FACTORS THAT INFLUENCE DISEASE DEVELOPMENT AND PROGRESSION IN COPD

This article is an excerpt from The GOLD Report 2013. The GOLD Report 2013 is an excellent work stating the current position on COPD from a worldwide perspective. This article is the best that I’ve seen describing how the disease progresses for most people. I do appreciate that it is a hard read, but do bear in mind that it was written by professionals for professionals worldwide. The authors come from many countries, and we have to bear in mind that environmental factors differ from one country to another. Poverty is an important indirect cause in many places, and not necessarily just in Third World Countries.

I hope you find it relevant, and not too hard going.

Although cigarette smoking is the best-studied COPD risk factor, it is not the only one and there is consistent evidence from epidemiologic studies that nonsmokers may also develop chronic airflow limitation. Much of the evidence concerning risk factors for COPD comes from cross-sectional epidemiological studies that identify associations rather than cause-and-effect relationships. Although several longitudinal studies of COPD have followed groups and populations for up to 20 years, none has monitored the progression of the disease through its entire course, or has included the pre-and perinatal periods which may be important in shaping an individual’s future COPD risk. Thus, current understanding of risk factors for COPD is in many respects still incomplete. COPD results from a gene-environment interaction. Among people with the same smoking history, not all will develop COPD due to differences in genetic predisposition to the disease, or in how long they live. Risk factors for COPD may also be related in more complex ways. For example, gender may influence whether a person takes up smoking or experiences certain occupational or environmental exposures; socioeconomic status may be linked to a child’s birth weight (as it impacts on lung growth and development and in turn on susceptibility to develop the disease); and longer life expectancy will allow greater lifetime exposure to risk factors. Understanding the relationships and interactions among risk factors requires further investigation.

Genes

The genetic risk factor that is best documented is a severe hereditary deficiency of alpha-1 antitrypsin, a major circulating inhibitor of serine proteases. Although alpha-1 antitrypsin deficiency is relevant to only a small part of the world’s population, it illustrates the interaction between genes and environmental exposures leading to COPD. A significant familial risk of airflow limitation has been observed in smoking siblings of patients with severe COPD, suggesting that genetic together with environmental factors could influence this susceptibility. Single genes such as the gene encoding matrix metalloproteinase 12 (MMP12) have been related to decline in lung function. Although several genome-wide association studies indicate a role of the gene for the alpha-nicotinic acetylcholine receptor as well as the hedge-hog interacting protein gene and possibly one or two others, there remains a discrepancy between findings from analyses of COPD and lung function as well as between genome-wide association study analyses and candidate gene analyses.

Age and Gender

Age is often listed as a risk factor for COPD. It is unclear if healthy aging as such leads to COPD or if age reflects the sum of cumulative exposures throughout life. In the past, most studies showed that COPD prevalence and mortality were greater among men than women but data from developed countries show that the prevalence of the disease is now almost equal in men and women, probably reflecting the changing patterns of tobacco smoking. Some studies have even suggested that women are more susceptible to the effects of tobacco smoke than men.

Lung Growth and Development

Lung growth is related to processes occurring during gestation, birth, and exposures during childhood and adolescence. Reduced maximal attained lung function (as measured by spirometry) may identify individuals who are at increased risk for the development of COPD. Any factor that affects lung growth during gestation and childhood has the potential for increasing an individual’s risk of developing COPD. For example, a large study and meta-analysis confirmed a positive association between birth weight and FEV1 in adulthood, and several studies have found an effect of early childhood lung infections. A study found that factors in early life termed “childhood disadvantage factors” were as important as heavy smoking in predicting lung function in early adult life.

Exposure to Particles

Across the world, cigarette smoking is the most commonly encountered risk factor for COPD. Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of decline in FEV1, and a greater COPD mortality rate than nonsmokers. Other types of tobacco (e.g., pipe, cigar, water pipe) and marijuanaare also risk factors for COPD. Passive exposure to cigarette smoke (also known as environmental tobacco smoke or ETS) may also contribute to respiratory symptoms and COPD by increasing the lung’s total burden of inhaled particles and gases. Smoking during pregnancy may also pose a risk for the foetus, by affecting lung growth and development in utero and possibly the priming of the immune system.

 Occupational exposures, including organic and inorganic dusts and chemical agents and fumes, are an under appreciated risk factor for COPD. An analysis of the large U.S. population-based NHANES III survey of almost 10,000 adults aged 30-75 years estimated the fraction of COPD attributable to work was 19.2% overall, and 31.1% among never-smokers. These estimates are consistent with a statement published by the American Thoracic Society that concluded that occupational exposures account for 10-20% of either symptoms or functional impairment consistent with COPD. The riskfrom occupational exposures in less regulated areas of the world is likely to be much higher than reported in studies from Europe and North America.

 Wood, animal dung, crop residues, and coal, typically burned in open fires or poorly functioning stoves, may lead to very high levels of indoor air pollution. Evidence continues to grow that indoor pollution from biomass cooking and heating in poorly ventilated dwellings is an important risk factor for COPD. Almost 3 billion people worldwide use biomass and coal as their main source of energy for cooking, heating, and other household needs, so the population at risk worldwide is very large.

 High levels of urban air pollution are harmful to individuals with existing heart or lung disease. The role of outdoor air pollution in causing COPD is unclear, but appears to be small when compared with that of cigarette smoking. It has also been difficult to assess the effects of single pollutants in long-term exposure to atmospheric pollution. However, air pollution from fossil fuel combustion, primarily from motor vehicle emissions in cities, is associated with decrements of respiratory function. The relative effects of short-term, high-peak exposures and long-term, low-level exposures are yet to be resolved.

Socio-economic Status

Poverty is clearly a risk factor for COPD but the components of poverty that contribute to this are unclear. There is strong evidence that the risk of developing COPD is inversely related to socioeconomic status. It is not clear, however, whether this pattern reflects exposures to indoor and outdoor air pollutants, crowding, poor nutrition, infections, or other factors that are related to low socioeconomic status.

Asthma/Bronchial Hyper reactivity

Asthma may be a risk factor for the development of COPD, although the evidence is not conclusive. In a report from a longitudinal cohort of the Tucson Epidemiological Study of Airway Obstructive Disease, adults with asthma were found to have a twelve-fold higher risk of acquiring COPD over time than those without asthma, after adjusting for smoking. Another longitudinal study of people with asthma found that around 20% of subjects developed irreversible airflow limitation and reduced transfer coefficient, and in a longitudinal study self-reported asthma was associated with excess loss of FEV1 in the general population. In the European Community Respiratory Health Survey, bronchial hyper responsiveness was second only to cigarette smoking as the leading risk factor for COPD, responsible for 15% of the population attributable risk (smoking had a population attributable risk of 39%). The pathology of chronic airflow limitation in asthmatic nonsmokers and non-asthmatic smokers is markedly different, suggesting that the two disease entities may remain different even when presenting with similarly reduced lung function. However, clinically separating asthma from COPD may not be easy.

Bronchial hyper reactivity can exist without a clinical diagnosis of asthma and has been shown to be an independent predictor of COPD in population studies as well as an indicator of risk of excess decline in lung function in patients with mild COPD.

Chronic Bronchitis

In the seminal study by Fletcher and co-workers, chronic bronchitis was not associated with decline in lung function. However, subsequent studies have found an association between mucus hyper-secretion and FEV1 decline, and in younger adults who smoke the presence of chronic bronchitis is associated with an increased likelihood of developing COPD.

Infections

A history of severe childhood respiratory infection has been associated with reduced lung function and increased respiratory symptoms in adulthood. Susceptibility to infections plays a role in exacerbations of COPD but the effect on the development of the disease is less clear. HIV infection has been shown to accelerate the onset of smoking-related emphysema. Tuberculosis has been found to be a risk factor for COPD. In addition, tuberculosis is both a differential diagnosis to COPD and a potential comorbidity.

PATHOLOGY, PATHOGENESIS

AND PATHOPHYSIOLOGY

Inhaled cigarette smoke and other noxious particles such as smoke from biomass fuels cause lung inflammation, a normal response that appears to be modified in patients who develop COPD. This chronic inflammatory response may induce parenchymal tissue destruction (resulting in emphysema), and disrupt normal repair and defense mechanisms (resulting in small airway fibrosis). These pathological changes lead to air trapping and progressive airflow limitation. A brief overview follows of the pathological changes in COPD, their cellular and molecular mechanisms, and how these underlie physiologic abnormalities and symptoms characteristic of the disease.

 Pathology

Pathological changes characteristic of COPD are found in the airways, lung parenchymal, and pulmonary vasculature. The pathological changes include chronic inflammation, with increased numbers of specific inflammatory cell types in different parts of the lung, and structural changes resulting from repeated injury and repair. In general, the inflammatory and structural changes in the airways increase with disease severity and persist on smoking cessation.

 Pathogenesis

The inflammation in the respiratory tract of COPD patients appears to be a modification of the inflammatory response of the respiratory tract to chronic irritants such as cigarette smoke. The mechanisms for this amplified inflammation are not yet understood but may be genetically determined. Patients can clearly develop COPD without smoking, but the nature of the inflammatory response in these patients is unknown. Oxidative stress and an excess of proteinases in the lung further modify lung inflammation. Together, these mechanisms lead to the characteristic pathological changes in COPD. Lung inflammation persists after smoking cessation through unknown mechanisms, although autoantigens and persistent microorganisms may play a role.

Oxidative Stress.

Oxidative stress may be an important amplifying mechanism in COPD. Biomarkers of oxidative stress (e.g., hydrogen peroxide, 8-isoprostane) are increased in the exhaled breath condensate, sputum, and systemic circulation of COPD patients. Oxidative stress is further increased in exacerbations. Oxidants are generated by cigarette smoke and other inhaled particulates, and released from activated inflammatory cells such as macrophages and neutrophils. There may also be a reduction in endogenous antioxidants in COPD patients as a result of reduction in a transcription factor called Nrf2 that regulates many antioxidant genes.

Protease-Antiprotease Imbalance.

There is compelling evidence for an imbalance in the lungs of COPD patients between proteases that break down connective tissue components and anti proteases that protect against this. Several proteases, derived from inflammatory cells and epithelial cells, are increased in COPD patients. There is increasing evidence that they may interact with each other. Protease-mediated destruction of elastin, a major connective tissue component in lung parenchyma, is believed to be an important feature of emphysema and is likely to be irreversible.

Inflammatory Cells.

COPD is characterized by a specific pattern of inflammation involving increased numbers of CD8+ (cytotoxic) Tc1 lymphocytes present only in smokers that develop the disease. These cells, together with neutrophils and macrophages, release inflammatory mediators and enzymes and interact with structural cells in the airways, lung parenchyma and pulmonary vasculature.

Inflammatory Mediators.

The wide variety of inflammatory mediators that have been shown to be increased in COPD patients attract inflammatory cells from the circulation (chemotactic factors), amplify the inflammatory process (pro inflammatory cytokines), and induce structural changes (growth factors).

 Differences in Inflammation Between COPD and Asthma.

Although both COPD and asthma are associated with chronic inflammation of the respiratory tract, there are differences in the inflammatory cells and mediators involved in the two diseases, which in turn account for differences in physiological effects, symptoms, and response to therapy. Some patients with COPD have features consistent with asthma and may have a mixed inflammatory pattern with increased eosinophils.

 Pathophysiology

There is now a good understanding of how the underlying disease process in COPD leads to the characteristic physiologic abnormalities and symptoms. For example, inflammation and narrowing of peripheral airways leads to decreased FEV1. Parenchymal destruction due to emphysema also contributes to airflow limitation and leads to decreased gas transfer

 Airflow Limitation and Air Trapping.

The extent of inflammation, fibrosis, and luminal exudates in small airways is correlated with the reduction in FEV1 and FEV1/FVC ratio, and probably with the accelerated decline in FEV1 characteristic of COPD. This peripheral airway obstruction progressively traps air during expiration, resulting in hyperinflation. Although emphysema is more associated with gas exchange abnormalities than with reduced FEV1, it does contribute to gas trapping during expiration. This is especially so as alveolar attachments to small airways are destroyed when the disease becomes more severe. Hyperinflation reduces inspiratory capacity such that functional residual capacity increases, particularly during exercise (dynamic hyperinflation), resulting in increased dyspnea and limitation of exercise capacity. These factors contribute to impairment of the intrinsic contractile properties of respiratory muscles; this results in up regulation of local pro-inflammatory cytokines. It is thought that hyperinflation develops early in the disease and is the main mechanism for exertional dyspnea. Bronchodilators acting on peripheral airways reduce air trapping, thereby reducing lung volumes and improving symptoms and exercise capacity.

Gas Exchange Abnormalities.

Gas exchange abnormalities result in hypoxaemia and hypercapnia, and have several mechanisms in COPD. In general, gas transfer for oxygen and carbon dioxide worsens as the disease progresses. Reduced ventilation may also be due to reduced ventilatory drive. This may lead to carbon dioxide retention when it is combined with reduced ventilation due to a high work of breathing because of severe obstruction and hyperinflation coupled with ventilatory muscle impairment. The abnormalities in alveolar ventilation and a reduced pulmonary vascular bed further worsen the VA/Q abnormalities.

 Mucus Hyper secretion.

Mucus hyper secretion, resulting in a chronic productive cough, is a feature of chronic bronchitis and is not necessarily associated with airflow limitation. Conversely, not all patients with COPD have symptomatic mucus hyper secretion. When present, it is due to an increased number of goblet cells and enlarged submucosal glands in response to chronic airway irritation by cigarette smoke and other noxious agents. Several mediators and proteases stimulate mucus hyper secretion and many of them exert their effects through the activation of epidermal growth factor receptor (EGFR).

 Pulmonary Hypertension.

Pulmonary hypertension may develop late in the course of COPD and is due mainly to hypoxic vasoconstriction of small pulmonary arteries, eventually resulting in structural changes that include intimal hyperplasia and later smooth muscle hypertrophy/hyperplasia. There is an inflammatory response in vessels similar to that seen in the airways and evidence of endothelial cell dysfunction. The loss of the pulmonary capillary bed in emphysema may also contribute to increased pressure in the pulmonary circulation. Progressive pulmonary hypertension may lead to right ventricular hypertrophy and eventually to right-side cardiac failure.

 Exacerbations.

Exacerbations of respiratory symptoms often occur in patients with COPD, triggered by infection with bacteria or viruses (which may coexist), environmental pollutants, or unknown factors. Patients with bacterial and viral episodes have a characteristic response with increased inflammation. During respiratory exacerbations there is increased hyperinflation and gas trapping, with reduced expiratory flow, thus accounting for the increased dyspnea. There is also worsening of VA/Q abnormalities, which can result in hypoxaemia. Other conditions (pneumonia, thromboembolism, and acute cardiac failure) may mimic or aggravate an exacerbation of COPD.

Systemic Features.

It is increasingly recognized that many patients with COPD have comorbidities that have a major impact on quality of life and survival. Airflow limitation and particularly hyperinflation affect cardiac function and gas exchange. Inflammatory mediators in the circulation may contribute to skeletal muscle wasting and cachexia, and may initiate or worsen comorbidities such as ischemic heart disease, heart failure, osteoporosis, normocytic anaemia, diabetes, metabolic syndrome, and depression.

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A STRATEGY FOR DEALING WITH STRESS

At some point, all of us get into some sort of a stressful situation. Maybe we’ve done too much too quickly, or had a shock of some sort. We end up with low oxygen levels, panting and panicky, and our heart rate goes up. We’re in trouble.
First thing to do is STOP. Whatever it is we’re doing STOP… NOW…. Find somewhere to sit (best option), or at least something to lean on. Take your rescue drugs (for me Ventolin and Atrovent). Start pursed lips breathing (most ‘old hands’ will do this automatically). Concentrate on blowing out more air than you breathe in. If you have a pulse/oximeter, use it. After about five minutes, if you are still struggling to get to regular breathing, repeat the rescue inhalers. All rescue drugs are safe for repeated use if needed. If another five minutes passes and you are not on the road to recovery, GET SOMEONE TO CALL AN AMBULANCE!!!! It could be that you need nebulised drugs and oxygen to get you to stabilise. If your breathing is still ragged and you are struggling, you do need help. There is nothing to gain by being a hero.
That’s the breathing side dealt with, what’s the heart doing meanwhile? Probably going like the clappers. I know that if I get into trouble, my heart rate goes up, a lot. My normal PR (Pulse Rate) at rest is about 105. A short walk will take it up to 120. Doing pulmonary exercises can take my PR up to just over 130. A panic attack? 150/160. Serious, and not good.
How to deal with this? Use a relaxation technique. The benefits of doing this was shown to me and others on the course when I attended a Pulmonary Rehabilitation course about two years ago. It was used as part of the exercise programme as a part of the finishing set. We all said that we felt the benefit. One the Occupational Therapists would lead this by reading a script about five minutes long, usually describing a gentle journey through a tranquil landscape. We would sit, close our eyes, a try to imagine ourselves following this journey. We all learned from this that we COULD in some way control our heart rate, and slow it down quicker than a ‘normal’ recovery. What made this work was the rhythm of the words, changing from fairly fast gradually to a good bit slower, along with a change in how the view was described. Clever writing! But, for me, this had a flaw, the scripts were too long, too much to remember when in a difficult situation. So I came up with a slightly different way of doing it, which did not need me to recall a long script. Here it is.
Imagine a ball. It’s about the size of a football. It’s red. It’s bouncing. One bounce for each of your heart beats. Feel your heart beat. Match the bounce. A low bounce is faster than a high bounce. When you have got the bounce right (with practise, you will do that in a few seconds), change the colour of the ball to orange, and make the bounce of the ball a little higher to slow it down a fraction. Be careful not to slow the ball too much, or you will lose the synchronisation with your heart beat. At the same time, do pursed lips breathing. In a few seconds (10 to 20) you should feel that your heart has slowed a little. Change the colour of the ball again, to yellow. Make the bounce a little higher again to slow it again. When you get your heart beat to match the bounce again, change the colour again, and so on. I find that I can usually slow my heart rate down by about 5 beats per minute using this, so from about 140 down to 110 takes 6 or 7 minutes, which I think is pretty good going. The colours. I go through the colours of the rainbow Red to Violet, because it’s easy to remember, and using the same sequence gives a comparison to previous times so you know how it’s going THIS TIME. If your recovery is much longer than usual, it’s often an indication of something wrong that needs to be seen to. The ball. Not important, just something comfortable that you can bounce in your mind.
Remember, Red … Orange … Yellow … Green … Blue … Indigo … Violet.
When you have gone through the colours, if it’s not enough, start again.

Like many other exercises for helping out when we’re not so good, this needs to be practised when we’re OK, and on an even keel.

I hope that some of you might get something useful out of this. I know it works for me.

breathe easy

johnwr

A Description of Collateral Ventilation in Lung Disease

Recently, on another blog, there was a question where someone was asking for a good description of Collateral Ventilation in relation to lung disease. The following is the answer I gave. I have repeated it here in the hope that someone else may benefit from it.

Let’s see if I can help explain this for you. It may be a bit long-winded, so please bear with me.
In the lungs of a normal, healthy person, there is one single route inwards and out again for each of the alveoli (alveoli are the tiny cavities at the end of the airways where the gas exchange with the blood happens). Think in terms of a bunch of grapes. Alveoli are the grapes, the airways are the stalks.
When the lungs get damaged, whether through disease or pollution or irritation, if the membrane suffers extensive damage, then some of that membrane is replaced, as part of the healing process, with scar tissue. If there are repeated episodes of disease, or sustained exposure to pollution or other causes of irritation, then the amount of scarring can become significant.
Scar tissue is not as elastic as the original membrane. It also does not permit gas exchange. As our lungs expand and contract, if the sites where scarring has occurred have become a significant size, then some tearing can happen. This tearing is minute, and is no cause for concern in terms of day to day wear and tear. It is the long term combined effect over years that is the problem. This is where we now jump to, several year down the line. Imagine that two adjacent alveoli have a lot of scarring, and another inflaming infection takes hold, and one particular breath is deeper and heavier than normal, and it causes a tear that goes through the tissue between the alveoli. You now have a hole that will not close. The tissue will heal, but leaves an enlarged cavity because that requires less stretching than the original formation. For the bunch of grapes, two grapes have been replaced by one damson fed by two stalks. After several more years, a number of damsons have formed, and some of those have merged into much larger plums. This is now advanced Emphysema, with some large cavities (called bullae), and we are at the point where medical intervention is required. One of the things that has to be considered to determine which operation is best to go for is how this damage presents itself.
The structure of the lungs is that they are divided into zones called lobes, three in the right, and two in the left. Thinking in terms of the bunches of grapes, consider that each lobe is home to one complete bunch whose only contact normally is through the main stem (the main airway). If the damage within the lungs is confined within the individual bunches, in other words, does not cross the boundaries between the lobes, then there is no colateral ventilation. Collateral ventilation occurs when the the tissue damage permits the passage of air between the lobes through holes between the lobes.
As the damage progresses, as the cavities form, so the internal support structure of the lungs gets reduced. This allows the lungs to become longer and they over inflate because of the loss of elasticity. They sit on the diaphragm, the bottom lobe of each lung gets compressed and generally cannot continue to work properly. The diaphragm now has to lift this extra weight with each breath taken. Through a day, that adds up to a lot of extra hard work. Taken with the loss of alveoli, and the presence of frequent infections etc, the lungs are now operating at maybe as low as 15% of their full capability when in good condition. The patient is permanently fatigued and needs lots of medication to keep the airways open. Often oxygen is needed. At this point, the consultant decides that surgical intervention is required. The first choice at the moment for most consultants is to use pulmonary valves. They are easy to fit, they allow the blocked off part of the lung to continue to pass CO2 and the lungs natural secretions out. Most importantly, they are reversible (if need be, they can be removed easily). The biggest deciding factor in choice for or against valves is whether or not there is colateral ventilation. If there is none, or is very minor, then valves could be considered. If there is colateral ventilation, then the usual decision is to go for lung reduction surgery.
As you can see, at the stage where there needs to be a choice made, the presence or not of colateral ventilation is important. Links to some videos that may help follow:

http://pulmonx.com/en/downloads/videos/zephyr-videos/zephyr-animation/

http://pulmonx.com/en/downloads/videos/chartis-videos/collateral-ventilation/

breathe easy, everyone.

John

IS SOY AS DANGEROUS AS SOME SAY? (Updated 1st May 2013)

I came across this article. If any one finds a rebuttal article, I’ll include it to give balance. You can’t make an honest decision without knowing the evidence from both sides.

The Dangers of Soy Are Real–and Much Worse Than You Might Think

Promoting soy foods as health foods while ignoring the dangers of soy and soy derivatives should be considered a crime against humanity. If you think this statement is too extreme, read this article to the end, and then see what you think!

The dangers of soy are thoroughly documented in the scientific literature, which makes it hard to believe that many health and fitness communities and counselors, and most health food stores, still promote soy products as ultra-healthy foods.

Hopefully this harmful misrepresentation of soy foods will begin to change as the dangers of soy become better known.

A Summary of the Dangers of Soy

  • Soybeans and soy products contain high levels of phytic acid, which inhibits assimilation of calcium, magnesium, copper, iron, and zinc.
  • Soaking, sprouting, and long, slow cooking do not neutralize phytic acid.
  • Diets high in phytic acid have been shown to cause growth problems in children.
  • Trypsin inhibitors in soy interfere with protein digestion and may cause pancreatic disorders.
  • Test animals showed stunted growth when fed trypsin inhibitors from soy.
  • The plant estrogens found in soy, called phytoestrogens, disrupt endocrine function, that is, the proper functioning of the glands that produce hormones, and have the potential to cause infertility as well as to promote breast cancer in adult women.
  • Hypothyroidism and thyroid cancer may be caused by soy phytoestrogens.
  • Infant soy formula has been linked to autoimmune thyroid disease.
  • Soy has been found to increase the body’s need for vitamin B12 and vitamin D.
  • Fragile soy proteins are exposed to high temperatures during processing in order to make soy protein isolate and textured vegetable protein, making them unsuitable for human digestion.
  • This same process results in the formation of toxic lysinoalanine and highly carcinogenic nitrosamines. (Doesn’t sound like anything anyone would want to eat, does it?)
  • MSG, (also called free glutamic acid), a potent neurotoxin, is formed during soy food processing. Many soy products have extra MSG added as well. (See video on the dangers of Aspartame, MSG’s chemical first cousin.)
  • Soy foods contain elevated levels of toxic aluminum, which negatively effects the nervous system the kidneys and has been implicated in the onset of Alzheimer’s.

If this list of the dangers of soy isn’t enough to make you run out the door of your local health food store, keep reading. It gets worse.

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Feeding Babies Infant Soy Formula Is Like Giving Them Birth Control Pills

  • It’s been found that babies given infant soy formulas have 13,000 to 22,000 times more estrogen than babies fed milk-based formulas.
  • Babies fed exclusively on infant soy formula are receiving the estrogenic equivalent (based on body weight) of at least four or five birth control pills per day! You read that right. Four or five birth control pills per day! Here’s the reference so you can check this out for yourself. [Irvine, C. et al., “The Potential Adverse Effects of Soybean Phytoestrogens in Infant Feeding”, New Zealand Medical Journal May 24, 1995, p. 318.] By contrast, dairy-based infant formula contains almost no phytoestrogens, nor does human milk, even when the mother eats soy products. (Sally Fallon & Mary G. Enig, Ph.D.)
  • There has been an increase of delayed physical maturation among boys, including lack of development of sexual organs.
  • Conversely, many girls today show signs of puberty, such as breast development and pubic hair, before the age of eight, and some even before the age of three.
  • Both of these abnormal conditions have been linked to the use of soy formulas as well as to exposure to “environmental estrogens” such as PCBs (polychlorinated biphenyls) and DDE (dichlorodiphenyldichloroethylene)a breakdown product of DDT.

Would you want to knowingly expose your tiny infant to the dangers of soy formula?

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But Don’t Oriental Cultures Eat Lots of Soy?

It seems that historically, Oriental cultures consumed mostly traditionally fermented soy products such as miso, tempeh, natto, shoyu and tamari. (Tofu is not fermented, and falls into the dangerous soy foods category.) They consumed these soy foods in small amounts, as a condiment.

  • Soy foods account for only 1.5 percent of calories in the Chinese diet, researchers found. (1977 Chang KC)
  • The actual soybean consumed today is not the same one used by traditional Oriental cultures.
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Problems with Soy Protein Isolate

  • Furthermore, modern soy foods are very different from those consumed traditionally in Asia. Most are made with soy protein isolate (SPI), which is a protein-rich powder extracted by an industrial process from the waste product of soy oil manufacturing. It is the industry’s way of making a profit on a waste product. The industry spent over 30 years and billions of dollars developing SPI.
  • In feeding studies, SPI caused many deficiencies in rats. That soy causes deficiencies in B12 and zinc is widely recognized, but the range of deficiencies was surprising.
  • Although SPI is added to many foods, it was never granted GRAS status, meaning “Generally Recognized as Safe”. The FDA only granted GRAS status to SPI for use as a binder in cardboard boxes. During the processing of soy, many additional toxins are formed, including nitrates (which are carcinogens) and a toxin called lysinoalanine. It was concerns about lysinoalanine in SPI that led the FDA to deny GRAS status for SPI as a food additive.
  • In spite of all these dangers of soy protein isolate, SPI is the basic ingredient of soy infant formula. The FDA even allows a health claim for foods containing 6.25 grams SPI per serving.
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Scientific Studies Showing Adverse Effects of Dietary Soy

The Weston Price Foundation has a list of studies carried out from 1971 to 2003 showing the adverse effects of dietary soy.

To give you an idea of how condemning these studies are, here are just a few summaries. There are over 50 more!

1986
Fort P and others. Breast feeding and insulin-dependent diabetes mellitus in children. J Am Coll Nutr 1986;5(5):439-441. Twice as many soy-fed children developed diabetes as those in a control group that was breast fed or received milk-based formula. It was based on this study that the American Academy of Pediatrics took a position of opposition to the use of soy infant formula. This objection was later dropped after the AAP received substantial grants from the Infant Formula Council.

1994
Hawkins NM and others. Potential aluminium toxicity in infants fed special infant formula. J Pediatr Gastroenterol Nutr 1994;19(4):377-81 (1994). Researchers found aluminum concentrations of 534 micrograms/L in soy formula, as compared to 9.2 micrograms/L in breast milk. The authors concluded that infants may be at risk from aluminium toxicity when consuming formula containing more than 300 micrograms/L.

1999
Sheehan DM and Doerge DR, Letter to Dockets Management Branch (HFA-305) February 18, 1999. A strong letter of protest from two government researchers at the National Center for Toxicological Research urging that soy protein carry a warning label rather than a health claim.

1999
White L. Association of High Midlife Tofu Consumption with Accelerated Brain Aging. Plenary Session #8: Cognitive Function, The Third International Soy Symposium, Program, November 1999, page 26. An ongoing study of Japanese Americans living in Hawaii found a significant statistical relationship between two or more servings of tofu per week and “accelerated brain aging.” Those participants who consumed tofu in mid life had lower cognitive function in late life and a greater incidence of Alzheimer’s and dementia.

2001
Strom BL and others. Exposure to soy-based formula in infancy and endocrinological and reproductive outcomes in young adulthood. JAMA 2001 Nov 21;286(19):2402-3. Although reported in the media as a vindication of soy infant formula, the study actually found that soy-fed infants had more reproductive problems and more asthma as adults.

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The FDA Had the Scientific Information about the Dangers of Soy but Chose to Ignore It

You might think that people probably just didn’t know about the toxic effects of soybeans, that the food industry and the FDA must have just been misinformed about the supposed benefits, and very real dangers, of soy. Unfortunately for the FDA’s credibility, this was not the case.

If you simply do a search on ‘soybean’ at the Poisonous Plant Database of the United States FDA’s Center for Food Safety and Applied Nutrition, you can see this information yourself.

Right there in black and white you’ll find 288 studies on soy, many focused on the toxic properties and effects of soybeans. It’s not very easy to understand or get access to the actual studies, but it is cause for great concern that the FDA had this information and knowingly chose to ignore the dangers, just as it has done with so many other additives and pharmaceuticals.

It’s tragic to think of the human suffering that could have been avoided had the FDA just been more cautious and listened to their scientific advisors.

And it’s mind-boggling to think that the very federal agency whose mandate is, among other things, “to promote and protect the public health, to monitor products for continued safety after they are in use, and to help the public get the accurate, science-based information needed to improve health,” could knowingly do the apparent opposite.

This is one more example that highlights the need to educate yourself by finding good sources of information to base your health and diet decisions on, rather than relying on the FDA’s stamp of approval.

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More Confirmation on the Dangers of Soy: Medical Conditions Possibly Attributable to Soy Consumption

  • Asthma
  • Chronic Fatigue
  • Depression
  • Diabetes
  • Heart Arrhythmia
  • Heart or Liver Disease
  • Infertility/Reproductive Problems
  • Irritable Bowel Syndrome
  • Learning Disabilities/ADD/ADHD
  • Pancreatic Disorders
  • Premature or Delayed Puberty
  • Rheumatoid Arthritis
  • Thyroid Conditions:
    • Auto-Immune Thyroid Disorders (Graves’ or Hashimoto’s Disease)
    • Goiter
    • Hypothyroidism
    • Hyperthyroidism
    • Thyroid Nodules
    • Thyroid Cancer
    • Other thyroid disorders
  • Uterine Cancer
  • Weight Gain
Weston Price Foundation

Symptoms of Disorders Possibly Attributable to Soy

  • Always feeling cold or warm
  • Anemia
  • Behavioral problems
  • Brittle nails
  • Eczema
  • Hair thinning or loss
  • Hyperactivity
  • Learning deficiencies
  • Lethargy or low blood pressure
  • Sore bones and joints
  • Watery or swelling eyes
Weston Price Foundation

Do You Still Think We’re Exaggerating the Dangers of Soy?

When there is a pretty good possibility that something is harmful, as is the case with soy, common sense dictates that it’s better to avoid it!

The corporations who make billions from selling soy would like us to believe that until the dangers of soy are proven beyond a shadow of a doubt, we shouldn’t worry about them. This reminds me of Russian roulette: if a gun had a hundred chambers, and only one was loaded, I wouldn’t risk putting it to my head and pulling the trigger. Would you?

Or, as Roger Eichman, DDS, succinctly summed up the precautionary principle: “The precautionary principle requires action once the possibility of harm exists. It does not require proof beyond a shadow of a doubt.”

There’s more than enough sound scientific evidence to convince me. I used to think soy was a good dietary choice, but not anymore. I quit eating it a long time ago.

For more information about the dangers of soy, go to the Weston Price Foundation.

High Soy Rations Torture Prisoners: Nutrition Expert Asks Obama to Intervene

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UPDATE  (1st May 2013)   This article perhaps goes someway to give some balance to the discussion. You make up your own mind.

Soy Protein :: The Real Modern Research

Soy protein is widely used since 1959. In normal life there are so many soy foods which contain soy protein. This is  proved to be really good while thinking of its benefits. Commercially there are so many products which contain saturated or textured soy protein. Soy protein may have many benefits over some minor side effects to people with soy protein allergy.

What is soy protein?

A diet rich in soy and whey protein, found in ...

A diet rich in soy and whey protein, found in products such as soy milk and low-fat yogurt, has been shown to reduce breast cancer incidence in rats. (Photo credit: Wikipedia)

Soy protein is such a protein body which is mainly found in soybeans and secondarily in other pulses. When we talk about soy foods, we found many salad dressings, special soy milk, soy powered and many other things which contain high amount of soy protein in it. Here I am giving away a brief list of soy foods which contain soy protein.

  1. Salad Dressings
  2. Soups
  3. Soy Beverage Powder
  4. Meat Analogues
  5. Cheese
  6. Non-Dairy Creamer Products
  7. Infant Formulas

Soy Protein Varieties

Varieties or Proteins like Soy can be best explained in the following heads.

Soy Protein Isolate

The Soy Protein Isolate is highly refined form of soy protein which is also more saturated than the other soy protein varieties. Soy Protein Isolate contains normally more than 90% of pure, refined soy protein. Soy protein isolate is formed or produced using soy floor while isolating other non-protein components and fats which were present in the source.

Concentrate Soy Protein

The soy protein concentrate is mainly the form of protein which is extracted from soy floor however while extracting process the water-soluble carbohydrates are removed. In this form of soy protein the pure protein can be found around 70%.

Soy Protein  Effects

Soy Protein has many good and bad effects over human body. In my personal opinion the soy protein has more benefits than the side effects. Let me explain the dangers of soy protein as well as benefits of it.

Soy Protein Side Effects or Dangers

Textured Soy Protein Soup

Textured Soy Protein Soup (Photo credit: pykmi)

Many people has soy food allergy mostly in United States of America and Canada. People do want to know that what type of side effects or dangers are there in soy protein or soy products. The main danger of soy protein is the methods or processing the soy foods, normally soybeans are not as much dangerous as soy protein isolate or soy protein concentrate, Its due to the way, the industries process soy proteins from the raw source. The primary method contains some high temperature and high pressure methods with chemical processors.  During the processing of soy products, many good ingredients are removed and such a chemical results is occurred that the resulted soy products may stop or resits to let the body absorb many mineral particulars such as Zinc, Copper, Magnesium and Iron which are necessary to the human body to do certain functions.

Benefits of Soy Protein

  1. This do have such an energy inside which really imitate like meat products.
  2. According to FDA, this protein do reduce LDL Cholesterol from the human body, hence it lowers the risk of heart problems.
  3. Soy Protein Amino Acids inside, so improves the effect of other foods too.
  4. Soy protein, reduces the risk to many serious diseases such as Colon cancer, Osteoporosis and  Prostate Cancer.

ASPARTAME – IS IT DANGEROUS?


What you should know


Aspartame
, also marketed as Nutrasweet, Spoonful, Canderel and Equal as well as being a common additive in many foods and drinks (sometimes shown as the E number E951). Aspartame acts as a sugar replacement.
The EPA announced that there is an
epidemic of Multiple Sclerosis and Systemic Lupus and they did not know what toxin was causing this to be rampant across the US. Scientists have now found the answer to this question – Aspartame.

ASPARTAME. In temperatures exceeding 86 degrees F. the wood alcohol in Aspartame converts to Formaldehyde, and then to Formic Acid. Patients with methanol toxicity caused by drinking 3-4 Diet Coke or Diet Pepsi per day, have been caused to have MS or Systemic Lupus symptoms. In Systemic Lupus and MS case triggers by Aspartame, the victim is unaware that Aspartame is the culprit but continued use, in the case of Lupus, can be life threatening. On stopping Aspartame these patients usually lose all or most of their symptoms. Unfortunately the disease cannot be reversed.

Symptoms of Aspartame Disease are: Fibromyalgia symptoms, spasms, shooting pains, cramps, vertigo, numbness in the legs, dizziness, headaches, tinnitus, joint pain, depression, anxiety attacks, slurred speech, blurred vision, blindness and memory loss. Formaldehyde is classed with chemicals like Arsenic and Cyanide  DEADLY POISONS!
Kills as surely as the other two, only slower and causes all kinds of
neurological problems. It changes the brain s chemistry and is a reason for severe seizures. According to the College of Physicians, the Phenylalanine in Aspartame depletes Serotonin, and causes manic depression, panic attacks, rage and violence.

Aspartame is especially deadly for Diabetics, as it makes the food sugar level go out of control causing patients to suffer severe memory loss, coma and death. The memory loss is due to the fact that Aspartic Acid and Phenylalanine are neurotoxic without the other amino acids found in protein. Thus it goes past the blood brain barrier and deteriorates the neurons of the brain. Dr Russell Blaylock, neurosurgeon, said The ingredients stimulate the neurons of the brain to death, causing brain damage of varying degrees . Aspartame disease is rampant in the US, and most probably in 90 other countries (Including the UK and most of Europe) where over 5000 products containing Aspartame are sold. Aspartame Disease could also be to blame for Gulf War Syndrome. Several thousand pallets of diet drinks were stored and consumed in the heat of 120 degrees F (remember the heat liberates the methanol at 86 degrees F) Most Gulf War Syndrome symptoms are identical to Aspartame Poisoning. Dr. H. J. Roberts, world expert on Aspartame poisoning, says it also escalates Alzheimer s disease. Women as young as 30 are admitted to hospices with Alzheimer s disease! Dr Roberts also says that consuming Aspartame during conception can cause birth defects. According to Dr. Louis Elsas. Paediatrician Professor of Genetics the Phenylalanine concentrates in the placenta causing mental retardation. Another neurosurgeon said that when brain tumours were removed, high levels of Aspartame were found in them. Aspartame makes you crave carbohydrates, and stores in the fatty tissue, so even though it is used as a diet aid, it actually makes you FAT!

MONSANTO, the creator of Aspartame (the largest G M food company) knows all about the dangers, they fund the American Diabetics Association, Congress, and the Conference of the American College of Physicians. As proven in 1996, the American Diabetic Association takes money from the food industry to endorse their products. Therefore they cannot criticise MONSANTO. A bill that tried to warn people about the dangers of ASPARTAME, was killed off by the powerful drug and chemical lobbies, letting loose the hounds of disease and death on an unsuspecting public. And that includes all of us here in the UK! – Having read this, would you trust MONSANTO S GM food?

So, if it s labelled Sugar Free   DON T HAVE IT!


Article from Positive Health magazine  July 1999

Aspartame – Not all Sweetness and Light

Many patients diagnosed with Multiple Sclerosis (MS) may in fact be suffering from some of the 92 already documented neurological symptoms now being attributed to methanol toxicity or Aspartame Disease , including fibromyalgia, headaches, vertigo, tinnitus, numbness in the legs, blurred vision, slurred speech, depression and memory loss. In addition, an analysis of the incidence of brain tumours, carried out my Professor John Olney, Washington University, St Louis, USA, has demonstrated that there was an abrupt 10% increase in cases following the introduction of Aspartame in dry goods in 1981 and soft drinks in 1983.

Methanol, the toxin present in Aspartame, belongs to the same class of poisons as Cyanide and Arsenic. It is readily converted into formaldehyde and then into Formic Acid (the poison contained in the sting of Fire Ants) when subjected to prolonged storage of temperatures of 86 Degrees F or over in the body, this can result in metabolic acidosis and methanol toxicity affecting the brain, retina and nerves.

It is interesting to note that Aspartame is manufactured by the NutraSweet Corporation, a subsidiary of Monsanto, who, it is believed, are fully aware of the dangers of their product. However, as Monsanto also funds the American Diabetics Association, the American Dietetic Association, Congress and the Conference of the American College of Physicians, there appears to be a conspiracy of silence with regard to the dangers of this artificial sweetener which is contained in over 5,000 sugar-free products sold under the brand names of NutraSweet, Canderel, Equal and Spoonful. (Also listed as E Number E951)
The general advice is to read the labels and avoid!


Useful links on this subject:


http://www.myelitis.org/tmic/archive/22/0294.html
http://www.members.tripod.com/~aspartame/doubt.htm
http://www.acponline.org/public/aspartame.htm

http://www.nutritionist-resource.org.uk/blog/2012/10/04/the-sugar-trap-how-can-you-escape

I copied this article from elsewere. I believe that it had been copied to where I got it from.  There were no credits with it. If this article offends someone because of copyright issues, then get in touch with me by leaving a message in the comments.

GOLD REPORT (UPDATED 2013)

A new version of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Report has been published, dated February 2013. First quick look through shows many areas where the knowledge has been updated, which is very welcome.
If you do read it (it is heavy going in places), remember that in the UK we are quite advanced, and this document has to be relevant worldwide, so information from trials of new drugs and techniques are not included because as yet they are not accepted worldwide.
There is a lot of new information on drugs, how the work, and what they are used for.
All in all, a very useful reference tool.

To see it for yourself, follow this link:

http://www.goldcopd.org/uploads/us…

As always, breathe easy.

John