human health, such as chickens, cows, and trout. Some of the measurements taken from these animals are also unusual measures of human health, such as abdominal fat pad weight, total de-boned breast meat yield, and milk production.� In her examination of the full range of submittals to authorities in Australia and New Zealand, she says that there was no proper evaluation of �biochemistry, immunology, tissue pathology, and gut, liver, and kidney function.�92 Writing on behalf of the Public Health Association of Australia, Dr. Carman says, �The effects of feeding people high concentrations of the new protein over tens of years cannot be determined by feeding 20 mice a single oral gavage of a given high concentration of the protein and taking very basic data for 13-14 days.�93

The FDA’s Fake Safety Assessments

gmos Safety assessmentSubmissions to the US Food and Drug Administraion (FDA) may be worse than in other countries, since the agency doesn�t actually require any data. Their policy says that biotech companies can determine if their own foods are safe. Anything submitted is voluntary and, according to former Environmental Protection Agency scientist Doug Gurian-Sherman, PhD, �often lack[s] sufficient detail, such as necessary statistical analyses needed for an adequate safety evaluation.� Using Freedom of Information Requests, Dr. Gurian-Sherman analyzed more than a fourth of the data summaries (14 of 53) of GM crops reviewed by the FDA. He says, �The FDA consultation process does not allow the agency to require submission of data, misses obvious errors in company- submitted data summaries, provides insufficient testing guidance, and does not require sufficiently detailed data to enable the FDA to assure that GE crops are safe to eat.�94 Similarly, a Friends of the Earth review of company and FDA documents concluded:

�If industry chooses to submit faulty, unpublishable studies, it does so without consequence. If it should respond to an agency request with deficient data, it does so without reprimand or follow-up. . . . If a company finds it disadvantageous to characterize its product, then its properties remain uncertain or unknown. If a corporation chooses to ignore scientifically sound testing standards . . . then faulty tests are conducted instead, and the results are considered legitimate. In the area of genetically engineered food regulation, the �competent� agencies rarely if ever (know how to) conduct independent research to verify or supplement industry findings.� 95

At the end of the consultation, the FDA doesn�t actually approve the crops. Rather, they issue a letter that includes a statement such as the following:

�Based on the safety and nutritional assessment you have conducted, it is our understanding that Monsanto has concluded that corn products derived from this new variety are not materially different in composition, safety, and other relevant parameters from corn currently on the market, and that the genetically modified corn does not raise issues that would require premarket review or approval by FDA. . . . As you are aware, it is Monsanto�s responsibility to ensure that foods marketed by the firm are safe, wholesome and in compliance with all applicable legal and regulatory requirements.�96

Company Research Is Secret, Inadequate & Flawed

GMOs FDA health inspectorsThe unpublished industry studies submitted to regulators are typically kept secret based on the claim that it is �confidential business information.� The Royal Society of Canada is one of many organizations that condemn this practice. They wrote:

�In the judgment of the Expert Panel, the more regulatory agencies limit free access to the data upon which their decisions are based, the more compromised becomes the claim that the regulatory process is �science based.� This is due to a simple but well- understood requirement of the scientific method itself�that it be an open, completely transparent enterprise in which any and all aspects of scientific research are open to full review by scientific peers. Peer review and independent corroboration of research findings are axioms of the scientific method, and part of the very meaning of the objectivity and neutrality of science.�97

Whenever private submissions are made public through lawsuits or Freedom of Information Act Requests, it becomes clear why companies benefit from secrecy. The quality of their research is often miserable, incompetent, and unacceptable for peer-review. In 2000, for example, after the potentially allergenic StarLink corn was found to have contaminated the food supply, the corn�s producer, Aventis CropScience, presented wholly inadequate safety data to the EPA�s scientific advisory panel. One frustrated panel member, Dean Metcalfe, MD,�the government�s top allergist�said during a hearing, �Most of us review for a lot of journals. And if this were presented for publication in the journals that I review for, it would be sent back to the authors with all of these questions. It would be rejected.�98

Unscientific Assumptions Are The Basis Of Approvals

Professor Clark, who analyzed submissions to Canadian regulators, concluded, �Most or all of the conclusions of food safety for individual GM crops are based on inferences and assumptions, rather than on actual testing.� For example, rather than actually testing to see if the amino acid sequence produced by their inserted gene is correct, �the standard practice,� according to research analyst William Freese, �is to sequence just 5 to 25 amino acids,�99 even if the protein has more than 600 in total. If the short sample matches what is expected, they assume that the rest are also fine. If they are wrong, however, a rearranged protein could be quite dangerous.

Monsanto�s submission to Australian regulators on their high lysine GM corn provides an excellent example of overly optimistic assumptions used in place of science. The gene inserted into the corn produces a protein that is naturally found in soil. Monsanto claimed that since people consume small residues of soil on fruits and vegetables, the protein has a history of safe consumption. Based on the amount of GM corn protein an average US citizen would consume (if all their corn were Monsanto�s variety), they would eat up to 4 trillion times the amount normally consumed through soil. In other words, �for equivalent exposure� of the protein from soil �people would have to eat . . . nearly as much as 10,000kg [22,000 pounds, every] second 24 hours a day seven days a week.�100

Studies Are Rigged To Avoid Finding Problems

gmos analysis microsopeIn addition, to relying on untested assumptions, industry-funded research is often designed specifically to force a conclusion of safety. In the high lysine corn described above, for example, the levels of certain nutritional components (i.e. protein content, total dietary fiber, acid detergent fiber, and neutral detergent fiber) were far outside the normal range for corn. Instead of comparing their corn to normal controls, which would reveal this disparity, Monsanto compared it to obscure corn varieties that were also substantially outside the normal range on precisely these values. Thus, their study found no statistical differences by design.

When Monsanto learned that independent researchers were to publish a study in July 1999 showing that GM soy contains 12%-14% less cancer-fighting phytoestrogens, the company responded with its own study, concluding that soy�s phytoestrogen levels vary too much to even carry out a statistical analysis. Researchers failed to disclose, however, that they had instructed the laboratory to use an obsolete method of detection�one that had been prone to highly variable results.101

When Aventis prepared samples to see if the potential allergen in StarLink corn remained intact after cooking, instead of using the standard 30-minute treatment, they heated corn for two hours.102

To show that pasteurization destroyed bovine growth hormone in milk from cows treated with rbGH, scientists pasteurized the milk 120 times longer than normal. Unable to destroy more than 19%, they then spiked the milk with a huge amount of the hormone and repeated the long pasteurization, destroying 90%.103 (The FDA reported that pasteurization destroys 90% of the hormone.104) To demonstrate that injections of rbGH did not interfere with cow�s fertility, Monsanto apparently added cows to the study that were pregnant prior to injection.105

And in order to prove that the protein from their GM crops breaks down quickly during simulated digestion, biotech companies used thousands of times the amount of digestive enzymes and a much stronger acid compared to that recommended by the World Health Organization.106

Other methods used to hide problems are varied and plentiful. For example, researchers:

  • Use highly variable animal starting weights to hinder detection of food-related changes
  • Keep feeding studies short to miss long-term impacts
  • Test effects of Roundup Ready soybeans that have not been sprayed with Roundup
  • Avoid feeding animals the actual GM crop, but give them instead a single dose of the GM protein that was produced inside GM bacteria
  • Use too few subjects to derive statistically significant results
  • Use poor statistical methods or simply leave out essential methods, data, or statistics
  • Use irrelevant control groups, and employ insensitive evaluation techniques

Roundup Ready Soybeans: Case Study Of Flawed Research

gmos soybeansMonsanto�s 1996 Journal of Nutrition studies on Roundup Ready soybeans107,108 provide plenty of examples of scientific transgressions. Although the study has been used often by the industry as validation for safety claims, experts working in the field were not impressed. For example, Dr. Arpad Pusztai was commissioned at the time by the UK government to lead a 20 member consortium in three institutions to develop rigorous testing protocols on GM foods�protocols that were never implemented. Dr. Pusztai, who had published several studies in that same nutrition journal, said the Monsanto paper was not �up to the normal journal standards.� He said, �It was obvious that the study had been designed to avoid finding any problems. Everybody in our consortium knew this.� Some of the flaws include:

  • Researchers tested GM soy on mature animals, not young ones. Young animals use protein to build their muscles, tissues, and organs. Problems with GM food could therefore show up in organ and body weight. But adult animals use the protein for tissue renewal and energy. �With a nutritional study on mature animals,� says Dr. Pusztai, �you would never see any difference in organ weights even if the food turned out to be anti-nutritional. The animals would have to be emaciated or poisoned to show anything.�
  • If there were an organ development problem, the study wouldn�t have picked it up since the researchers didn�t even weigh the organs.
  • In one of the trials, researchers substituted only one tenth of the natural protein with GM soy protein. In two others, they diluted their GM soy six- and twelve-fold. 109 Scientists Ian Pryme, PhD, of Norway and Rolf Lembcke, PhD, of Denmark wrote, the �level of the GM soy was too low, and would probably ensure that any possible undesirable GM effects did not occur.�
  • Pryme and Lembcke, who published a paper in Nutrition and Health that analyzed all published peer-reviewed feeding studies on GM foods (10 as of 2003), also pointed out that the percentage of protein in the feed used in the Roundup Ready study was �artificially too high.� This �would almost certainly mask, or at least effectively reduce, any possible effect of the [GM soy].� They said it was �highly likely that all GM effects would have been diluted out.� 110
  • Proper compositional studies filter out effects of weather or geography by comparing plants grown at the same time in the same location. Monsanto, however, pooled data from several locations, which makes it difficult for differences to be statistically significant. Nonetheless, the data revealed significant differences in the ash, fat, and carbohydrate content. Roundup Ready soy meal also contained 27% more trypsin inhibitor, a potential allergen. Also, cows fed GM soy produced milk with a higher fat content, demonstrating another disparity between the two types of soy.
  • One field trial, however, did grow GM and non-GM plants next to each other, but this data was not included in the paper. Years after the study appeared, medical writer Barbara Keeler recovered the data that had been omitted. It showed that Monsanto�s GM soy had significantly lower levels of protein, a fatty acid, and phenylalanine, an essential amino acid. Also, toasted GM soy meal contained nearly twice the amount of a lectin�a substance that may interfere with the body�s ability to assimilate other nutrients. And the amount of trypsin inhibitor in cooked GM soy was as much as seven times higher than in a cooked non-GM control.
  • The study also omitted many details normally required for a published paper. According to Pryme and Lembcke, �No data were given for most of the parameters.�
  • And when researchers tested the effects of Roundup Ready protein on animals, they didn�t extract the protein from the soybeans. Instead, they derived it from GM bacteria, claiming the two forms of protein were equivalent. There are numerous ways, however, in which the protein in the soy may be different. In fact, nine years after this study was published, another study showed that the gene inserted into the soybeans produced unintended aberrant RNA strands, meaning that the protein may be quite different than what was intended.111

In Pryme and Lembcke�s analysis, it came as no surprise that this Monsanto study, along with the other four peer-reviewed animal feeding studies that were �performed more or less in collaboration with private companies,� reported no negative effects of the GM diet. �On the other hand,� they wrote, �adverse effects were reported (but not explained) in [the five] independent studies.� They added, �It is remarkable that these effects have all been observed after feeding for only 10�14 days.�112

Toxic GM Foods Could Have Been Approved

Two GM foods whose commercialization was stopped because of negative test results give a chilling example of what may be getting through. Rats fed GM potatoes had potentially precancerous cell growth in the stomach and intestines, less developed brains, livers, and testicles, partial atrophy of the liver, and damaged immune systems.113 GM peas provoked an inflammatory response in mice, suggesting that the peas might trigger a deadly anaphylactic shock in allergic humans.114 Both of these dangerous crops, however, could easily have been approved. The problems were only discovered because the researchers used advanced tests that were never applied to GM crops already on the market. Both would have passed the normal tests that companies typically use to get their products approved.

Ironically, when Monsanto was asked to comment on the pea study, their spokesperson said it demonstrated that the regulatory system works. He failed to disclose that none of his company�s GM crops had been put through such rigorous tests.

Rampant, Unrelenting Industry Bias

Industry-funded research that favors the funders is not new. Bias has been identified across several industries. In pharmaceuticals, for example, positive results are four times more likely if the drug�s manufacturer funds the study.115 When companies pay for the economic analyses of their own cancer drugs, the results are eight times more likely to be favorable.116 Compared to drug research, the potential for industry manipulation in GM crop studies is considerably higher. Unlike pharmaceutical testing, GM research has no standardized procedures dictated by regulators. GM studies are not usually published in peer-reviewed journals and are typically kept secret by companies and governments. There is little money available for rigorous independent research, so company evidence usually goes unchallenged and unverified. Most importantly, whereas drugs can show serious side-effects and still be approved, GM food cannot. There is no tolerance for adverse reactions; feeding trials must show no problems.

Thus, when industry studies show problems (in spite of their efforts to avoid them), serious adverse reactions and even deaths among GM-fed animals are ignored or dismissed as �not biologically significant� or due to �natural variations.� In the critical arena of food safety research, the biotech industry is without accountability, standards, or peer-review. They�ve got bad science down to a science.

Promoting & Regulating Don’t Mix

While such self-serving behavior may be expected from corporations, how come government bodies let such blatant scientific contortions pass without comment? One reason is that several regulatory agencies are also charged with promoting the interests of biotechnology. This is the official position of the FDA and other US government bodies, for example. Suzanne Wuerthele, PhD, a US EPA toxicologist, says, �This technology is being promoted, in the face of concerns by respectable scientists and in the face of data to the contrary, by the very agencies which are supposed to be protecting human health and the environment. The bottom line in my view is that we are confronted with the most powerful technology the world has ever known, and it is being rapidly deployed with almost no thought whatsoever to its consequences.�117

Canadian regulators are similarly conflicted. The Royal Society of Canada reported that, �In meetings with senior managers from the various Canadian regulatory departments . . . their responses uniformly stressed the importance of maintaining a favorable climate for the biotechnology industry to develop new products and submit them for approval on the Canadian market. . . . The conflict of interest involved in both promoting and regulating an industry or technology . . . is also a factor in the issue of maintaining the transparency, and therefore the scientific integrity, of the regulatory process. In effect, the public interest in a regulatory system that is �science based�. . . is significantly compromised when that openness is negotiated away by regulators in exchange for cordial and supportive relationships with the industries being regulated.�118

Many scientists on the European Food Safety Authority (EFSA) GMO Panel are personally aligned with biotech interests. According to Friends of the Earth (FOE), �One member has direct financial links with the biotech industry and others have indirect links, such as close involvement with major conferences organized by the biotech industry. Two members have even appeared in promotional videos produced by the biotech industry. . . . Several members of the Panel, including the chair Professor Kuiper, have been involved with the EU-funded ENTRANSFOOD project. The aim of this project was to agree [to] safety assessment, risk management, and risk communication procedures that would �facilitate market introduction of GMOs in Europe, and therefore bring the European industry in a competitive position.� Professor Kuiper, who coordinated the ENTRANSFOOD project, sat on a working group that also included staff from Monsanto, Bayer CropScience, and Syngenta.� In a statement reminiscent of the deceptive policy statement by the FDA, the FOE report concludes that EFSA is �being used to create a false impression of scientific agreement when the real situation is one of intense and continuing debate and uncertainty.�119

The pro-GM European Commission repeats the same ruse. According to leaked documents obtained by FOE, while they privately appreciate �the uncertainties and gaps in knowledge that exist in relation to the safety of GM crops, . . . the Commission normally keeps this uncertainty concealed from the public whilst presenting its decisions about the safety of GM crops and foods as being certain and scientifically based.� For example, the Commission privately condemned the submission information for one crop as �mixed, scarce, delivered consecutively all over years, and not convincing.� They said there is �No sufficient experimental evidence to assess the safety.�120

With an agenda to promote GM foods, regulators regularly violate their own laws. In Europe, the law requires that when EFSA and member states have different opinions, they �are obliged to co-operate with a view to either resolving the divergence or preparing a joint document clarifying the contentious scientific issues and identifying the relevant uncertainties in the data.�121 According to FOE, in the case of all GM crop reviews, none of these legal obligations were followed.122 The declaration of GRAS status by the FDA also deviated from the Food and Cosmetic Act and years of legal precedent. Some violations are more blatant. In India, one official tampered with the report on Bt cotton to increase the yield figures to favor Monsanto.123 In Mexico, a senior government official allegedly threatened a University of California professor, implying �We know where your children go to school,� trying to get him not to publish incriminating evidence that would delay GM approvals.124 In Indonesia, Monsanto gave bribes and questionable payments to at least 140 officials, attempting to get their genetically modified (GM) cotton approved.125

Manipulation Of Public Opinion

gmos manipulationWhen governments fail in their duty to keep corporations in check, the �protector� role should shift to the media, which acts as a watchdog to expose public dangers and governmental shortcomings. But mainstream media around the world has largely overlooked the serious problems associated with GM crops and their regulation. The reason for this oversight is varied and includes contributions from an aggressive public relations and disinformation campaign by the biotech industry, legal threats by biotech companies, and in some cases, the fear of losing advertising accounts. This last reason is particularly prevalent among the farm press, which receives much of its income from the biotech industry.

Threatening letters from Monsanto�s attorneys have resulted in the cancellation of a five-part news series on their genetically engineered bovine growth hormone scheduled for a Fox TV station in Florida, as well as the cancellation of a book critical of Monsanto�s GMO products. A printer also shredded 14,000 copies of the Ecologist magazine issue entitled �The Monsanto Files,� due to fear of a Monsanto lawsuit. (See the chapter �Muscling the Media� in Seeds of Deception126 for more examples.)

The methods that biotech advocates use to manipulate public opinion research has become an art form. Consumer surveys by the International Food Information Council (IFIC), for example,whose supporters include the major biotech seed companies, offers conclusions such as �A growing majority of Americans support the benefits of food biotechnology as well as the US Food and Drug Administration�s (FDA) labeling policy.� But communications professor James Beniger, who was past president of the American Association for Public Opinion Research, described the surveys as �so biased with leading questions favoring positive responses that any results are meaningless.�127 The 2003 survey, for example, included gems such as:

�All things being equal, how likely would you be to buy a variety of produce, like tomatoes or potatoes, if it had been modified by biotechnology to taste better or fresher?� and

�Biotechnology has also been used to enhance plants that yield foods like cooking oils. If cooking oil with reduced saturated fat made from these new plants was available, what effect would the use of biotechnology have on your decision to buy this cooking oil?�128

A similar tactic was used at a December 11, 2007 focus group in Columbus, Ohio �designed� to show that consumers wanted to make it illegal for dairies to label their milk as free from Monsanto�s genetically engineered bovine hormone rBST. The facilitator said, �All milk contains hormones. There is no such thing as hormone-free milk. The composition of both types of milk is the same in all aspects. Now what do you think of a label that says �no added hormones?� Don�t you think it is deceiving and inappropriate to put �rBST-free� on labels?� Not only was the facilitator �leading the witness,� he presented false information. Milk from cows treated with rBST has substantially higher levels of Insulin-like Growth Factor-1,129 which has been linked to higher risk of cancer,130 and higher incidence of fraternal twins.131 It also has higher levels of bovine growth hormone, pus, and in some cases, antibiotics.

Another example of manipulated consumer opinion was found in a 2004 article in the British Food Journal, authored by four advocates of genetically modified (GM) foods.132 According to the peer-reviewed paper, when shoppers in a Canadian farm store were confronted with an informed and unbiased choice between GM corn and non-GM corn, most purchased the GM variety. This finding flew in the face of worldwide consumer resistance to GM foods, which had shut markets in Europe, Japan, and elsewhere. It also challenged studies that showed that the more information on genetically modified organisms (GMOs) consumers have, the less they trust them.133 The study, which was funded by the biotech-industry front group, Council for Biotechnology Information and the industry�s trade association, the Crop Protection Institute of Canada (now Croplife Canada), was given the Journal�s prestigious Award for Excellence for the Most Outstanding Paper of 2004 and has been cited often by biotech advocates.

Stuart Laidlaw, a reporter from Canada�s Toronto Star, visited the farm store several times during the study and described the scenario in his book Secret Ingredients. Far from offering unbiased choices, key elements appeared rigged to favor GM corn purchases. The consumer education fact sheets were entirely pro-GMO, and Doug Powell, the lead researcher, enthusiastically demonstrated to Laidlaw how he could convince shoppers to buy the GM varieties. He confronted a farmer who had already�purchased non-GM corn. After pitching his case for GMOs, Powell proudly had the farmer tell Laidlaw that he had changed his opinion and would buy GM corn in his next shopping trip.

Powell�s interference with shoppers� �unbiased� choices was nothing compared to the effect of the signs placed over the corn bins. The sign above the non-GM corn read, �Would you eat wormy sweet corn?� It further listed the chemicals that were sprayed during the season. By contrast, the sign above the GM corn stated, �Here�s What Went into Producing Quality Sweet Corn.� It is no wonder that 60% of shoppers avoided the �wormy corn.� In fact, it may be a testament to people�s distrust of GMOs that 40% still went for the �wormy� option.

Powell and his colleagues did not mention the controversial signage in their study. They claimed that the corn bins in the farm store were �fully labelled��either �genetically engineered Bt sweet corn� or �Regular sweet corn.� When Laidlaw�s book came out, however, Powell�s �wormy� sign was featured in a photograph,134 exposing what was later described by Cambridge University�s Dr. Richard Jennings as �flagrant fraud.� Jennings, who is a leading researcher on scientific ethics, says, �It was a sin of omission by failing to divulge information which quite clearly should have been disclosed.�135

In his defence, Powell claimed that his signs merely used the language of consumers and was �not intended to manipulate consumer purchasing patterns.� He also claimed that the �wormy� corn sign was only there for the first week of the trial and was then replaced by other educational messages. But eye witnesses and photographs demonstrate the presence of the sign long after Powell�s suggested date of replacement.136

Several scientists and outraged citizens say the paper should be withdrawn, but the Journal refused. In fact, the Journal�s editor has not even agreed to reconsider its Award for Excellence. A blatant propaganda exercise still stands validated as exemplary science.

Critics & Independent Scientists Are Attacked

gmos scientistOne of the most troubling aspects of the biotech debate is the attack strategy used on GMO critics and independent scientists. Not only are adverse findings by independent scientists often suppressed, ignored, or denied, researchers that discover problems from GM foods have been fired, stripped of responsibilities, deprived of tenure, and even threatened. Consider Dr. Pusztai, the world�s leading scientist in his field, who inadvertently discovered in 1998 that unpredictable changes in GM crops caused massive damage in rats. He went public with his concerns, was a hero at his prestigious institute for two days, and then, after the director received two phone calls allegedly from the UK Prime Minister�s office, was fired after 35 years and silenced with threats of a lawsuit. False statements were circulated to trash his reputation, which are recited by GMO advocates today.

After University of California Professor Ignacio Chapela, PhD, published evidence that GM corn contaminated Mexico�s indigenous varieties, two fictitious internet characters created by Monsanto�s PR firm, the Bivings Group, initiated a brutal internet smear campaign, lying about Dr. Chapela and his research.

Irina Ermakova, PhD, a leading scientist at the Russian National Academy of Sciences, fed female rats GM soy and was stunned to discover that more than half their offspring died within three weeks�compared to only 10% from mothers fed non-GM soy. Without funding to extend her analysis, she labeled her work �preliminary,� published it in a Russian journal, and implored the scientific community to repeat the study. Two years later, no one has repeated it, but advocates use false or irrelevant arguments to divert attention from the shocking results and have tried to vilify Dr. Ermakova.

A New Zealand MP testified at the 2001 Royal Commission of Inquiry on Genetic Modification, �I have been contacted by telephone and e-mail by a number of scientists who have serious concerns . . . but who are convinced that if they express these fears publicly. . . or even if they asked the awkward and difficult questions, they will be eased out of their institution.� Indeed in 2007, after Professor Christian Velot, PhD, raised the difficult questions on GMOs at public conferences, his 2008 research funds were confiscated, his student assistants were re-assigned, and his position at the University of Paris-Sud faces early termination.

We Are The Guinea Pigs

gmos family eatingSince GM foods are not properly tested before they enter the market, consumers are the guinea pigs. But this doesn�t even qualify as an experiment. There are no controls and no monitoring. Given the mounting of evidence of harm, it is likely that GM foods are contributing to the deterioration of health in the United States, Canada, and other countries where it is consumed. But without post- marketing surveillance, the chances of tracing health problems to GM food are low. The incidence of a disease would have to increase dramatically before it was noticed, meaning that millions may have to get sick before a change is investigated. Tracking the impact of GM foods is even more difficult in North America, where the foods are not labeled.

Regulators at Health Canada announced in 2002 that they would monitor Canadians for health problems from eating GM foods. A spokesperson said, �I think it�s just prudent and what the public expects, that we will keep a careful eye on the health of Canadians.� But according to CBC TV news, Health Canada �abandoned that research less than a year later saying it was �too difficult to put an effective surveillance system in place.�� The news anchor added, �So at this point, there is little research into the health effects of genetically modified food. So will we ever know for sure if it�s safe?�137

Not with the biotech companies in charge. Consider the following statement in a report submitted to county officials in California by pro-GM members of a task force. �[It is] generally agreed that long-term monitoring of the human health risks of GM food through epidemiological studies is not necessary because there is no scientific evidence suggesting any long-term harm from these foods.�138 Note the circular logic: Because no long-term epidemiological studies are in place, we have no evidence showing long- term harm. And since we don�t have any evidence of long-term harm, we don�t need studies to look for it.

What are these people thinking? Insight into the pro-GM mindset was provided by Dan Glickman, the US Secretary of Agriculture under President Clinton.

�What I saw generically on the pro-biotech side was the attitude that the technology was good, and that it was almost immoral to say that it wasn�t good, because it was going to solve the problems of the human race and feed the hungry and clothe the naked. . . . And there was a lot of money that had been invested in this, and if you�re against it, you�re Luddites, you�re stupid. That, frankly, was the side our government was on. Without thinking, we had basically taken this issue as a trade issue and they, whoever �they� were, wanted to keep our product out of their market. And they were foolish, or stupid, and didn�t have an effective regulatory system. There was rhetoric like that even here in this department. You felt like you were almost an alien, disloyal, by trying to present an open-minded view on some of the issues being raised. So I pretty much spouted the rhetoric that everybody else around here spouted; it was written into my speeches.�139

Fortunately, not everyone feels that questioning GM foods is disloyal. On the contrary, millions of people around the world are unwilling to participate in this uncontrolled experiment. They refuse to eat GM foods. Manufacturers in Europe and Japan have committed to avoid using GM ingredients. And the US natural foods industry, not waiting for the government to test or label GMOs, is now engaged in removing all remaining GM ingredients from their sector using a third party verification system. The Campaign for Healthier Eating in America will circulate non-GMO shopping guides in stores nationwide so that consumers have clear, healthy non-GMO choices. With no governmental regulation of biotech corporations, it is left to consumers to protect ourselves.

For a guide to avoiding GMOs, go to www.NonGMOShoppingGuide.com.

International bestselling author and independent filmmaker Jeffrey M. Smith is the Executive Director of the Institute for Responsible Technology and a leading spokesperson on the health dangers of GMOs. His first book, Seeds of Deception, is the world�s bestselling book on the subject. His second, Genetic Roulette: The Documented Health Risks of Genetically Engineered Foods, identifies 65 risks of GMOs and demonstrates how superficial government approvals are not competent to find most of them. Mr. Smith has pioneered the Campaign for Healthier Eating in America, designed to create the tipping point of consumer rejection against GMOs. See www.ResponsibleTechnology.org, www.NonGMOShoppingGuide.com.

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References:

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26 Stanley W. B. Ewen and Arpad Pusztai, �Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat
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27 Arpad Pusztai, �Facts Behind the GM Pea Controversy: Epigenetics, Transgenic Plants & Risk Assessment,� Proceedings of the Conference,
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28 Arpad Pusztai, �Can science give us the tools for recognizing possible health risks of GM food,� Nutrition and Health, 2002, Vol 16 Pp 73-84.
29 John M. Burns, �13-Week Dietary Subchronic Comparison Study with MON 863 Corn in Rats Preceded by a 1-Week Baseline Food
Consumption Determination with PMI Certified Rodent Diet #5002,� December 17, 2002
www.monsanto.com/pdf/products/fullratstudy863.pdf
30 R. Tudisco, P. Lombardi, F. Bovera, D. d�Angelo, M. I. Cutrignelli, V. Mastellone, V. Terzi, L. Avallone, F. Infascelli, �Genetically Modified
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31 Comments to ANZFA about Applications A346, A362 and A363 from the Food Legislation and Regulation Advisory Group (FLRAG) of the
Public Health Association of Australia (PHAA) on behalf of the PHAA, �Food produced from glyphosate-tolerant canola line GT73.�
32 M. Malatesta, C. Caporaloni, S. Gavaudan, M. B. Rocchi, S. Serafini, C. Tiberi, G. Gazzanelli, �Ultrastructural Morphometrical and
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33 Jeffrey M. Smith, Genetic Roulette: The Documented Health Risks of Genetically Engineered Foods, Yes! Books, Fairfield, IA USA 2007
34 Irina Ermakova, �Experimental Evidence of GMO Hazards,� Presentation at Scientists for a GM Free Europe, EU Parliament, Brussels, June
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35 Arpad Pusztai, �Can Science Give Us the Tools for Recognizing Possible Health Risks for GM Food?� Nutrition and Health 16 (2002): 73�84.
36 S. Leeson, �The Effect of Glufosinate Resistant Corn on Growth of Male Broiler Chickens,� Department of Animal and Poultry Sciences,
University of Guelph, Report No. A56379, July 12, 1996.
37 Malatesta, et al, �Ultrastructural Analysis of Pancreatic Acinar Cells from Mice Fed on Genetically modified Soybean,� J Anat. 2002
November; 201(5): 409�415; see also M. Malatesta, M. Biggiogera, E. Manuali, M. B. L. Rocchi, B. Baldelli, G. Gazzanelli, �Fine Structural
Analyses of Pancreatic Acinar Cell Nuclei from Mice Fed on GM Soybean,� Eur J Histochem 47 (2003): 385�388.
38 Arpad Pusztai, �Can science give us the tools for recognizing possible health risks of GM food,� Nutrition and Health, 2002, Vol 16 Pp 73-84
39 R. Tudisco, P. Lombardi, F. Bovera, D. d�Angelo, M. I. Cutrignelli, V. Mastellone, V. Terzi, L. Avallone, F. Infascelli, �Genetically Modified
Soya Bean in Rabbit Feeding: Detection of DNA Fragments and Evaluation of Metabolic Effects by Enzymatic Analysis,� Animal Science 82
(2006): 193�199.
40 John M. Burns, �13-Week Dietary Subchronic Comparison Study with MON 863 Corn in Rats Preceded by a 1-Week Baseline Food
Consumption Determination with PMI Certified Rodent Diet #5002,� December 17, 2002
www.monsanto.com/pdf/products/fullratstudy863.pdf
41 R. Tudisco, P. Lombardi, F. Bovera, D. d�Angelo, M. I. Cutrignelli, V. Mastellone, V. Terzi, L. Avallone, F. Infascelli, �Genetically Modified
Soya Bean in Rabbit Feeding: Detection of DNA Fragments and Evaluation of Metabolic Effects by Enzymatic Analysis,� Animal Science 82
(2006): 193�199.
42 Arpad Pusztai, �Can science give us the tools for recognizing possible health risks of GM food,� Nutrition and Health, 2002, Vol 16 Pp 73-84
43 de Vend�mois JS, Roullier F, Cellier D, S�ralini GE. A Comparison of the Effects of Three GM Corn Varieties on Mammalian Health. Int J
Biol Sci 2009; 5:706-726. Available from www.biolsci.org/v05p0706.htm
44 S�ralini, G.-E., et al. Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food
Chem. Toxicol. (2012), dx.doi.org/10.1016/j.fct.2012.08.005
45 Irina Ermakova, �Experimental Evidence of GMO Hazards,� Presentation at Scientists for a GM Free Europe, EU Parliament, Brussels, June
12, 2007
46 L. Vecchio et al, �Ultrastructural Analysis of Testes from Mice Fed on Genetically Modified Soybean,� European Journal of Histochemistry
48, no. 4 (Oct�Dec 2004):449�454.
47 Oliveri et al., �Temporary Depression of Transcription in Mouse Pre-implantion Embryos from Mice Fed on Genetically Modified Soybean,�
48th Symposium of the Society for Histochemistry, Lake Maggiore (Italy), September 7�10, 2006.
48 Fl�via Bittencourt Brasil, et al, �The Impact of Dietary Organic and Transgenic Soy on the Reproductive System of Female Adult Rat,� The
Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology Volume 292, Issue 4, pages 587-594, April 2009
onlinelibrary.wiley.com/doi/10.1002/ar.20878/abstract
49 Jeffrey M. Smith, �Genetically Modified Soy Linked to Sterility, Infant Mortality,� based on correspondence with study authors and press
reports, Institute for Responsible Technology www.responsibletechnology.org/article-gmo-soy-linked-to-sterility
50 Alberta Velimirov and Claudia Binter, �Biological effects of transgenic maize NK603xMON810 fed in long term reproduction studies in
mice,� Forschungsberichte der Sektion IV, Band 3/2008. Report-Federal Ministry of Health, Family and Youth. 2008.
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51 I.V.Ermakova, �Genetically Modified Organisms and Biological Risks,� Proceedings of International Disaster Reduction Conference (IDRC)
Davos, Switzerland August 27th � September 1st, 2006: 168�172. eco-irina-ermakova.narod.ru/eng/art/art16.html
52 Irina Ermakova, �Genetically modified soy leads to the decrease of weight and high mortality of rat pups of the first generation. Preliminary
studies,� Ecosinform 1 (2006): 4�9.
53 Irina Ermakova, �Experimental Evidence of GMO Hazards,� Presentation at Scientists for a GM Free Europe, EU Parliament, Brussels, June
12, 2007
54 I.V.Ermakova �GMO: Life itself intervened into the experiments,� Letter, EcosInform N2 (2006): 3�4.
55 Jeffrey M. Smith, Genetic Roulette: The Documented Health Risks of Genetically Engineered Foods, Yes! Books, Fairfield, IA USA 2007
56 �Mortality in Sheep Flocks after Grazing on Bt Cotton Fields�Warangal District, Andhra Pradesh� Report of the Preliminary Assessment,
April 2006, gmwatch.org/latest-listing/1-news-items/6416-mortality-in-sheep-flocks-after-grazing-on-bt-cotton-fields-warangal-districtandhra-pradesh-2942006

57 Personal communication and visit by Jeffrey Smith with village members, near Warangal, Andhra Pradesh, January 2009.
58 John M. Burns, �13-Week Dietary Subchronic Comparison Study with MON 863 Corn in Rats Preceded by a 1-Week Baseline Food
Consumption Determination with PMI Certified Rodent Diet #5002,� December 17, 2002
www.monsanto.com/monsanto/content/sci_tech/prod_safety/fullratstudy.pdf, see also St�phane Foucart, �Controversy Surrounds a GMO,�
Le Monde, 14 December 2004; and Jeffrey M. Smith, �Genetically Modified Corn Study Reveals Health Damage and Cover-up,� Spilling the
Beans, June 2005, www.seedsofdeception.com/Public/Newsletter/June05GMCornHealthDangerExposed/index.cfm
59 Arpad Pusztai, �Can science give us the tools for recognizing possible health risks of GM food,� Nutrition and Health, 2002, Vol 16 Pp 73-84
60 V. E. Prescott, et al, �Transgenic Expression of Bean r-Amylase Inhibitor in Peas Results in Altered Structure and
Immunogenicity,� Journal of Agricultural Food Chemistry (2005): 53.
61 Yearly food sensitivity assessment of York Laboratory, as reported in Mark Townsend, �Why soya is a hidden destroyer,� Daily Express,
March 12, 1999.
62 G. A. Kleter and A. A. C. M. Peijnenburg, �Screening of transgenic proteins expressed in transgenic food crops for the presence of short amino
acid sequences indentical to potential, IgE-binding linear epitopes of allergens,� BMC Structural Biology 2 (2002): 8�19.
63 Netherwood et al, �Assessing the survival of transgenic plant DNA in the human gastrointestinal tract,� Nature Biotechnology 22 (2004): 2.
64 Hye-Yung Yum, Soo-Young Lee, Kyung-Eun Lee, Myung-Hyun Sohn, Kyu-Earn Kim, �Genetically Modified and Wild Soybeans: An
immunologic comparison,� Allergy and Asthma Proceedings 26, no. 3 (May�June 2005): 210-216(7).
65 Stephen R. Padgette et al, �The Composition of Glyphosate-Tolerant Soybean Seeds Is Equivalent to That of Conventional Soybeans,� The
Journal of Nutrition 126, no. 4, (April 1996); including data in the journal archives from the same study; see also A. Pusztai and S. Bardocz,
�GMO in animal nutrition: potential benefits and risks,� Chapter 17, Biology of Nutrition in Growing Animals (Elsevier, 2005).
66 Manuela Malatesta, et al, �Ultrastructural Analysis of Pancreatic Acinar Cells from Mice Fed on Genetically modified Soybean,� Journal of
Anatomy 201, no. 5 (November 2002): 409; see also M. Malatesta, M. Biggiogera, E. Manuali, M. B. L. Rocchi, B. Baldelli, G. Gazzanelli, �Fine
Structural Analyses of Pancreatic Acinar Cell Nuclei from Mice Fed on GM Soybean,� Eur J Histochem 47 (2003): 385�388.
67 See for example, Scott H. Sicherer et al., �Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit
dial telephone survey: A 5-year follow-up study,� Journal of allergy and clinical immunology, March 2003, vol. 112, n 6, 1203-1207); and Ricki
Helm et al., �Hypoallergenic Foods�Soybeans and Peanuts,� Information Systems for Biotechnology News Report, October 1, 2002.
68 Vazquez et al, “Intragastric and intraperitoneal administration of Cry1Ac protoxin from Bacillus thuringiensis induces systemic and mucosal
antibody responses in mice,” Life Sciences, 64, no. 21 (1999): 1897�1912; Vazquez et al, �Characterization of the mucosal and systemic immune
response induced by Cry1Ac protein from Bacillus thuringiensis HD 73 in mice,� Brazilian Journal of Medical and Biological Research 33 (2000):
147�155.
69 R. I. V�zquez, L. Moreno-Fierros, L. Neri-Baz�n, et al., �Bacillus thuringiensis Cry1Ac Protoxin Is a Potent Systemic and Mucosal Adjuvant,�
Scandinavian Journal of Immunology 49 (1999): 578�84. See also Vazquez-Padron, RI. Et al. (2000b) Characterization of the mucosal and
systemic immune response induced by Cry1Ac protein from Bacillus thuringiensis HD 73 in mice. Brazilian Journal of Medical and Biological
Research 33, 147-155.
70 Nagui H. Fares, Adel K. El-Sayed, �Fine Structural Changes in the Ileum of Mice Fed on Endotoxin Treated Potatoes and Transgenic
Potatoes,� Natural Toxins 6, no. 6 (1998): 219�233.
71 Alberto Finamore, et al, �Intestinal and Peripheral Immune Response to MON810 Maize Ingestion in Weaning and Old Mice,� J. Agric. Food
Chem., 2008, 56 (23), pp 11533�11539, November 14, 2008
72 Washington State Department of Health, �Report of health surveillance activities: Asian gypsy moth control program,� (Olympia, WA:
Washington State Dept. of Health, 1993).
73 M. Green, et al., �Public health implications of the microbial pesticide Bacillus thuringiensis: An epidemiological study, Oregon, 1985-86,�
Amer. J. Public Health 80, no. 7(1990): 848�852.
74 M.A. Noble, P.D. Riben, and G. J. Cook, �Microbiological and epidemiological surveillance program to monitor the health effects of Foray
48B BTK spray� (Vancouver, B.C.: Ministry of Forests, Province of British Columbi, Sep. 30, 1992).
75 A. Edamura, MD, �Affidavit of the Federal Court of Canada, Trial Division. Dale Edwards and Citizens Against Aerial Spraying vs. Her
Majesty the Queen, Represented by the Minister of Agriculture,� (May 6, 1993); as reported in Carrie Swadener, �Bacillus thuringiensis (B.t.),�
Journal of Pesticide Reform, 14, no, 3 (Fall 1994).
76 J. R. Samples, and H. Buettner, �Ocular infection caused by a biological insecticide,� J. Infectious Dis. 148, no. 3 (1983): 614; as reported in
Carrie Swadener, �Bacillus thuringiensis (B.t.)�, Journal of Pesticide Reform 14, no. 3 (Fall 1994)
77 M. Green, et al., �Public health implications of the microbial pesticide Bacillus thuringiensis: An epidemiological study, Oregon, 1985-86,�
Amer. J. Public Health, 80, no. 7 (1990): 848�852.
78 A. Edamura, MD, �Affidavit of the Federal Court of Canada, Trial Division. Dale Edwards and Citizens Against Aerial Spraying vs. Her
Majesty the Queen, Represented by the Minister of Agriculture,� (May 6, 1993); as reported in Carrie Swadener, �Bacillus thuringiensis (B.t.),�
Journal of Pesticide Reform, 14, no, 3 (Fall 1994).
79 Carrie Swadener, �Bacillus thuringiensis (B.t.),� Journal of Pesticide Reform 14, no. 3 (Fall 1994).
80 Terje Traavik and Jack Heinemann, �Genetic Engineering and Omitted Health Research: Still No Answers to Ageing Questions, 2006. Cited in
their quote was: G. Stotzky, �Release, persistence, and biological activity in soil of insecticidal proteins from Bacillus thuringiensis,� found in
Deborah K. Letourneau and Beth E. Burrows, Genetically Engineered Organisms. Assessing Environmental and Human Health Effects (cBoca
Raton, FL: CRC Press LLC, 2002), 187�222.
81 See for example, A. Dutton, H. Klein, J. Romeis, and F. Bigler, �Uptake of Bt-toxin by herbivores feeding on transgenic maize and
consequences for the predator Chrysoperla carnea,� Ecological Entomology 27 (2002): 441�7; and J. Romeis, A. Dutton, and F. Bigler, �Bacillus
thuringiensis toxin (Cry1Ab) has no direct effect on larvae of the green lacewing Chrysoperla carnea (Stephens) (Neuroptera: Chrysopidae),�
Journal of Insect Physiology 50, no. 2�3 (2004): 175�183.
82 Mesnage R, Clair E, Gress S, Then C, Sz�k�cs A, S�ralini, GE. (2012). Cytotoxicity on human cells of Cry1Ab and Cry1Ac Bt insecticidal
toxins alone or with a glyphosate-based herbicide. J. Appl. Toxicol. doi: 10.1002/jat.2712
83 Aris A, Leblanc S. Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada.
Reprod Toxicol (2011), doi:10.1016/j.reprotox.2011.02.004 www.ncbi.nlm.nih.gov/pubmed/21338670
84 N. Tomlinson of UK MAFF’s Joint Food Safety and Standards Group 4, December 1998 letter to the U.S. FDA, commenting on its draft
document, �Guidance for Industry: Use of Antibiotic Resistance Marker Genes in Transgenic Plants.�
85 Jeffrey M. Smith, �Bt-maize (corn) during pollination, may trigger disease in people living near the cornfield,� Press Release, February 2004,
www.responsibletechnology.org/gmo-dangers/health-risks/articles-about-risks-by-jeffrey-smith/Genetically-Engineered-Foods-May-CauseRising-Food-Allergies-Genetically-Engineered-Corn-June-2007;
and Allen V. Estabillo, �Farmer’s group urges ban on planting Bt corn; says it
could be cause of illnesses,� Mindanews, October 19, 2004 www.gmwatch.org/latest-listing/43-2004/5635-farmers-group-urges-ban-onplanting-bt-corn-20102004
86 Mae-Wan Ho, �GM Ban Long Overdue, Dozens Ill & Five Deaths in the Philippines,� ISIS Press Release, June 2, 2006. www.isis.org.uk/GMBanLongOverdue.php
87 Ashish Gupta et. al., �Impact of Bt Cotton on Farmers� Health (in Barwani and Dhar District of Madhya Pradesh),� Investigation Report, Oct�
Dec 2005.
88 Jeffrey M. Smith, Genetic Roulette: The Documented Health Risks of Genetically Engineered Foods, Yes! Books, Fairfield, IA USA 2007
89 E. Ann Clark, �Food Safety of GM Crops in Canada: toxicity and allergenicity,� GE Alert, 2000.
www.plant.uoguelph.ca/research/homepages/eclark/safety.htm
90 FLRAG of the PHAA of behalf of the PHAA, �Comments to ANZFA about Applications A372, A375, A378 and A379.�
91 Judy Carman, �Is GM Food Safe to Eat?� in R. Hindmarsh, G. Lawrence, eds., Recoding Nature Critical Perspectives on Genetic Engineering
(Sydney: UNSW Press, 2004): 82�93.
92 Judy Carman, �Is GM Food Safe to Eat?� in R. Hindmarsh, G. Lawrence, eds., Recoding Nature Critical Perspectives on Genetic Engineering
(Sydney: UNSW Press, 2004): 82�93.
93 FLRAG, �Comments to ANZFA about Applications A346, A362 and A363,� www.iher.org.au/
94 Doug Gurian-Sherman, �Holes in the Biotech Safety Net, FDA Policy Does Not Assure the Safety of Genetically Engineered Foods,� Center
for Science in the Public Interest, www.cspinet.org/new/pdf/fda_report__final.pdf
95 Bill Freese, �The StarLink Affair, Submission by Friends of the Earth to the FIFRA Scientific Advisory Panel considering Assessment of
Additional Scientific Information Concerning StarLink Corn,� July 17�19, 2001.
96 FDA Letter, Letter from Alan M. Rulis, Office of Premarket Approval, Center for Food Safety and Applied Nutrition, FDA to Dr. Kent Croon,
Regulatory Affairs Manager, Monsanto Company, Sept 25, 1996. See Letter for BNF No. 34 at
www.fda.gov/Food/Biotechnology/Submissions/ucm161107.htm
97 �Elements of Precaution: Recommendations for the Regulation of Food Biotechnology in Canada; An Expert Panel Report on the Future of
Food Biotechnology prepared by The Royal Society of Canada at the request of Health Canada Canadian Food Inspection Agency and
Environment Canada� The Royal Society of Canada, January 2001. www.canadians.org/food/documents/rsc_feb05.pdf
98 FIFRA Scientific Advisory Panel (SAP), Open Meeting, July 17, 2001. www.epa.gov/scipoly/sap/meetings/2001/july/julyfinal.pdf
99 Bill Freese, Crop testing, New Scientist, Letter to the Editor, issue 2530, December 17, 2005
100 M. Cretenet, J. Goven, J. A. Heinemann, B. Moore, and C. Rodriguez-Beltran, �Submission on the DAR for application A549 Food Derived
from High-Lysine Corn LY038: to permit the use in food of high-lysine corn, 2006, www.inbi.canterbury.ac.nz
101 Marc Lapp� and Britt Bailey, �ASA Response,� June 25, 1999, www.environmentalcommons.org/cetos/articles/asaresponse.html
102 Bill Freese, �The StarLink Affair, Submission by Friends of the Earth to the FIFRA Scientific Advisory Panel considering Assessment of
Additional Scientific Information Concerning StarLink Corn,� July 17-19, 2001
103 Paul P. Groenewegen, Brian W. McBride, John H. Burton, Theodore H. Elsasser. “Bioactivity of Milk from bST-Treated Cows.” J. Nutrition
120, 1990, pp. 514-519
104 Judith C. Juskevich and C. Greg Guyer. “Bovine Growth Hormone: Human Food Safety Evaluation.” Science, vol. 249. August 24, 1990, pp.
875-884
105 Pete Hardin, �rbGH: Appropriate Studies Haven�t Been Done,� The Milkweed, July 2000
106 See for example, Doug Gurian-Sherman, �Holes in the Biotech Safety Net, FDA Policy Does Not Assure the Safety of Genetically Engineered
Foods,� Center for Science in the Public Interest, www.cspinet.org/new/pdf/fda_report__final.pdf
107 S. R. Padgette, N. B.Taylor, D. L. Nida, M. R. Bailey, J. MacDonald, L. R. Holden, R. L. Fuchs, �The composition of glyphosate-tolerant
soybean seeds is equivalent to that of conventional soybeans,� J. Nutr. 126 (1996):702�716.
108 B. G. Hammond, J. L. Vicini, G. F. Hartnell, M. W. Naylor, C. D. Knight, E. H. Robinson, R. L. Fuchs, and S. R. Padgette, �The feeding
value of soybeans fed to rats, chickens, catfish, and dairy cattle is not altered by genetic incorporation of glyphosate tolerance,� J. Nutr. 126
(1996): 717�727.
109 A. Pusztai and S. Bardocz, �GMO in animal nutrition: potential benefits and risks,� Chapter 17, Biology of Nutrition in Growing Animals
(Elsevier, October 2005). earlier
110 Ian F. Pryme and Rolf Lembcke, �In Vivo Studies on Possible Health Consequences of Genetically Modified Food and Feed�with Particular
Regard to Ingredients Consisting of Genetically Modified Plan Materials,� Nutrition and Health 17(2003): 1�8.
111 Andreas Rang, et al, �Detection of RNA variants transcribed from the transgene in Roundup Ready soybean,� Eur Food
Res Technol 220 (2005): 438�443.
112 Ian F. Pryme and Rolf Lembcke, �In Vivo Studies on Possible Health Consequences of Genetically Modified Food and Feed�with Particular
Regard to Ingredients Consisting of Genetically Modified Plan Materials,� Nutrition and Health 17(2003): 1�8.
113 Arpad Pusztai, �Can science give us the tools for recognizing possible health risks of GM food,� Nutrition and Health, 2002, Vol 16 Pp 73-84;
Stanley W. B. Ewen and Arpad Pusztai, �Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small
intestine,� Lancet, 1999 Oct 16; 354 (9187): 1353-4; Arpad Pusztai, �Genetically Modified Foods: Are They a Risk to Human/Animal Health?�
June 2001 Action Bioscience www.actionbioscience.org/biotech/pusztai.html; and A. Pusztai and S. Bardocz, �GMO in animal nutrition:
potential benefits and risks,� Chapter 17, Biology of Nutrition in Growing Animals, R. Mosenthin, J. Zentek and T. Zebrowska (Eds.) Elsevier,
October 2005
114 V. E. Prescott, et al, �Transgenic Expression of Bean r-Amylase Inhibitor in Peas Results in Altered Structure and Immunogenicity,� Journal
of Agricultural Food Chemistry (2005): 53.
115 J. Lexchin, L. A. Bero, B. Djulbegovic, and O. Clark, �Pharmaceutical industry sponsorship and research outcome and quality: systematic
review,� BMJ 326 (2003):1167�1176.
116 Mark Friedberg, et al, �Evaluation of Conflict of Interest in Economic Analyses of New Drugs Used in Oncology,� JAMA 282 (1999):1453�
1457.
117 Suzanne Wuerthele quoted here: archive.sare.org/sanet-mg/archives/html-home/23-html/0195.html
118 �Elements of Precaution,� The Royal Society of Canada, January 2001. www.canadians.org/food/documents/rsc_feb05.pdf
119 Friends of the Earth Europe, �Throwing Caution to the Wind: A review of the European Food Safety Authority and its work on genetically
modified foods and crops,� November 2004.
120 European Communities submission to World Trade Organization dispute panel, 28 January 2005, reported in Hidden uncertainties – risks of
GMOs, 23 April 2006, Friends of the Earth / Greenpeace www.non-gm-farmers.com/news_print.asp?ID=2731
121 EU Regulation 178/2002 (Article 30.4)
122 Friends of the Earth Europe, �Throwing Caution to the Wind: A review of the European Food Safety Authority and its work on genetically
modified foods and crops,� November 2004.
123 �Greenpeace exposes Government-Monsanto nexus to cheat Indian farmers: calls on GEAC to revoke BT cotton permission,� Press release,
March 3, 2005, www.greenpeace.org/india_en/news/details?item_id=771071
124 Jeffrey M. Smith, Seeds of Deception, (Iowa: Yes! Books, 2003), 224.
125 �Monsanto Bribery Charges in Indonesia by DoJ and USSEC,� Third World Network, Malaysia, Jan 27, 2005,
www.mindfully.org/GE/2005/Monsanto-Indonesia-Bribery27jan05.htm
126 Jeffrey M. Smith, Seeds of Deception, Yes! Books, Fairfield, Iowa 2003
127 Karen Charman, The Professor Who Can Read Your Mind, PR Watch Newsletter Fourth Quarter 1999, Volume 6, No. 4
128 www.gmwatch.org/latest-listing/41-2002/3068-support-for-food-biotechnology-holds-in-the-us-
129 Estimates of increased IGF-1 levels vary considerably. In Mepham et al, �Safety of milk from cows treated with bovine somatotropin,� The
Lancet 2 (1994):197, IGF-1 levels were up to 10 times higher. The methods used may also underestimate IGF-1 levels considerably. See Samuel
S. Epstein, �Unlabeled Milk From Cows Treated With Biosynthetic Growth Hormones: A Case of Regulatory Abdication,� International Journal
of Health Services 26(1996): 173�185; and Samuel S. Epstein, What�s In Your Milk? (Victoria, British Columbia, Canada:Trafford Publishing,
2006), 197�204.
130 For a review of literature linking elevated levels of IGF-1 with increased risks of breast, colon and prostate cancers, see Samuel S. Epstein,
What�s In Your Milk?, 197�204.
131 Gary Steinman, �Mechanisms of Twinning VII. Effect of Diet and Heredity on the Human Twinning Rate,� Journal of Reproductive
Medicine, May 2006; S.E. Echternkamp et al, �Ovarian Follicular Development in Cattle Selected for Twin Ovulations and Births,� Journal of
Animal Science 82 no. 2 (2004): 459�471; and S. E. Echternkamp et al, �Concentrations of insulin-like growth factor-I in blood and ovarian
follicular fluid of cattle selected for twins,� Biology of Reproduction, 43(1990): 8�14.
132 Powell D.A.; Blaine K.; Morris S.; Wilson J., Agronomic and consumer considerations for Bt and conventional sweet-corn, British Food
Journal, Volume: 105, Issue: 10, Page: 700-713 (Nov 2003)
133 GM Nation? The findings of the public debate, www.gmnation.org.uk/ut_09/ut_9_6.htm#summary
134 To see the Toronto Star photo in Laidlaw�s book, go to www.gmwatch.org/p1temp.asp?pid=72&page=1 or
www.powerbase.info/index.php/Shane_Morris
135 Corn Fakes, Private Eye, No. 1194, 28 September-11 October 2007 www.gmwatch.org/latest-listing/46-2007/7525-award-winningpaper-qa-flagrant-fraudq-cambridge-expert-2692007
136 Tim Lambert, Would you eat wormy corn?, September 7 2007
scienceblogs.com/deltoid/2007/09/would_you_eat_wormy_sweet_corn.php
137 �Genetically modified foods, who knows how safe they are?� CBC News and Current Affairs, September 25, 2006.
138 Mike Zelina, et al., The Health Effects of Genetically Engineered Crops on San Luis Obispo County,� A Citizen Response to the SLO Health
Commission GMO Task Force Report, 2006.
139 Bill Lambrecht, Dinner at the New Gene Caf�, St. Martin’s Press, September 2001, pg 139
Photo credits
Stanley W. B. Ewen and Arpad Pusztai, �Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small
intestine,� Lancet, 1999 Oct 16; 354 (9187): 1353-4.
M. Malatesta, C. Caporaloni, S. Gavaudan, M. B. Rocchi, S. Serafini, C. Tiberi, G. Gazzanelli, �Ultrastructural Morphometrical and
Immunocytochemical Analyses of Hepatocyte Nuclei from Mice Fed on Genetically Modified Soybean,� Cell Struct Funct. 27 (2002): 173�180
Irina Ermakova, �Experimental Evidence of GMO Hazards,� Presentation at Scientists for a GM Free Europe, EU Parliament, Brussels, June 12,
2007
Irina Ermakova, �Genetically modified soy leads to the decrease of weight and high mortality of rat pups of the first generation. Preliminary
studies,� Ecosinform 1 (2006): 4�9.

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Boosting Energy with Hypothyroidism | Wellness Clinic

Boosting Energy with Hypothyroidism | Wellness Clinic

The cornerstone of treating hypothyroidism and reducing its symptom involves following the proper treatment. People with hypothyroidism receive the maximum relief from exhaustion when they balance their thyroid-stimulating hormone (TSH) levels, often to below 2.5 milliunits per liter (mU/L), based on study published in the Kansas Journal of Medicine.

 

“Most experts agree that after hypothyroidism is diagnosed, 1 mU/L into 3 mU/L has been an appropriate TSH range,” explains Victor Bernet, MD, an endocrinologist and assistant professor of medicine at the Mayo Clinic in Jacksonville, Fla.. However, it may take time to achieve that goal, and your symptoms, such as energy, could persist for awhile. Managing fatigue as you wait is an issue of making healthy lifestyle choices and getting enough sleep.

 

Take the Recommended Treatment

 

The good news about hypothyroidism treatment is that thyroid medication is successful for most people, especially when taken as prescribed. This means that you should follow your physician’s instructions. The most severe cases of hypothyroidism see symptoms improve with treatment within six months, states Jan Hoffman, MD, an endocrinologist and leader of the section of endocrinology at the Via Christi Clinic in Wichita, Kan.. But some individuals may continue to feel tiredness. For these individuals, Dr. Hoffman suggests medication adjustments to comprise both the T3 and T4 hormones. This is not yet a mainstream treatment, if you haven’t been getting good results from your present drug 35, about trying it, but you might talk to your primary care doctor or endocrinologist.

 

Balance Your Diet

 

Eating a nutritious diet rich in fruits and vegetables, whole grains, and proteins can help give you. Cut back on added sugars, which can increase the fatigue you are feeling out of migraines. “There is certainly an advantage to maintaining a wholesome, well-balanced diet with regular exercise to improve health generally,” Hoffman says. Because sleep quality can be reduced by this, additionally you may need to avoid eating large meals within a few hours of bedtime. Instead, opt for a dinner and a snack before bed.

 

Try Cognitive Behavioral Therapy

 

Cognitive behavioral therapy (CBT) is a style of therapy that helps you to change negative thought patterns and replace them with more positive ones. In studies looking at physical action, CBT, and fatigue, researchers have observed that this kind of therapy appears to help people feel like they’re more active or capable of being active, and so less fatigued, even if they aren’t really increasing their physical activity levels. This is in part as counter the belief that you’re simply tired from the consequences of hypothyroidism to do anything and one tactic of CBT is to assist you.

 

Limit Alcohol and Caffeine

 

If you’re fighting fatigue from hypothyroidism, it’s easy to slip into a cycle of drinking lots of drinks during the day and then using a nightcap to bring you back down. It will not tackle fatigue although caffeine can occasionally give you a elevator, such as feeling perkier in the morning. What’s worse, this cycle of caffeine and alcohol to wind down could be sapping your energy over and beyond the fatigue. Both caffeine and alcohol interfere with your body’s ability to achieve sleep. Cut back on carbonated beverages, adhering before noon, and have one alcoholic beverage if any, in the day.

 

Engage in Physical Activity

 

You may believe eczema has left you but physical activity, even a little at a time, can help counter fatigue, enhance your energy levels also improve your sleep quality. Try for the national recommendations for physical activity that is healthy: being active for at least 30 minutes. Exercising in the evening can make it difficult to get to sleep later try to schedule your workouts for earlier in the day.

 

Take Steps to Sleep More Soundly

 

Obtaining enough high-quality sleep people need seven can help fight fatigue. Deep sleep requires the appropriate “stage”: A slightly cool, dark, sound-free site. To get your body to the sleep rhythm, set a regular time to go to wake up and to sleepon weekends and holidays. If you’ve taken these measures to boost your sleep however are still lacking energy during the day and suspect you are not sleeping well, think about a sleep evaluation to determine if you have some sleeping disorders, such as sleep apnea, that may be robbing you of a good night’s sleep.

 

Stop Smoking

 

Nicotine is a stimulant. So even though smoking can feel as a relaxing routine, it’s interfering with your sleep quality and, in turn, adding to fatigue. Individuals who stop smoking find that once they’ve made it during the withdrawal period, they’ve sleep and more energy. Smoking is known to contribute to autoimmune disease, which might be challenging your hypothyroidism treatment plan’s development. Take note that hypothyroidism can be also complicated by smoking cessation, so be certain you quit smoking under the supervision of your doctor.

 

Get Routine Medical Tests

 

Dr. Bernet contrasts thyroid function into a well-functioning vehicle. “If your car is acting up and your oil is low or you have not changed it in awhile, you need oil,” he says. This is the equivalent of taking medication to get your thyroid hormone levels back to normal. This, too, applies to sleeplessness therapy. If your thyroid screening indicates you are at normal levels after treatment but you are still feeling exhausted, ask for further evaluation. About one in five people experience fatigue, but hypothyroidism is simply one cause of exhaustion that is ongoing.

 

The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
 

By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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TRENDING TOPIC: EXTRA EXTRA: About Chiropractic

 

 

About Thyroid Disease and Fatigue | Wellness Clinic

About Thyroid Disease and Fatigue | Wellness Clinic

Are you tired of being tired? Whatever you call it, exhaustion, fatigue, lethargy, or feeling run down, overtired, or just plainly pooped out, fatigue is a frequent symptom associated with thyroid disease.

 

How does thyroid disease cause fatigue?

 

We’re not talking about regular fatigue after a late night. This is a debilitating fatigue. You might find yourself needing a rest in the afternoon to endure until dinnertime. Or you wake up tired and still sleep ten to twelve hours a night. Or you’re less able to work out, and your endurance is reduced because you are weak and lethargic. Or brain-fogged and exhausted out may just walk around about exactly the quantity of sleep that used to make you feeling refreshed.

 

There are a number of important things to know about the connections between thyroid disease and fatigue, and ten of the most significant things to know about boosting your energy and battling fatigue are mentioned below.

 

Fatigue and Hypothyroidism

 

Fatigue is a really common symptom of hypothyroidism, an underactive or reduced thyroid function, in many individuals. Many patients report that their fatigue is diminished or even completely solved after the treatment for hypothyroidism is optimized. Various treatment approaches, including functional medicine can help improve hypothyroidism.

 

Fatigue and Hyperthyroidism

 

Fatigue is also a symptom of hyperthyroidism, an overactive or increased thyroid function, in some patients. Exhaustion is present even when you have gotten an adequate quantity of sleep. In other scenarios, exhaustion or fatigue associated with hyperthyroidism may result from insomnia, anxiety, or disrupted sleep patterns. Typically, treatment for hyperthyroidism can help resolve the patient’s overall symptoms.

 

Autoimmune Thyroid Disease and Fatigue

 

Even when thyroid function tests demonstrate that the thyroid gland is “normal” and hormone levels fall within the benchmark range, the existence of elevated thyroid antibodies, which may indicate autoimmune Hashimoto’s disease or Graves’ disease, may lead to fatigue as a symptom in some patients.

 

Dietary Changes

 

Some thyroid patients, including individuals who don’t have celiac disease or gluten intolerance, have reported a decrease in fatigue when they switch into a gluten-free diet plan. A gluten-free diet is a nutrition plan free of wheat and gluten products. Others have reported similar effects by removing sugar, dairy, or other foods in the diet.

 

Unrefreshing Sleep

 

Some people experience fatigue due to what is called unrefreshing sleep. This indicates that you’ve had enough sleep seven or more hours, but you wake up and feel tired, because the sleep has been of poor quality, interrupted, or did not reach levels that are restorative. Unrefreshing sleep could be associated with dysfunction, in addition to chronic fatigue syndrome and fibromyalgia in most cases.

 

Iron

 

Some thyroid patients suffering from fatigue may be reduced in iron, in particular, the saved form of iron known as ferritin. It is worth having ferritin levels assessed by your healthcare professional, and if they are not optimal (in the upper end of the reference range), talk with your doctor about supplementing with iron, or even incorporating more iron to your diet through foods. An excess of iron, in particular, a hereditary condition called hemochromatosis, may also be related to fatigue. There is a link between thyroid conditions and an increased probability of hemochromatosis.

 

Chronic Fatigue Syndrome and Fibromyalgia

 

In case you have long-term, debilitating fatigue, and the tiredness is accompanied by other symptoms like enlarged lymph nodes, a chronic sore throat, and/or body/muscle aches pains, you may have other conditions such as chronic fatigue syndrome and/or fibromyalgia. These conditions are common in thyroid patients than in the general populace.

 

T3 and Natural Thyroid

 

Some thyroid patients on thyroid hormone replacement have reported a rise in their exhaustion levels or fatigue when switching from a T4 only treatment (i.e., levothyroxine), to some T4/T3 treatment, for example, the inclusion of artificial T3, or use of a natural desiccated thyroid medication.

 

Sleep Apnea

 

Thyroid patients are at greater risk of sleep apnea, and at which breathing stops for short periods during sleep. Sleep apnea can contribute to fatigue, due to an improper oxygen intake when sleeping. Thyroid patients experiencing fatigue should speak with a healthcare professional about having a sleep study or evaluation completed to determine if sleep abnormalities, such as apnea, may be contributing to the fatigue.

 

Get Better and More Sleep

 

Be sure you receive optimum treatment for your thyroid illness and address any sleeping disorders, food sensitivities, and imbalances on your iron levels. Also, make sure you get adequate sleep. According to the National Sleep Foundation, many adults need a minimum of seven to eight hours each night, and a considerable proportion of us aren’t currently getting this level of sleep on a regular basis.

 

Here are some tips to help avoid fatigue by getting better and more sleep:

 

  • Try to maintain the same sleep schedule weekdays and weekends
  • Keep your bedroom cool
  • Don’t watch television or work in your bedroom
  • Avoid alcohol and caffeine in the day, and before bedtime
  • Don’t take naps
  • Don’t exercise after dinner period
  • Have a hot shower or bath before bedtime
  • Use a sound conditioner or earplugs to block noise
  • Avoid large meals before bedtime
  • Boost light exposure during the day
  • Minimize lighting into your bedroom by using blinds or blackout curtains, turn off tv and computer at night, prevent illuminated clocks, and don’t read from or look at backlit devices or smart phones at nighttime
  • Listen to relaxation or guided imagery audios to help fall asleep.
  • Do not drink too much liquid in the evening
  • Restrict changes in your job shifts
  • Drink a natural or relaxation tea at bedtime
  • Have a bedtime snack with protein

 

The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
 

By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

blog picture of cartoon paperboy big news

 

TRENDING TOPIC: EXTRA EXTRA: About Chiropractic

 

 

Three Metabolic Energy Systems

Three Metabolic Energy Systems

Personal Training 101

energy personal trainer

How You Get Energy & How You Use It

energy asparagus eggs tomatos We usually talk of energy in general terms, as in �I don�t have a lot of energy today� or �You can feel the energy in the room.� But what really is energy? Where do we get the energy to move? How do we use it? How do we get more of it? Ultimately, what controls our movements? The three metabolic energy pathways are the�phosphagen system, glycolysis�and the�aerobic system.�How do they work, and what is their effect?

Albert Einstein, in his infinite wisdom, discovered that the total energy of an object is equal to the mass of the object multiplied by the square of the speed of light. His formula for atomic energy, E = mc2, has become the most recognized mathematical formula in the world. According to his equation, any change in the energy of an object causes a change in the mass of that object. The change in energy can come in many forms, including mechanical, thermal, electromagnetic, chemical, electrical or nuclear. Energy is all around us. The lights in your home, a microwave, a telephone, the sun; all transmit energy. Even though the solar energy that heats the earth is quite different from the energy used to run up a hill, energy, as the first law of thermodynamics tells us, can be neither created nor destroyed. It is simply changed from one form to another.

ATP Re-Synthesis

energyThe energy for all physical activity comes from the conversion of high-energy phosphates (adenosine�triphosphate�ATP) to lower-energy phosphates (adenosine�diphosphate�ADP; adenosine�monophosphate�AMP; and inorganic phosphate, Pi). During this breakdown (hydrolysis) of ATP, which is a water-requiring process, a proton, energy and heat are produced: ATP + H2O ��ADP + Pi�+ H+�+ energy + heat. Since our muscles don�t store much ATP, we must constantly resynthesize it. The hydrolysis and resynthesis of ATP is thus a circular process�ATP is hydrolyzed into ADP and Pi, and then ADP and Pi�combine to resynthesize ATP. Alternatively, two ADP molecules can combine to produce ATP and AMP: ADP + ADP ��ATP + AMP.

Like many other animals, humans produce ATP through three metabolic pathways that consist of many enzyme-catalyzed chemical reactions: the phosphagen system, glycolysis and the aerobic system. Which pathway your clients use for the primary production of ATP depends on how quickly they need it and how much of it they need. Lifting heavy weights, for instance, requires energy much more quickly than jogging on the treadmill, necessitating the reliance on different energy systems. However, the production of ATP is never achieved by the exclusive use of one energy system, but rather by the coordinated response of all energy systems contributing to different degrees.

1. Phosphagen System

energy woman sit-ups on machineDuring short-term, intense activities, a large amount of power needs to be produced by the muscles, creating a high demand for ATP. The phosphagen system (also called the ATP-CP system) is the quickest way to resynthesize ATP (Robergs & Roberts 1997). Creatine phosphate (CP), which is stored in skeletal muscles, donates a phosphate to ADP to produce ATP: ADP + CP ��ATP + C. No carbohydrate or fat is used in this process; the regeneration of ATP comes solely from stored CP. Since this process does not need oxygen to resynthesize ATP, it is anaerobic, or oxygen-independent. As the fastest way to resynthesize ATP, the phosphagen system is the predominant energy system used for all-out exercise lasting up to about 10 seconds. However, since there is a limited amount of stored CP and ATP in skeletal muscles, fatigue occurs rapidly.

2. Glycolysis

energyGlycolysis is the predominant energy system used for all-out exercise lasting from 30 seconds to about 2 minutes and is the second-fastest way to resynthesize ATP. During glycolysis, carbohydrate�in the form of either blood glucose (sugar) or muscle glycogen (the stored form of glucose)�is broken down through a series of chemical reactions to form pyruvate (glycogen is first broken down into glucose through a process called�glycogenolysis). For every molecule of glucose broken down to pyruvate through glycolysis, two molecules of usable ATP are produced (Brooks et al. 2000). Thus, very little energy is produced through this pathway, but the trade-off is that you get the energy quickly. Once pyruvate is formed, it has two fates: conversion to lactate or conversion to a metabolic intermediary molecule called acetyl coenzyme A (acetyl-CoA), which enters the mitochondria for oxidation and the production of more ATP (Robergs & Roberts 1997). Conversion to lactate occurs when the demand for oxygen is greater than the supply (i.e., during anaerobic exercise). Conversely, when there is enough oxygen available to meet the muscles� needs (i.e., during aerobic exercise), pyruvate (via acetyl-CoA) enters the mitochondria and goes through aerobic metabolism.

When oxygen is not supplied fast enough to meet the muscles� needs (anaerobic glycolysis), there is an increase in hydrogen ions (which causes the muscle pH to decrease; a condition called acidosis) and other metabolites (ADP, Pi�and potassium ions). Acidosis and the accumulation of these other metabolites cause a number of problems inside the muscles, including inhibition of specific enzymes involved in metabolism and muscle contraction, inhibition of the release of calcium (the trigger for muscle contraction) from its storage site in muscles, and interference with the muscles� electrical charges (Enoka & Stuart 1992; Glaister 2005; McLester 1997). As a result of these changes, muscles lose their ability to contract effectively, and muscle force production and exercise intensity ultimately decrease.

3. Aerobic System

energySince humans evolved for aerobic activities (Hochachka, Gunga & Kirsch 1998; Hochachka & Monge 2000), it�s not surprising that the aerobic system, which is dependent on oxygen, is the most complex of the three energy systems. The metabolic reactions that take place in the presence of oxygen are responsible for most of the cellular energy produced by the body. However, aerobic metabolism is the slowest way to resynthesize ATP. Oxygen, as the patriarch of metabolism, knows that it is worth the wait, as it controls the fate of endurance and is the sustenance of life. �I�m oxygen,� it says to the muscle, with more than a hint of superiority. �I can give you a lot of ATP, but you will have to wait for it.�

The aerobic system�which includes the�Krebs cycle�(also called the�citric acid cycle or TCA cycle) and the�electron transport chain�uses blood glucose, glycogen and fat as fuels to resynthesize ATP in the mitochondria of muscle cells (see the sidebar �Energy System Characteristics�). Given its location, the aerobic system is also called�mitochondrial respiration.�When using carbohydrate, glucose and glycogen are first metabolized through glycolysis, with the resulting pyruvate used to form acetyl-CoA, which enters the Krebs cycle. The electrons produced in the Krebs cycle are then transported through the electron transport chain, where ATP and water are produced (a process called�oxidative phosphorylation) (Robergs & Roberts 1997). Complete oxidation of glucose via glycolysis, the Krebs cycle and the electron transport chain produces 36 molecules of ATP for every molecule of glucose broken down (Robergs & Roberts 1997). Thus, the aerobic system produces 18 times more ATP than does anaerobic glycolysis from each glucose molecule.

energyFat, which is stored as triglyceride in adipose tissue underneath the skin and within skeletal muscles (called�intramuscular triglyceride), is the other major fuel for the aerobic system, and is the largest store of energy in the body. When using fat, triglycerides are first broken down into free fatty acids and glycerol (a process called�lipolysis). The free fatty acids, which are composed of a long chain of carbon atoms, are transported to the muscle mitochondria, where the carbon atoms are used to produce acetyl-CoA (a process called�beta-oxidation).

Following acetyl-CoA formation, fat metabolism is identical to carbohydrate metabolism, with acetyl-CoA entering the Krebs cycle and the electrons being transported to the electron transport chain to form ATP and water. The oxidation of free fatty acids yields many more ATP molecules than the oxidation of glucose or glycogen. For example, the oxidation of the fatty acid palmitate produces 129 molecules of ATP (Brooks et al. 2000). No wonder clients can sustain an aerobic activity longer than an anaerobic one!

Understanding how energy is produced for physical activity is important when it comes to programming exercise at the proper intensity and duration for your clients. So the next time your clients get done with a workout and think, �I have a lot of energy,� you�ll know exactly where they got it.

Energy System Characteristics
energy

Energy System Workouts

Have clients warm up and cool down before and after each workout.

Phosphagen System

An effective workout for this system is short, very fast sprints on the treadmill or bike lasting 5�15 seconds with 3�5 minutes of rest between each. The long rest periods allow for complete replenishment of creatine phosphate in the muscles so it can be reused for the next interval.

  • 2 sets of 8 x 5 seconds at close to top speed with 3:00 passive rest and 5:00 rest between sets
  • 5 x 10 seconds at close to top speed with 3:00�4:00 passive rest

Glycolysis

This system can be trained using fast intervals lasting 30 seconds to 2 minutes with an active-recovery period twice as long as the work period (1:2 work-to-rest ratio).

  • 8�10 x 30 seconds fast with 1:00 active recovery
  • 4 x 1:30 fast with 3:00 active recovery

Aerobic System

While the phosphagen system and glycolysis are best trained with intervals, because those metabolic systems are emphasized only during high-intensity activities, the aerobic system can be trained with both continuous exercise and intervals.

  • 60 minutes at 70%�75% maximum heart rate
  • 15- to 20-minute tempo workout at lactate threshold intensity (about 80%�85% maximum heart rate)
  • 5 x 3:00 at 95%�100% maximum heart rate with 3:00 active recovery

by�Jason Karp, PhD

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References:

Brooks, G.A., et al. 2000.�Exercise Physiology: Human Bioenergetics and Its Applications.Mountain View, CA: Mayfield.

Enoka, R.M., & Stuart, D.G. 1992. Neurobiology of muscle fatigue.�Journal of Applied Physiology, 72�(5), 1631�48.

Glaister, M. 2005. Multiple sprint work: Physiological responses, mechanisms of fatigue and the influence of aerobic fitness.�Sports Medicine, 35�(9), 757�77.

Hochachka, P.W., Gunga, H.C., & Kirsch, K. 1998. Our ancestral physiological phenotype: An adaptation for hypoxia tolerance and for endurance performance?�Proceedings of the National Academy of Sciences, 95,�1915�20.

Hochachka, P.W., & Monge, C. 2000. Evolution of human hypoxia tolerance physiology.�Advances in Experimental and Medical Biology, 475,�25�43.

McLester, J.R. 1997. Muscle contraction and fatigue: The role of adenosine 5′-diphosphate and inorganic phosphate.�Sports Medicine, 23�(5), 287�305.

Robergs, R.A. & Roberts, S.O. 1997.�Exercise Physiology: Exercise, Performance, and Clinical Applications.�Boston: William C. Brown.

Dietary Strategies: Treatment Of Metabolic Syndrome

Dietary Strategies: Treatment Of Metabolic Syndrome

Dietary Strategies:

Abstract: Metabolic syndrome (MetS) is established as the combination of central obesity and different metabolic disturbances, such as insulin resistance, hypertension and dyslipidemia. This cluster of factors affects approximately 10%�50% of adults worldwide and the prevalence has been increasing in epidemic proportions over the last years. Thus, dietary strategies to treat this heterogenic disease are under continuous study. In this sense, diets based on negative-energy-balance, the Mediterranean dietary pattern, n-3 fatty acids, total antioxidant capacity and meal frequency have been suggested as effective approaches to treat MetS. Furthermore, the type and percentage of carbohydrates, the glycemic index or glycemic load, and dietary fiber content are some of the most relevant aspects related to insulin resistance and impaired glucose tolerance, which are important co-morbidities of MetS. Finally, new studies focused on the molecular action of specific nutritional bioactive compounds with positive effects on the MetS are currently an objective of scientific research worldwide. The present review summarizes some of the most relevant dietary approaches and bioactive compounds employed in the treatment of the MetS to date.

Keywords: metabolic syndrome; dietary strategies; bioactive compounds

1. Metabolic Syndrome

dietary healthy unhealthy foodIt was during the period between 1910 and 1920 when it was suggested for the first time that a cluster of associated metabolic disturbances tended to coexist together [1]. Since then, different health organisms have suggested diverse definitions for metabolic syndrome (MetS) but there has not yet been a well-established consensus. The most common definitions are summarized in Table 1. What is clear for all of these is that the MetS is a clinical entity of substantial heterogeneity, commonly represented by the combination of obesity (especially abdominal obesity), hyperglycemia, dyslipidemia and/or hypertension [2�6].

dietary table 1

Obesity consists of an abnormal or excessive fat accumulation, for which the main cause is a chronic imbalance between energy intake and energy expenditure [7,8]. The excess of energy consumed is primarily deposited in the adipose tissue as triglycerides (TG) [9].

Dyslipidemia encompasses elevated serum TG levels, increased low density lipoprotein- cholesterol (LDL-c) particles, and reduced levels of high density lipoprotein-cholesterol (HDL-c) [10]. It is associated with hepatic steatosis [11], dysfunction of pancreatic ?-cells [12] and elevated risk of atherosclerosis [13], among others.

Another main modifiable MetS manifestation is hypertension, which is mainly defined as a resting systolic blood pressure (SBP) ? 140 mmHg or diastolic blood pressure (DBP) ? 90 mmHg or drug prescription to lower hypertension [14]. It usually involves narrowed arteries and is identified as a major cardiovascular and renal risk factor, related to heart and vascular disease, stroke and myocardial infarction [13,15�17].

Hyperglycemia, related insulin resistance and type 2 diabetes mellitus are characterized by an impaired uptake of glucose by the cells, that lead to elevated plasma glucose levels, glycosuria and ketoacidosis [18]. It is responsible for different tissue damage that shortens the life expectancy of diabetics, involving cardiovascular diseases (CVD), atherosclerosis, hypertension [19], ?-cell dysfunction [12], kidney disease [20] or blindness [21]. Currently, diabetes is considered the leading cause of death in developed countries [22].

Moreover, oxidative stress and low grade inflammation are two important mechanisms implicated in the etiology, pathogenesis, and development of MetS [23]. Oxidative stress is defined as an imbalance between the pro-oxidants and antioxidants in the body [24]. It plays a key role in the development of atherosclerosis by different mechanisms such as the oxidation of LDL-c particles [25] or impairment of HDL-c functions [26]. Inflammation is an immune system response to injury hypothesized to be a major mechanism in the pathogenesis and progression of obesity related disorders and the link between adiposity, insulin resistance, MetS and CVD [27].

Although the prevalence of the MetS varies broadly around the word and depends on the source used for its definition, it is clear that over the last 40�50 years the number of people presenting with this syndrome has risen in epidemic proportions [28]. Moreover, the frequency of this syndrome is increased in developed countries, sedentary people, smokers, low socioeconomic status population, as well as in individuals with unhealthy dietary habits [29,30].

For all of this, there is currently a wide concern to find effective strategies to detect, treat and control the comorbidities associated with MetS. This is a complex challenge as MetS is a clinical entity of substantial heterogeneity and therefore, the different cornerstones implicated in its development should be addressed. In this review we compiled and examined different dietary patterns and bioactive compounds that have pointed out to be effective in MetS treatment.

2. Dietary Patterns

dietarySeveral dietary strategies and their potential positive effects on the prevention and treatment of the different metabolic complications associated to the MetS, are described below and summarized in Table 2.

dietary table 22.1. Energy-Restricted Diet Strategies

dietary

Energy restricted diets are probably the most commonly used and studied dietary strategies for combating excess weight and related comorbidities. They consist in personalized regimes that supply less calories than the total energy expended by a specific individual [31].

A hypocaloric diet results in a negative energy balance and subsequently, in body weight reduction [31]. Weight loss is achieved via fat mobilization from different body compartments as a consequence of the lipolysis process necessary to provide energy substrate [32,33]. In people who are overweight or suffering from obesity, as is the case of most people with MetS, weight loss is important as it is associated with improvement of related disorders such as abdominal obesity (visceral adipose tissue), type 2 diabetes, CVD or inflammation [32�36].

Moreover, as described above, low grade inflammation is associated with MetS and obesity. Therefore, of particular importance is the fact that in obese individuals following a hypocaloric diet, a depletion of plasma inflammatory markers such as interleukin (IL)-6 has been observed [34]. Thus, caloric restriction in obese people suffering MetS may improve the whole-body pro-inflammatory state.

At the same time, body weight reduction is associated with improvements in cellular insulin signal transduction, increments in peripheral insulin sensitivity and higher robustness in insulin secretory responses [32,36]. People with excess body weight who are at risk of developing type 2 diabetes, may benefit from a hypocaloric regime by improving plasma glucose levels and insulin resistance.

In addition, different intervention trials have reported a relationship between energy restricted diets and lower risk of developing CVD. In this sense, in studies with obese people following a hypocaloric diet, improvements in lipid profile variables such as reductions of LDL-c and plasma�TG levels, as well as improvements in hypertension via depletion of SBP and DBP levels have been observed [35,37].

Among the different nutritional intervention trials, a reduction of 500�600 kcal a day of the energy requirements is a well-established hypocaloric dietary strategy, which has demonstrated to be effective in weight reduction [38,39]. However, the challenge lies in maintaining the weight loss over time, as many subjects can follow a prescribed diet for a few months, but most people have difficulty in maintaining the acquired habits over the long term [40,41].

2.2. Diets Rich in Omega-3 Fatty Acids

dietary foods omega 3 infographicThe very long-chain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are essential omega-3 polyunsaturated fatty acids (n-3 PUFAs) for human physiology. Their main dietary sources are fish and algal oils and fatty fish, but they can also be synthesized by humans from ?-linolenic acid [40].

There is a moderate body of evidence suggesting that n-3 PUFAs, mainly EPA and DHA, have a positive role in the prevention and treatment of the pathologies associated to MetS [42].

In this context, it has been described that EPA and DHA have the ability to reduce the risk of developing CVD and cardiometabolic abnormalities as well as CVD-related mortality [42]. These beneficial effects are thought to be mainly due to the ability of these essential fatty acids to reduce plasma TG levels [43].

Moreover, different studies have shown that people following an increased n-3 PUFA diet have reduced plasma levels of the pro-inflammatory cytokines IL-6 and tumor necrosis factor-alpha (TNF?), as well as plasma C-reactive protein (CRP) [44]. These effects are probably mediated by resolvins, maresins and protectins, which are EPA and DHA metabolic products with anti-inflammatory properties [44].

There are some studies that have observed an association between n-3 ingestion and improvements or prevention of type 2 diabetes development. However, other studies found opposite results [44]. Thus, it cannot be made any specific affirmation in this respect.

The European Food Safety Authority recommends and intake of 250 mg EPA + DHA a day, in the general healthy population as a primary prevention of CVD [45]. These amounts can be achieved with an ingestion of 1�2 fatty fish meals per week [45].

2.3. Diets Based on Low Glycemic Index/Load

dietary salad unconstructedOver the last ten years, the concern about the quality of the carbohydrates (CHO) consumed has risen [46]. In this context, the glycemic index (GI) is used as a CHO quality measure. It consists in a ranking on a scale from 0 to 100 that classifies carbohydrate-containing foods according to the postprandial glucose response [47]. The higher the index, the more promptly the postprandial serum glucose rises and the more rapid the insulin response. A quick insulin response leads to rapid hypoglycemia, which is suggested to be associated with an increment of the feeling of hunger and to a subsequent higher caloric intake [47]. The glycemic load (GL) is equal to the GI multiplied by the number of grams of CHO in a serving [48].

There is a theory which states that MetS is a consequence of an elevated intake of high GI foods over time, among others unhealthy dietary habits [49]. In this sense, following a diet rich in high GI CHO has been associated with hyperglycemia, insulin resistance, type 2 diabetes, hypertriglyceridemia, CVD, and obesity [47,50,51], abnormalities directly related to MetS.

On the contrary, a low GI diet has been associated with slower absorption of the CHO and subsequently smaller blood glucose fluctuations, which indicate better glycemic control [46]. In patients with type 2 diabetes, diets based on low GI are associated with reductions in glycated hemoglobin (HbA1c) and fructosamine blood levels, two biomarkers used as key monitoring factors in diabetes management [52,53].

For all of this, it is common to find the limitation of CHO at high GI among the advice for MetS treatment [28], in particular with respect to �ready-to-eat processed foods� including sweetened beverages, soft drinks, cookies, cakes, candy, juice drinks, and other foods which contain high amounts of added sugars [54].

2.4. Diets with High Total Antioxidant Capacity

dietary antioxidant foodsDietary total antioxidant capacity (TAC) is an indicator of diet quality defined as the sum of antioxidant activities of the pool of antioxidants present in a food [55]. These antioxidants have the capacity to act as scavengers of free radicals and other reactive species produced in the organisms [56]. Taking into account that oxidative stress is one of the remarkable unfortunate physiological states of MetS, dietary antioxidants are of main interest in the prevention and treatment of this multifactorial disorder [57]. Accordingly, it is well-accepted that diets with a high content of spices, herbs, fruits, vegetables, nuts and chocolate, are associated with a decreased risk of oxidative stress-related diseases development [58�60]. Moreover, several studies have analyzed the effects of dietary TAC in individuals suffering from MetS or related diseases [61,62]. In the Tehran Lipid and Glucose Study it was demonstrated that a high TAC has beneficial effects on metabolic disorders and especially prevents weight and abdominal fat gain [61]. In the same line, research conducted in our institutions also evidenced that beneficial effects on body weight, oxidative stress biomarkers and other MetS features were positively related with higher TAC consumption in patients suffering from MetS [63�65].

In this sense, the World Health Organization (WHO) recommendation for fruit and vegetables consumption (high TAC foods) for the general population is a minimum of 400 g a day [66]. Moreover, cooking with spices is recommended in order to increase the TAC dietary intake and, at the same time, maintain flavor while reducing salt [67].

2.5. Moderate-High Protein Diets

dietary Protein rich FoodsThe macronutrient distribution set in a weight loss dietary plan has commonly been 50%�55% total caloric value from CHO, 15% from proteins and 30% from lipids [57,68]. However, as most people have difficulty in maintaining weight loss achievements over time [69,70], research on increment of protein intake (>20%) at the expense of CHO was carried out [71�77].

Two mechanisms have been proposed to explain the potential beneficial effects of high-moderate protein diets: the increment of diet-induced thermogenesis [73] and the increase of satiety [78]. The increment of the thermogenesis is explained by the synthesis of peptide bonds, production of urea and gluconeogenesis, which are processes with a higher energy requirement than the metabolism of lipids or CHO [75]. An increment of different appetite-control hormones such as insulin, cholecystokinin or glucagon-like peptide 1, may clarify the satiety effect [79].

Other beneficial effects attributed to moderate-high protein diets in the literature are the improvement of glucose homeostasis [80], the possibility of lower blood lipids [81], the reduction of blood pressure [82], the preservation of lean body mass [83] or the lower of cardiometabolic disease risk [84,85]. However, there are other studies that have not found benefits associated to a moderate-high protein diet [76]. This fact may be explained by the different type of proteins and their amino acid composition [80], as well as by the different type of populations included in each study [85]. Therefore, more research in the field is needed in order to make these results consistent.

In any case, when a hypocaloric diet is implemented, it is necessary to slightly increase the amount of proteins. Otherwise it would be difficult to reach the protein energy requirements, established as 0.83 g/kg/day for isocaloric diets and which should probably be at least 1 g/kg/day for energy-restricted diets [86].

2.6. High Meal Frequency Pattern

dietary eating time

The pattern of increasing meal frequency in weight loss and weight control interventions has currently become popular among professionals [87,88]. The idea is to distribute the total daily energy�intake into more frequently and smaller meals. However, there is no strong evidence about the efficacy of this habit yet [89]. While some investigations have found an inverse association between the increment of meals per day and body weight, body mass index (BMI), fat mass percentage or metabolic diseases such as coronary heart disease or type 2 diabetes [71,88,90�92], others have found no association [93�95].

Different mechanisms by which high meal frequency can have a positive effect on weight and metabolism management have been proposed. An increment of energy expenditure was hypothesized; however, the studies carried out in this line have concluded that total energy expenditure does not differ among different meal frequencies [96,97]. Another postulated hypothesis is that the greater the number of meals a day, the higher the fat oxidation, but again no consensus has been achieved [89,98]. An additional suggested mechanism is that increasing meal frequency leads to plasma glucose levels with lower oscillations and reduced insulin secretion which is thought to contribute to a better appetite control. However, these associations have been found in population with overweight or high glucose levels but in normal-weight or normoglycaemic individuals the results are still inconsistent [93,99�101].

2.7. The Mediterranean Diet

dietary Mediterranean DietThe concept of the Mediterranean Diet (MedDiet) was for the first time defined by the scientific Ancel Keys who observed that those countries around the Mediterranean Sea, which had a characteristic diet, had less risk of suffering coronary heart diseases [102,103].

The traditional MedDiet is characterized by a high intake of extra-virgin olive oil and plant foods (fruits, vegetables, cereals, whole grains, legumes, tree nuts, seeds and olives), low intakes of sweets and red meat and moderate consumption of dairy products, fish and red wine [104].

There is a lot of literature supporting the general health benefits of the MedDiet. In this sense, it has been reported that a high adherence to this dietary pattern protects against mortality and morbidity from several causes [105]. Thus, different studies suggested the MedDiet as a successful tool for the prevention and treatment of MetS and related comorbidities [106�108]. Moreover, recent meta-analysis concluded that the MedDiet is associated with less risk of developing type 2 diabetes and with a better glycemic control in people with this metabolic disorder [107,109,110]. Other studies have found a positive correlation between the adherence to a MedDiet pattern and reduced risk of developing CVD [111�114]. In fact, many studies have found a positive association between following a MedDiet and improvements in lipid profile by reduction of total cholesterol, LDL-c and TG, and an increase in HDL-c [111�115]. Finally, different studies also suggest that the MedDiet pattern may be a good strategy for obesity treatment as it has been associated with significant reductions in body weight and waist circumference [108,116,117].

The high amount of fiber which, among other beneficial effects, helps to weight control providing satiety; and the high antioxidants and anti-inflammatory nutrients such as n-3 fatty acids, oleic acid or phenolic compounds, are thought to be the main contributors to the positive effects attributed to the MedDiet [118].

For all these reasons, efforts to maintain the MedDiet pattern in Mediterranean countries and to implement this dietary habits in westernized countries with unhealthy nutritional patterns should be made.

3. Dietary: Single Nutrients and Bioactive Compounds

dietary Nutrition single nutrientNew studies focused on the molecular action of nutritional bioactive compounds with positive effects on MetS are currently an objective of scientific research worldwide with the aim of designing more personalized strategies in the framework of molecular nutrition. Among them, flavonoids and antioxidant vitamins are some of the most studied compounds with different potential benefits such as antioxidant, vasodilatory, anti-atherogenic, antithrombotic, and anti-inflammatory effects [119]. Table 3 summarizes different nutritional bioactive compounds with potential positive effects on MetS, including the possible molecular mechanism of action involved.

dietary table 3

3.1. Ascorbate

dietary AscorbateVitamin C, ascorbic acid or ascorbate is an essential nutrient as human beings cannot synthesize it. It is a water-soluble antioxidant mainly found in fruits, especially citrus (lemon, orange), and vegetables (pepper, kale) [120]. Several beneficial effects have been associated to this vitamin such as antioxidant and anti-inflammatory properties and prevention or treatment of CVD and type 2 diabetes [121�123].

This dietary component produces its antioxidant effect primarily by quenching damaging free radicals and other reactive oxygen and nitrogen species and therefore preventing molecules such as LDL-c from oxidation [122]. It can also regenerate other oxidized antioxidants like tocopherol [124].

Moreover, it has been described that ascorbic acid may reduce inflammation as it is associated with depletion of CRP levels [125]. This is an important outcome to take in consideration in the treatment of MetS sufferers, as they usually present low grade inflammation [27].

Supplementation with vitamin C have also been associated with prevention of CVD by improving the endothelial function [126] and probably by lowering blood pressure [121]. These effects are thought to be exerted by the ability of vitamin C to enhance the endothelial nitric oxide synthase enzyme (eNOS) activity and to reduce HDL-c glycation [127].

Additionally, several studies have attributed to ascorbate supplementation an antidiabetic effect by improving whole body insulin sensitivity and glucose control in people with type 2 diabetes [123]. These antidiabetic properties are thought to be mediated by optimization of the insulin secretory function of the pancreatic islet cells by increasing muscle sodium-dependent vitamin C transporters (SVCTs) [128].

Despite all of this, it should be taken into account that most people reach ascorbic acid requirements (established at 95�110 mg/day in the general population) from diet and do not need supplementation [122,129]. Besides, it should be considered that an excess of vitamin C ingestion leads to the opposite effect and oxidative particles are formed [130,131].

3.2. Hydroxytyrosol

dietary HydroxytyrosolHydroxytyrosol (3,4-dihydroxyphenylethanol) is a phenolic compound mainly found in olives [132].

It is considered the strongest antioxidant of olive oil and one of the main antioxidants in nature [133]. It acts as a powerful scavenger of free radicals, as a radical chain breaker and as metal chelator [134]. It has the ability of inhibiting LDL-c oxidation by macrophages [132]. In this sense, it is the only phenol recognized by the European Food Safety Authority (EFSA) as a protector of blood lipids from oxidative damage [135].

Hydroxytyrosol has also been reported to have anti-inflammatory effects, probably by suppressing cyclooxygenase activity and inducing eNOS expression [136]. Thus, enhancement of olives/olive oil intakes or hydroxytyroxol supplementation in people suffering from MetS may be a good strategy in order to improve inflammatory status.

Another beneficial effect attributed to this phenolic compound is its cardiovascular protective effect. It presents anti-atherogenic properties by decreasing the expression of vascular cell adhesion protein 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) [132,137], which are probably the result of an inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF?B), activator protein 1 (AP-1), GATA transcription factor and nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase [138,139]. Hydroxytyrosol also provides antidyslipidemic effects by lowering plasma levels of LDL-c, total cholesterol and TG, and by rising HDL-c [138].

Despite the beneficial effects attributed to hydfroxytyrosol as an antioxidant, for its antiinflamatory properties and as cardiovascular protector, it should be taken into account that most studies focused on this compound have been performed with mixtures of olive phenols, thus a synergic effect cannot be excluded [140].

3.3. Quercetin

dietaryQuercetin is a predominant flavanol naturally present in vegetables, fruits, green tea or red wine. It is commonly found as glycoside forms, where rutin is the most common and important structure found in nature [141].

Many beneficial effects that can contribute to MetS improvement have been attributed to quercetin. Among them, its antioxidant capacity should be highlighted, as it has been reported to inhibit lipid peroxidation and increase antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) or glutathione peroxidase (GPX) [142].

Moreover, an anti-inflammatory effect mediated via attenuation of tumor necrosis factor ? (TNF-?), NF?B and mitogen-activated protein kinases (MAPK), as well as depletion of IL-6, IL-1?, IL-8 or monocyte chemoattractant protein-1 (MCP-1) gene expression has also been attributed to this polyphenol [143].

As most people with MetS are overweight or obese, the role of quercetin in body weight reduction and obesity prevention has been of special interest. In this sense, it stands out the capacity of quercetin to inhibit adipogenesis through inducing the activation of AMP-activated protein kinase (AMPK) and decreasing the expression of CCAAT-enhancer-binding protein-? (C/EBP?), peroxisome�proliferator-activated receptor gamma (PPAR?), and sterol regulatory element-binding protein 1 (SREBP-1) [141,144].

According to the antidiabetic effects, it is proposed that quercetin may act as an agonist of peroxisome proliferator-activated receptor gamma (PPAR?), and thus improve insulin-stimulated glucose uptake in mature adipocytes [145]. Moreover, quercetin may ameliorate hyperglycemia by inhibiting glucose transporter 2 (GLUT2) and insulin dependent phosphatidylinositol-3-kinase (PI3K) and blocking tyrosine kinase (TK) [142].

Finally, different studies observed that quercetin has the ability to reduce blood pressure [146�148]. However, the mechanisms of action are not clear, since some authors have suggested that quercetin increases eNOS, contributing to inhibition of platelet aggregation and improvement of the endothelial function [146,147], but there are other studies that have not come across these results [148].

3.4. Resveratrol

dietary

Resveratrol (3,5,4?-trihidroxiestilben) is a phenolic compound mainly found in red grapes and derived products (red wine, grape juice) [149]. It has shown antioxidant and anti-inflammatory activities, and cardioprotective, anti-obesity and antidiabetic capacities [150�156].

The antioxidant effects of resveratrol have been reported to be carried out by scavenging of hydroxyl, superoxide, and metal-induced radicals as well as by antioxidant effects in cells producing reactive oxygen species (ROS) [150].

Moreover, it has been reported that the anti-inflammatory effects of resveratrol are mediated by inhibiting NF?B signaling [151]. Furthermore, this polyphenol reduces the expression of proinflammatory cytokines such as interleukin 6 (IL-6), interleukin 8 (IL-8), TNF-?, monocyte chemoattractant protein-1 (MCP-1) and eNOS [152]. In addition, resveratrol inhibits the cyclooxygenase (COX) expression and activity, a pathway involved in the synthesis of proinflammatory lipid mediators [152].

Concerning the effects of resveratrol against development of type 2 diabetes, it has been reported that treatment of diabetes patients with this polyphenol provides significant improvements in the status of multiple clinically relevant biomarkers such as fasting glucose levels, insulin concentrations or glycated hemoglobin and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) [153,154].

Additionally, cardioprotective effects have been attributed to resveratrol. In this sense, it is suggested that resveratrol improves the endothelial function by producing nitric oxide (NO) through increasing the activity and expression of eNOS. This effect is thought to be conducted through activation of nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (Sirt 1) and 5? AMP-activated protein kinase (AMPK) [155]. Besides, resveratrol exerts endothelial protection by stimulation of NF-E2-related factor 2 (Nrf2) [156] and decreasing the expression of adhesion proteins such as ICAM-1 and VCAM-1 [152].

Finally, it has been described that resveratrol may have a role in preventing obesity as it has been related with energy metabolism improvement, increasing lipolysis and reducing lipogenesis [157]. However, more studies are needed in order to corroborate these findings.

3.5. Tocopherol

dietary vitamin e TocopherolTocopherols, also known as vitamin E, are a family of eight fat-soluble phenolic compounds whose main dietary sources are vegetable oils, nuts and seeds [130,158].

For a long time, it has been suggested that vitamin E could prevent different metabolic diseases as a potent antioxidant, acting as scavenger of lipid peroxyl radicals by hydrogen donating [159]. In this sense, it was described that tocopherols inhibit peroxidation of membrane phospholipids and prevent generation of free radicals in cell membranes [160].

Moreover, it has been shown that supplementation with ?-tocopherol or ?-tocopherol, two of the different isoforms of vitamin E, could have an effect on inflammation status by reducing CRP levels [161]. Additionally, inhibition of COX and protein kinase C (PKC) and reduction of cytokines�such as IL-8 or plasminogen activator inhibitor-1 (PAI-1) are other mechanisms that may contribute to these anti-inflammatory effects [162,163].

However, the beneficial effects attributed to this vitamin previously have lately became controversial as different clinical trials have not come across such benefits, but ineffective or even harmful effects have been observed [164]. It has been recently suggested that this may be explained by the fact that vitamin E may lose most of the antioxidant capacity when ingested by human beings through different mechanisms [162].

3.6. Anthocyanins

dietary Anthocyanins

Anthocyanins are water-soluble polyphenolic compounds responsible for the red, blue and purple colors of berries, black currants, black grapes, peaches, cherries, plums, pomegranate, eggplant, black beans, red radishes, red onions, red cabbage, purple corn or purple sweet potatoes [165�167]. Actually, they are the most abundant polyphenols in fruits and vegetables [167]. Moreover, they can also be found in teas, honey, nuts, olive oil, cocoa, and cereals [168].

These compounds have high antioxidant capacity inhibiting or decreasing free radicals by donating or transferring electrons from hydrogen atoms [167].

Regarding clinical studies, it has been shown that these bioactive compounds may prevent type 2 diabetes development by improving insulin sensitivity [169]. The exact mechanisms by which anthocyanins exert their antidiabetic effect are not yet clear, but an enhancement of the glucose uptake by muscle and adipocyte cells in an insulin-independent manner has been suggested [169].

Moreover, it has been shown that anthocyanins may have the capacity to prevent CVD development by improving endothelial function via increasing brachial artery flow-mediated dilation and HDL-c, and decreasing serum VCAM-1 and LDL-c concentrations [170�173].

Finally, these polyphenolic compounds may exert anti-inflamatory effects via reducing proinflamatory molecules such as IL-8, IL-1? or CRP [172,174].

However, most studies have used anthocyanin-rich extracts instead of purified anthocyanins; thus, a synergic effect with other polyphenols cannot be discarded.

3.7. Catechins

dietary tea leaves CatechinsCatechins are polyphenols that can be found in a variety of foods including fruits, vegetables, chocolate, wine, and tea [175]. The epigallocatechin 3-gallate present in tea leaves is the catechin class most studied [176].

Anti-obesity effects have been attributed to these polyphenols in different studies [176]. The mechanisms of action suggested to explain these beneficial effects on body weight are: increasing energy expenditure and fat oxidation, and reducing fat absorption [177]. It is thought that energy expenditure is enhanced by catechol-O-methyltransferase and phosphodiesterase inhibition, which stimulates the sympathetic nervous system causing an activation of the brown adipose tissue [178]. Fat oxidation is mediated by upregulation of acyl-CoA dehydrogenase and peroxisomal b-oxidation enzymes [178,179].

Moreover, catechin intake has also been associated with lower risk of CVD development by improving lipid biomarkers. Thus, it has been reported that consumption of this kind of polyphenols may increase HDL-c and decrease LDL-c and total cholesterol [180].

Finally, and antidiabetic effect has also been related to catechin comsumption, lowering fasting glucose levels [175] and improving insulin sensitivity [178].

4. Conclusions

As the prevalence of MetS reaches epidemic rates, the finding of an effective and easy-to-follow dietary strategy to combat this heterogenic disease is still a pending subject. This work recompiled different dietary nutrients and nutritional patterns with potential benefits in the prevention and�treatment of MetS and related comorbidities (Figure 1) with the aim of facilitating future clinical�studies in this area. The challenge now is to introduce precision bioactive compounds in personalized�nutritional patterns in order to gain the most benefits for prevention and treatment of this disease�through nutrition.

dietary fig 1

Conflicts of Interest: The authors declare no conflict of interest.

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Lifestyle Changes for Managing Thyroid Disease | Wellness Clinic

Lifestyle Changes for Managing Thyroid Disease | Wellness Clinic

A butterfly-shaped gland found at the front of the neck, the thyroid gland, may not look like much, but it can wreak havoc on your health, when it isn’t functioning properly. The thyroid gland produces thyroxin (T4) and triiodothyronine (T3), hormones which control the metabolism, respiration, temperature and other essential functions of the human body. Too much or too little of these hormones can lead to thyroid disease, such as hypothyroidism and hyperthyroidism.

 

What can you do to treat thyroid disorders?

 

To treat thyroid disorders, drugs and medications are often prescribed. The most commonly prescribed medication for treating hypothyroidism is levothyroxine, while treatment for hyperthyroidism includes anti-thyroid medicines, such as propylthiouracil or methimazole, radioactive iodine which may destroy the thyroid gland and stop the excess production of thyroid hormones, even surgery to remove the thyroid gland altogether.

 

A dissatisfaction with normal care, however, has resulted in an increasing interest in a more holistic approach to thyroid disease treatment, one which prefers natural, lifestyle changes, not drugs or medications. Jen Wittman, CHHC, AADP, creator of Thyroid Loving Care and a certified holistic health expert, chef and writer, is an advocate of this strategy. Wittman was diagnosed with Hashimoto’s thyroid disease, an autoimmune disorder which attacks the thyroid gland itself, but was able to undo the illness without the use of medicines.

 

“In my experience, changing diet, improving gut health, managing stress and maintaining overall health and wellness helps support the body so that medicine is unnecessary, or at minimum, may work more effectively,” Wittman said.

 

Adopting a Healthy Diet

 

Wittman recommends eliminating gluten, caffeine and soy, in addition to reducing sugar for all thyroid diseases, however, she says that diets are contingent on the individual.

 

She clarified that some folks gain from a Paleo or Autoimmune Paleo protocol, while others will need to avoid foods like nightshades such as paprika, cayenne, tomatoes, bell peppers, eggplant and potatoes or polyunsaturated fatty acids such as peppermint and vegetable oils. Others also find cutting out milk or alcohol from their diet helps.

 

“There is not any effective one-size fits all approach when it comes to reversing autoimmune and thyroid conditions”.

 

According to Charlie Seltzer, MD, owner of Lean4Life Weight Loss & Fitness Solutions, another change some healthcare professionals suggest for individuals suffering from thyroid disease is to avoid eating raw goitrogenic foods like cruciferous vegetables, such as broccoli and kale, that interfere with the function of the thyroid gland.

 

But comments on diet’s influence on thyroid function have a tendency to vary. Jabbour, for example, doesn’t believe that exercise and diet can cure thyroid disorder. But one thing they could all agree on though is that eating healthier can fight weight gain and reduce a few of the symptoms like fatigue and depression, especially in the first six months of hormonal therapy when a balance of hormones has not yet been attained.

 

To Supplement or Not?

 

Too much or too little of certain nutrients can greatly impact thyroid function. Stella Lucia Volpe, PhD, RD, LDN, FACSM, professor and chair of the department of nutrition sciences at Drexel University at the College of Nursing & Health Professions, clarified that some thyroid diseases could be, but not necessarily is, a consequence of iodine deficiency. Iron or Zinc deficiencies can be variables as well. For instance, the thyroid converts iodine into thyroxin (T4) and triiodothyronine (T3) so a deficiency of iodine in your diet can interfere with hormone production.

 

But iodine deficiency is uncommon in the USA, Jabbour cautioned. Therefore supplementation could be harmful if no authentic deficiency is present, leading to the specific opposite problem. Too much iodine in your diet can also be an issue if you’re at risk for thyroid disease. Mario Skugor, MD, advises his patients with Graves’ disease, another autoimmune thyroid disease, because their thyroid is secreting a surplus of both T4 and T3 to prevent foods.

 

Wittman considers that most people with thyroid disorder need supplements at least short-term, but that they often can be weaned off them. “There is just not one simple way to reverse these conditions in everybody,” Wittman said. “Rather there are several unique supplements, lifestyle changes, healing modalities and dietary alterations which can be used to reverse the conditions and eliminate symptoms.” Seltzer cautioned against supplementing on your own. See your doctor and get appropriate testing first to make sure it’s necessary in the first location.

 

Exercise & Your Thyroid

 

Opinions on exercise also differ. Seltzer does not see it playing an important role in proper thyroid function while exercise in general is good for everybody. “The best exercise routine is the one that a individual is most likely to stay with,” Seltzer said. “I enjoy resistance training supplemented with cardiovascular exercise, with a focus on interval training, but if someone hates lifting weights, then anything is better than nothing.”

 

Wittman advises her clients to choose exercises which don’t tax the adrenal gland like gentle yoga, walking or Tai Chi. Jabbour and Skugor say patients with hyperthyroidism must watch the intensity and duration of the workouts because exercise may exacerbate an already rapid heart rate along with other symptoms.

 

What is the Best Strategy?

 

The absence of consensus on holistic approaches will likely cause your head to spin, right? Can you choose alternative remedies or would you rather stick with normal care for treating thyroid disease? The American Thyroid Association recommends that you work with your healthcare professional about the best strategies to include alternative or complementary medicine and always keep the lines of communication open if your doctor doesn’t approve of these practices. Your well-being is the priority, and a few inappropriate options, could interfere with your treatment.

 

The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss options on the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .�
 

By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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