The relationship between the liver, exercise and candida
The liver is a ingenious detox factory. Through two steps, Phase I and II, toxins, pesticides, heavy metals, additives are dismantled and disarmed and removed from the body via the urine e.g.
Phase I
During this process toxic substances undergo a treatment which converts them into bio-active substances. This makes them much more toxic but it is necessary to be able to bind to water in stage II. The cytochrome P 450 enzymes get in action during this phase.
Phase II
The bio-active substances are converted into bio-inactive substances. For example, they can bind to water and avoids toxic loads that are stacked in the liver. During this phase the toxins lose their fragrance.
The enzymes responsible for the conversion of glutathione, glutathione transferase, in particular, are also active during the second phase of detoxification. They need a co-enzyme to function, in particular: selenium, zinc, magnesium, vitamin B (3, 6, 8, 11, 12), and alpha-lipoic acid.
Phase II proceeds via glutathione transferases but on one condition only. It needs (daily) exercise to be useful. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid.
Cysteine is a troublemaker if there is no exercise. How come? Cysteine can always be present into the cell. Outside the cell, only if there is sufficient cysteine to be converted via exercise.
If the person moves insufficiently, then the cell imports cystine. The cell is equipped with cystine channels. Only 1 cystine can pass at a time. This in turn gives a glutathione.
A cystine => a cysteine => 1 glutathione
Suppose the person exercises enough, no need to import cystine. Cysteine passes via specific channels, 10 cysteine enter at the same time the cell. Thus, it produces 10 times more glutathione.
Someone who has little chance to move or exercise, will detox 10x less than a active person. This is not without consequences.
Another stumbling block for Phase II of the detoxification is Candida or fungus. This causes leaky gut and too little recognized by mainstream medicine. Fungus produces acetyldehyde via the enzyme pyruvate decarboxylase. Acetyldehyde is dismantled by cysteine. The more candida, the greater the use of cysteine. Moreover, it compeeds with vitamine B6 and affects normal detox processes.
The effects of candida are far-reaching. The chemical by-products react with serotonin and dopamine. Acetaldehyde is then transformed into opiate substances that affect the functioning of the brains. The neurons are able to communicate less well and influences the red blood cells negatively. They have more trouble to transport oxygen. Thus, you are tired of candida.
Interesting to know is that everyday substances can limit stage II. These are coffee and tea, sugar and lactose (milk and cheese), smoking and alcohol, stress, paracetamol and too little exercise as previously cited.
Nature is generous, and also provides ways to stimulate phase II. Daily exercise is an obvious move with the knowledge what the lack of exercise can do. Vegetables and plants have to offer: onion, garlic, leeks, chicory, endive, artichoke, broccoli, radish, spinach, olive oil, fatty fish, avocado, turmeric, milk thistle, dandelion, Swedish herb, liver herb.
dinsdag 7 februari 2012
maandag 6 februari 2012
Kill the virus with
Viri Balance
https://www.gezondheidaanhuis.nl/nl/product/10195/Viri-Balance-Pervital-30-ml
Lymfo Balance
https://www.gezondheidaanhuis.nl/nl/product/13749/Lymfo-Balance-Pervital-30-ml
Detox Balance
https://www.gezondheidaanhuis.nl/nl/product/11801/Detox-Balance-Pervital-30-ml
Brand: Pervital
http://www.nutramin.nl/
If results are not satisfying, add Elaps Balance.
https://www.gezondheidaanhuis.nl/nl/product/13747/Elaps-Balance-Pervital-30-ml
Also helpful against HPV (human papilloma virus responsible for cervix cancer).
https://www.gezondheidaanhuis.nl/nl/product/10195/Viri-Balance-Pervital-30-ml
Lymfo Balance
https://www.gezondheidaanhuis.nl/nl/product/13749/Lymfo-Balance-Pervital-30-ml
Detox Balance
https://www.gezondheidaanhuis.nl/nl/product/11801/Detox-Balance-Pervital-30-ml
Brand: Pervital
http://www.nutramin.nl/
If results are not satisfying, add Elaps Balance.
https://www.gezondheidaanhuis.nl/nl/product/13747/Elaps-Balance-Pervital-30-ml
Also helpful against HPV (human papilloma virus responsible for cervix cancer).
zondag 5 februari 2012
Living is ...
"Perhaps it is true that we do not really exist until there is someone there to see us existing;
that we cannot properly speak until there is someone there who can understand what we are saying;
that, in essence, we are not wholly alive until we are loved."
Alain de Botton: On Love
that we cannot properly speak until there is someone there who can understand what we are saying;
that, in essence, we are not wholly alive until we are loved."
Alain de Botton: On Love
woensdag 1 februari 2012
Mitochondrial changes associated with glutathione deficiency
http://www.sciencedirect.com/science/article/pii/092544399500007Q
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with Ks of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species = damaging free radicals) ; this is opposed by reactions involving glutathione.
Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate (= vitamin C). Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with Ks of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species = damaging free radicals) ; this is opposed by reactions involving glutathione.
Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate (= vitamin C). Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.
dinsdag 31 januari 2012
Regular laughter equals regular exercise
In contrast, the subjects who watched the humorous video had changes in blood pressure and also changes in the leptin and ghrelin levels. Specifically, the level of leptin decreased as the level of ghrelin increased, much like the acute effect of moderate physical exercise that is often associated with increased appetite.
Berk explains that this research does not conclude that humor increases appetite. He explains, "The ultimate reality of this research is that laughter causes a wide variety of modulation and that the body's response to repetitive laughter is similar to the effect of repetitive exercise. The value of the research is that it may provide for those who are health care providers with new insights and understandings, and thus further potential options for patients who cannot use physical activity to normalize or enhance their appetite."
Source: http://www.the-aps.org/mm/hp/Audiences/Public-Press/For-the-Press/releases/10/12.html
Definitively an option for many ME and CFS sufferers who are bed- or housebound!
Berk explains that this research does not conclude that humor increases appetite. He explains, "The ultimate reality of this research is that laughter causes a wide variety of modulation and that the body's response to repetitive laughter is similar to the effect of repetitive exercise. The value of the research is that it may provide for those who are health care providers with new insights and understandings, and thus further potential options for patients who cannot use physical activity to normalize or enhance their appetite."
Source: http://www.the-aps.org/mm/hp/Audiences/Public-Press/For-the-Press/releases/10/12.html
Definitively an option for many ME and CFS sufferers who are bed- or housebound!
Multiparous pregnancy causes liver inflammation and weight gain
http://www.the-aps.org/mm/hp/Audiences/Public-Press/For-the-Press/releases/12/1.html
January 30, 2012
Contact: Donna Krupa
Office: (301) 634-7209
dkrupa@the-aps.org
@Phyziochick Multiple Births Lead to Weight Gains and Other Problems for Mouse Moms and Their Male Offspring
Article published in the American Journal of Physiology—Endocrinology and Metabolism
Bethesda, Md. (January 26, 2012)—Women have long bemoaned the fact that as they have more children, their weight gain from pregnancy becomes more difficult to lose. A new study using a mouse model that mimics the human effects of multiparity (giving birth more than once) has found that mouse moms who gave birth four times accrued significantly more fat compared to primiparous females (those giving birth once) of similar age. The study also found significantly more inflammation in the livers of multiparous animals. Multiparity’s effect also extended to the male offspring, who showed significant weight gain during adulthood. Their primiparous counterparts did not, despite similar levels of food consumption. The findings are contained in a study entitled “Multiparity Leads to Obesity and Inflammation in Mothers and Obesity in Male Offspring,” and appear in the American Journal of Physiology – Endocrinology and Metabolism, published by the American Physiological Society.
Methodology
Researchers at the University of Cincinnati designed the study in two parts. In the first part, they established the mouse model that mimics multiparity-induced obesity in humans. In the second part, they examined male offspring of the multiparous females.
The researchers compared one group of mice that gave birth four times with a second group of mice that gave birth only once, some of these at the same age that the first group had its fourth litter and some at a younger age.
The researchers weighed these animals and assessed the size of their fat deposits. They also performed glucose tolerance tests in all the mice and measured biochemical markers of inflammation. Additionally, the researchers performed similar tests in the male offspring of primiparous and multiparous mice, and measured weight, fat deposits, and glucose tolerance. They also measured the expression levels of various genes involved in storing versus using fat.
Results
The first part of the study showed that giving birth multiple times was a significant contributor to obesity regardless of age, with mice who gave birth multiple times being up to 45 percent heavier than those who had a single litter at the same age that the first animals had their fourth. The multiparous animals had fat deposits several times larger than those in typically-mated primiparous mice, as well as significantly larger glucose spikes after meals, a warning sign for diabetes. Multiparous moms also showed elevated markers for inflammation in numerous body tissues, a condition linked to heart disease, diabetes, cancer, and a variety of other diseases, as compared to the primiparous mice as well as age-matched females fed a high fat diet.
The second part of the study revealed that male offspring of multiparous mice weighed as much as 40 percent more than the male offspring of primiparous mice, despite eating no more food. Interestingly, the differences became apparent when the offspring were older, suggesting that excess energy was stored as fat only after growth rate slowed down. When the researchers examined genes responsible for storing versus using fat, the offspring of multiparous animals appeared to use less fat compared to those of the primiparous animals.
Importance, Implications of the Findings
These findings confirm that in mice, as in humans, giving birth multiple times, regardless of age, can lead to significant weight gain, and inflammation. The results also support the theory that multiple pregnancies induce metabolic stresses on females that have heritable consequences and may be part of an obesity cycle between mothers and offspring.
The authors suggest that finding effective ways to help women lose weight between pregnancies will assist in maintaining their health and that of their children, though additional interventions will likely be required as multiple pregnancies appear to have an adverse effect on women that is independent of her fat mass. “The current studies are important in supporting a healthier, less obese population in that we have defined specific metabolic pathways that are likely involved in the programming of obesity and can be targeted in either the mother or her offspring,” the authors say.
Study Team
The study was conducted by Sandra R. Rebholz, Thomas Jones, Katie T. Burke, Anja Jaeschke, Patrick Tso, David A. D’Alessio, and Laura A. Woollett, all of the University of Cincinnati College of Medicine.
January 30, 2012
Contact: Donna Krupa
Office: (301) 634-7209
dkrupa@the-aps.org
@Phyziochick Multiple Births Lead to Weight Gains and Other Problems for Mouse Moms and Their Male Offspring
Article published in the American Journal of Physiology—Endocrinology and Metabolism
Bethesda, Md. (January 26, 2012)—Women have long bemoaned the fact that as they have more children, their weight gain from pregnancy becomes more difficult to lose. A new study using a mouse model that mimics the human effects of multiparity (giving birth more than once) has found that mouse moms who gave birth four times accrued significantly more fat compared to primiparous females (those giving birth once) of similar age. The study also found significantly more inflammation in the livers of multiparous animals. Multiparity’s effect also extended to the male offspring, who showed significant weight gain during adulthood. Their primiparous counterparts did not, despite similar levels of food consumption. The findings are contained in a study entitled “Multiparity Leads to Obesity and Inflammation in Mothers and Obesity in Male Offspring,” and appear in the American Journal of Physiology – Endocrinology and Metabolism, published by the American Physiological Society.
Methodology
Researchers at the University of Cincinnati designed the study in two parts. In the first part, they established the mouse model that mimics multiparity-induced obesity in humans. In the second part, they examined male offspring of the multiparous females.
The researchers compared one group of mice that gave birth four times with a second group of mice that gave birth only once, some of these at the same age that the first group had its fourth litter and some at a younger age.
The researchers weighed these animals and assessed the size of their fat deposits. They also performed glucose tolerance tests in all the mice and measured biochemical markers of inflammation. Additionally, the researchers performed similar tests in the male offspring of primiparous and multiparous mice, and measured weight, fat deposits, and glucose tolerance. They also measured the expression levels of various genes involved in storing versus using fat.
Results
The first part of the study showed that giving birth multiple times was a significant contributor to obesity regardless of age, with mice who gave birth multiple times being up to 45 percent heavier than those who had a single litter at the same age that the first animals had their fourth. The multiparous animals had fat deposits several times larger than those in typically-mated primiparous mice, as well as significantly larger glucose spikes after meals, a warning sign for diabetes. Multiparous moms also showed elevated markers for inflammation in numerous body tissues, a condition linked to heart disease, diabetes, cancer, and a variety of other diseases, as compared to the primiparous mice as well as age-matched females fed a high fat diet.
The second part of the study revealed that male offspring of multiparous mice weighed as much as 40 percent more than the male offspring of primiparous mice, despite eating no more food. Interestingly, the differences became apparent when the offspring were older, suggesting that excess energy was stored as fat only after growth rate slowed down. When the researchers examined genes responsible for storing versus using fat, the offspring of multiparous animals appeared to use less fat compared to those of the primiparous animals.
Importance, Implications of the Findings
These findings confirm that in mice, as in humans, giving birth multiple times, regardless of age, can lead to significant weight gain, and inflammation. The results also support the theory that multiple pregnancies induce metabolic stresses on females that have heritable consequences and may be part of an obesity cycle between mothers and offspring.
The authors suggest that finding effective ways to help women lose weight between pregnancies will assist in maintaining their health and that of their children, though additional interventions will likely be required as multiple pregnancies appear to have an adverse effect on women that is independent of her fat mass. “The current studies are important in supporting a healthier, less obese population in that we have defined specific metabolic pathways that are likely involved in the programming of obesity and can be targeted in either the mother or her offspring,” the authors say.
Study Team
The study was conducted by Sandra R. Rebholz, Thomas Jones, Katie T. Burke, Anja Jaeschke, Patrick Tso, David A. D’Alessio, and Laura A. Woollett, all of the University of Cincinnati College of Medicine.
maandag 30 januari 2012
Factors that may possibly induce liver disease
Host factors that may enhance susceptibility to drugs, possibly inducing liver disease
Female - Halothane, nitrofurantoin, sulindac
Male - Amoxicillin-clavulanic acid (Augmentin)
Old age - Acetaminophen, halothane, INH, amoxicillin-clavulanic acid
Young age - Salicylates, valproic acid
Fasting or malnutrition - Acetaminophen
Large body mass index/obesity - Halothane
Diabetes mellitus - Methotrexate, niacin
Renal failure - Tetracycline, allopurinol
AIDS - Dapsone, trimethoprim-sulfamethoxazole
Hepatitis C - Ibuprofen, ritonavir, flutamide
Preexisting liver disease - Niacin, tetracycline, methotrexate
Source: http://emedicine.medscape.com/article/169814-overview
Female - Halothane, nitrofurantoin, sulindac
Male - Amoxicillin-clavulanic acid (Augmentin)
Old age - Acetaminophen, halothane, INH, amoxicillin-clavulanic acid
Young age - Salicylates, valproic acid
Fasting or malnutrition - Acetaminophen
Large body mass index/obesity - Halothane
Diabetes mellitus - Methotrexate, niacin
Renal failure - Tetracycline, allopurinol
AIDS - Dapsone, trimethoprim-sulfamethoxazole
Hepatitis C - Ibuprofen, ritonavir, flutamide
Preexisting liver disease - Niacin, tetracycline, methotrexate
Source: http://emedicine.medscape.com/article/169814-overview
zondag 29 januari 2012
Kwikvergiftiging en zijn symptomen
http://www.patrikpeters.amalgaam.be/symptomen_kwikvergiftiging.htm
Extract:
Het zweet breekt over heel het lichaam uit. Het is te vergelijken met hoge koorts, met dit verschil dat de lichaamstemperatuur normaal blijft. Men heeft het dus niet te warm of te koud. Het vele zweet kan natuurlijk wel een afkoelend effect hebben.
Mensen welke neiging hebben tot tandenknarsen, doen dit vooral 's nachts tijdens hun slaap. Dit is in vele gevallen als gevolg van stress. In dat geval zullen ze dan ook vooral 's nachts last hebben van het zweten. Dit begint dan doorgaans een paar uur na het inslapen en kan nog de hele nacht verder duren. Binnen de kortste keren is de kleding, de lakens en het hoofdkussen helemaal doorweekt. Sommige mensen gebruiken dan badlakens om tussen te slapen. Deze moeten ze dan verscheidene malen per nacht vervangen. Het zweet laat doorgaans bruin-roze plekken achter op het ondergoed. Die plekken zijn dikwijls moeilijk uit te wassen.
Extract:
Het zweet breekt over heel het lichaam uit. Het is te vergelijken met hoge koorts, met dit verschil dat de lichaamstemperatuur normaal blijft. Men heeft het dus niet te warm of te koud. Het vele zweet kan natuurlijk wel een afkoelend effect hebben.
Mensen welke neiging hebben tot tandenknarsen, doen dit vooral 's nachts tijdens hun slaap. Dit is in vele gevallen als gevolg van stress. In dat geval zullen ze dan ook vooral 's nachts last hebben van het zweten. Dit begint dan doorgaans een paar uur na het inslapen en kan nog de hele nacht verder duren. Binnen de kortste keren is de kleding, de lakens en het hoofdkussen helemaal doorweekt. Sommige mensen gebruiken dan badlakens om tussen te slapen. Deze moeten ze dan verscheidene malen per nacht vervangen. Het zweet laat doorgaans bruin-roze plekken achter op het ondergoed. Die plekken zijn dikwijls moeilijk uit te wassen.
Acetaminophen depletes glutathion
Acetaminophen = paracetamol
http://www.rjsharpe.com/acetaminophen/hypothesis.shtml
Acetaminophen: The Case for a Link to Neurodegenerative Diseases
Acetaminophen either decreases or depletes the endogenous anti-oxidant glutathione in mammalian cells. Without the protective effects of glutathione, mammalian cell damage or cell death occurs. Neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease and disorders of retinal cells, such as age associated macular degeneration, are due at least in part to cellular damage induced by free radicals and oxidative stress. By reducing or depleting neuronal and retinal glutathione, acetaminophen might trigger, accelerate or otherwise worsen these diseases.
Presentation of the Hypothesis
Although acetaminophen lacks the gastric toxicity and anti-platelet activity of aspirin and other classic NSAIDs, it is well known to have hepatotoxicity [7]. Chronic long term acetaminophen use increases the risk of liver failure and acute overdosage can cause fulminant liver necrosis and failure [7]. The mechanism by which acetaminophen causes liver toxicity is probably due to depletion of glutathione by this drug [7]. The hepatic cells are then unable to neutralize the toxic effects of peroxides, superoxide species and free radicals which are generated during the normal course of metabolism.
Neurons within the CNS are very metabolically active, moreover, there is evidence that the glutathione levels within CNS neurons fall with advancing age [8-10]. Others have postulated a role for oxidative stress in neurodegenerative diseases, including Parkinson’s’ disease and Alzheimer’s disease [8, 9].
Given the ability of acetaminophen to cross the blood-brain barrier and its glutathione reducing activity, I postulate that the use of acetaminophen amplifies the toxic effects of oxidative stress on CNS neurons as well as retinal cells and their neuronal network. Further, I hypothesize that the reduction of glutathione levels due to natural aging causes increased sensitivity to the toxic effects of acetaminophen in the elderly. Acetaminophen may thus be a direct cause of neurodegenerative and oculodegenerative diseases of the retina or may be a co-factor in the development and the acceleration of neuronal damage and loss in these diseases.
http://www.rjsharpe.com/acetaminophen/hypothesis.shtml
In the United States, approximately 2000 cases of acute liver failure occur annually and drugs account for over 50% of them (39% are due to acetaminophen, 13% are idiosyncratic reactions due to other medications).
http://emedicine.medscape.com/article/169814-overview
http://www.rjsharpe.com/acetaminophen/hypothesis.shtml
Acetaminophen: The Case for a Link to Neurodegenerative Diseases
Acetaminophen either decreases or depletes the endogenous anti-oxidant glutathione in mammalian cells. Without the protective effects of glutathione, mammalian cell damage or cell death occurs. Neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease and disorders of retinal cells, such as age associated macular degeneration, are due at least in part to cellular damage induced by free radicals and oxidative stress. By reducing or depleting neuronal and retinal glutathione, acetaminophen might trigger, accelerate or otherwise worsen these diseases.
Presentation of the Hypothesis
Although acetaminophen lacks the gastric toxicity and anti-platelet activity of aspirin and other classic NSAIDs, it is well known to have hepatotoxicity [7]. Chronic long term acetaminophen use increases the risk of liver failure and acute overdosage can cause fulminant liver necrosis and failure [7]. The mechanism by which acetaminophen causes liver toxicity is probably due to depletion of glutathione by this drug [7]. The hepatic cells are then unable to neutralize the toxic effects of peroxides, superoxide species and free radicals which are generated during the normal course of metabolism.
Neurons within the CNS are very metabolically active, moreover, there is evidence that the glutathione levels within CNS neurons fall with advancing age [8-10]. Others have postulated a role for oxidative stress in neurodegenerative diseases, including Parkinson’s’ disease and Alzheimer’s disease [8, 9].
Given the ability of acetaminophen to cross the blood-brain barrier and its glutathione reducing activity, I postulate that the use of acetaminophen amplifies the toxic effects of oxidative stress on CNS neurons as well as retinal cells and their neuronal network. Further, I hypothesize that the reduction of glutathione levels due to natural aging causes increased sensitivity to the toxic effects of acetaminophen in the elderly. Acetaminophen may thus be a direct cause of neurodegenerative and oculodegenerative diseases of the retina or may be a co-factor in the development and the acceleration of neuronal damage and loss in these diseases.
http://www.rjsharpe.com/acetaminophen/hypothesis.shtml
In the United States, approximately 2000 cases of acute liver failure occur annually and drugs account for over 50% of them (39% are due to acetaminophen, 13% are idiosyncratic reactions due to other medications).
http://emedicine.medscape.com/article/169814-overview
Antidepressants increase death rate 1,6 times
http://www.gaia-health.com/articles451/000458-antidepressants-increase-death-rate.shtml
Antidepressants Increase Death Rate: Non-Pharma Funded Research
Huge numbers of older men are dying from the use of antidepressants. A PLoS ONE study documents the extent of the carnage.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011266
by Heidi Stevenson
18 May 2011
A shocking study that should have received serious attention from the press and doctors seems to have been ignored. It documents that the death rate of depressed people who take antidepressants is, on average, 1.6 times greater than those who don't take them.
The respected journal, PLoS ONE, published the study in June 2010. It will come as no surprise that there was no pharmaceutical money funding the study. Performed in Australia, the study followed 5,276 men aged 68-88. The claim that depression is a deadly disease is true. The death rate of those diagnosed as depressed is significantly greater than others, and that mortality increases with increasing severity. Those points were the authors' focus. However, the study also shows that the men who are depressed and take trycyclic, SSRI, or any other antidepressants die at a significantly greater rate than those who don't.
The Figures for Increased Death with Antidepressants
One of the saddest things about the study is that the authors didn't dare tell the entire truth in their conclusion. Rather than point out that the death rate is 1.6 times higher for depressed men taking antidepressants, they simply stated:
The use of antidepressants does not reduce the mortality rates of older men with persistent symptoms of depression.
Technically, that's true—but it is, in effect, a lie. The reality is that antidepressants are clearly causing deaths in older men. Here is the graph they produced that documents the increased risk of death for each type of antidepressant compared with the death rate of undrugged patients:
(I have added legends to make it easy to see the results at a glance.)
he graph is based on hazard ratios, which are the increased rates of death. For example, a hazard ratio of 2 would refer to a doubled risk of death. Each of the bars shows the increased rate of death for the men taking a particular type of antidepressant. Here is a table of the results shown above:
You'll notice that the morbiditiy risk ratio figures for the types of antidepressants is specified as approximate. That's because the authors didn't present figures for those, so I estimated them from the graph.
Though the authors did present the specific risk ratios for causes of death, they avoided presenting the figures for increased morbidity for each type of antidepressant. While the reasons for death are certainly interesting, it should be obvious that the most important issue is simply whether and how much a drug increases the risk.
One of the primary reasons used to push antidepressants is that depression is a deadly disease. It sounds good, and this study shows that it's true. However, the implication that taking drugs saves lives is nothing short of a lie. And this particular lie is obviously killing people—yet not a single one of them is counted among the numbers who die from pharmaceutical drugs, nor are they counted as iatrogenic injuries.
Causes of Death
Now, let's take a look at how older men die. The tale becomes even murkier. The study revealed that the rate of suicides and accidents goes up in only one group: men with no depression who are given antidepressants. While the increase is small, it's certainly interesting.
The most significant causes of increased morbidity with antidepressants were cardiovascular diseases and cancer. Each of these nearly doubled with antidepressant use in depressed men over those who were depressed but did not take antidepressants. In men who were not depressed, there was little change. Deaths from infections nearly doubled, too.
This study is not definitive, with the most important factor being that it focused only on men over age 68. Nonetheless, the following conclusions should have been made:
•Men over age 68 should never take antidepressants.
•The claim that one should take antidepressants because depression is a deadly disease is obviously based on nothing.
•People of any age should question taking antidepressants. If they result in hugely increased death rates in older men, why should anyone assume that the story is different in women or younger people?
As documented in Gaia Health, antidepressants have been shown to cause increases in miscarriages, deformities in the babies of women who take them during pregnancy, and violence.
http://www.cbc.ca/news/canada/british-columbia/story/2011/09/19/bc-depressionbabies.html
This study, along with others for men and women of all ages—not to mention children!—should have been done years ago. The reason they haven't been done is inadvertently demonstrated by the fact that the authors assiduously avoided expressing the most startling results of their study: that antidepressants are clearly causing the deaths of thousands, possibly millions, of people.
Even when there was no Big Pharma money funding the study, the authors apparently feared to tell the truth about their findings. Instead, they hid the results behind dissembling words, words designed to give a false impression. Their data clearly shows that antidepressants are killing older men, and doing so at incredibly high numbers. Yet, they didn't utter a word of that in their conclusion. That demonstrates the fear that even honest researchers must be facing when their results show something that Big Pharma and Big Medicine would prefer not be revealed.
Sources:
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011266
http://www.gaia-health.com/articles451/000458-antidepressants-increase-death-rate.shtml
http://www.cbc.ca/news/canada/british-columbia/story/2011/09/19/bc-depressionbabies.html
Antidepressants Increase Death Rate: Non-Pharma Funded Research
Huge numbers of older men are dying from the use of antidepressants. A PLoS ONE study documents the extent of the carnage.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011266
by Heidi Stevenson
18 May 2011
A shocking study that should have received serious attention from the press and doctors seems to have been ignored. It documents that the death rate of depressed people who take antidepressants is, on average, 1.6 times greater than those who don't take them.
The respected journal, PLoS ONE, published the study in June 2010. It will come as no surprise that there was no pharmaceutical money funding the study. Performed in Australia, the study followed 5,276 men aged 68-88. The claim that depression is a deadly disease is true. The death rate of those diagnosed as depressed is significantly greater than others, and that mortality increases with increasing severity. Those points were the authors' focus. However, the study also shows that the men who are depressed and take trycyclic, SSRI, or any other antidepressants die at a significantly greater rate than those who don't.
The Figures for Increased Death with Antidepressants
One of the saddest things about the study is that the authors didn't dare tell the entire truth in their conclusion. Rather than point out that the death rate is 1.6 times higher for depressed men taking antidepressants, they simply stated:
The use of antidepressants does not reduce the mortality rates of older men with persistent symptoms of depression.
Technically, that's true—but it is, in effect, a lie. The reality is that antidepressants are clearly causing deaths in older men. Here is the graph they produced that documents the increased risk of death for each type of antidepressant compared with the death rate of undrugged patients:
(I have added legends to make it easy to see the results at a glance.)
he graph is based on hazard ratios, which are the increased rates of death. For example, a hazard ratio of 2 would refer to a doubled risk of death. Each of the bars shows the increased rate of death for the men taking a particular type of antidepressant. Here is a table of the results shown above:
You'll notice that the morbiditiy risk ratio figures for the types of antidepressants is specified as approximate. That's because the authors didn't present figures for those, so I estimated them from the graph.
Though the authors did present the specific risk ratios for causes of death, they avoided presenting the figures for increased morbidity for each type of antidepressant. While the reasons for death are certainly interesting, it should be obvious that the most important issue is simply whether and how much a drug increases the risk.
One of the primary reasons used to push antidepressants is that depression is a deadly disease. It sounds good, and this study shows that it's true. However, the implication that taking drugs saves lives is nothing short of a lie. And this particular lie is obviously killing people—yet not a single one of them is counted among the numbers who die from pharmaceutical drugs, nor are they counted as iatrogenic injuries.
Causes of Death
Now, let's take a look at how older men die. The tale becomes even murkier. The study revealed that the rate of suicides and accidents goes up in only one group: men with no depression who are given antidepressants. While the increase is small, it's certainly interesting.
The most significant causes of increased morbidity with antidepressants were cardiovascular diseases and cancer. Each of these nearly doubled with antidepressant use in depressed men over those who were depressed but did not take antidepressants. In men who were not depressed, there was little change. Deaths from infections nearly doubled, too.
This study is not definitive, with the most important factor being that it focused only on men over age 68. Nonetheless, the following conclusions should have been made:
•Men over age 68 should never take antidepressants.
•The claim that one should take antidepressants because depression is a deadly disease is obviously based on nothing.
•People of any age should question taking antidepressants. If they result in hugely increased death rates in older men, why should anyone assume that the story is different in women or younger people?
As documented in Gaia Health, antidepressants have been shown to cause increases in miscarriages, deformities in the babies of women who take them during pregnancy, and violence.
http://www.cbc.ca/news/canada/british-columbia/story/2011/09/19/bc-depressionbabies.html
This study, along with others for men and women of all ages—not to mention children!—should have been done years ago. The reason they haven't been done is inadvertently demonstrated by the fact that the authors assiduously avoided expressing the most startling results of their study: that antidepressants are clearly causing the deaths of thousands, possibly millions, of people.
Even when there was no Big Pharma money funding the study, the authors apparently feared to tell the truth about their findings. Instead, they hid the results behind dissembling words, words designed to give a false impression. Their data clearly shows that antidepressants are killing older men, and doing so at incredibly high numbers. Yet, they didn't utter a word of that in their conclusion. That demonstrates the fear that even honest researchers must be facing when their results show something that Big Pharma and Big Medicine would prefer not be revealed.
Sources:
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011266
http://www.gaia-health.com/articles451/000458-antidepressants-increase-death-rate.shtml
http://www.cbc.ca/news/canada/british-columbia/story/2011/09/19/bc-depressionbabies.html
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