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Definiendo la pobreza infantil desde un enfoque de derechos humanos

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It is a lipoprotein that is manufactured in the guts and the liver, and it contains a small amount of cholesterol. This is all complete rubbish. People taking the Atkins diet even had the cheek to find that their cholesterol levels dropped. This is all great stuff, and many thousands of people who used to die are now being saved. Well, not quite, but I once chased down a reference linking heart disease to impotence and found the source reference from a study in Germany in In German. To quote a riddle that my son came home with the other day: Sin embargo, el enfoque monetario es parcial y, en ciertos aspectos, contra productivo en la forma de medir la pobreza.

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However, excess alcohol consumption creates rebound platelet stickiness platelets are hugely important in blood-clotting. For example, the hypothesis that mankind is causing global warming by burning fossil fuels. At which point they are reabsorbed into the liver, or other cells. But surely, everyone knows that there is a placebo effect; it really exists. The duration of intervention was three months. Because people start using terms like alpha-linoleic, and stearic and Omega-3, and cis-bonds and uncle Tom Cobbly and all.

My areas of interest include therapeutic endoscopy, inflammatory bowel diseases, as well as liver and pancreatic disease. Having a special passion for teaching, I strive to educate patients about their illnesses to enable them to be an active participant in their care.

Lewey graduated from osteopathic medical school where he embraced the tradition of treating the whole person. He went on to complete his residency and fellowship training with board certifications in the specialties of internal medicine, pediatrics, and gastroenterology.

For almost three decades, Dr. Lewey has practiced medicine, educated medical students and patients, and conducted clinical research. His interest in these celiac disease and non-celiac gluten sensitivity stem from his personal and family experiences with allergies, celiac disease, and gluten and dairy sensitivity.

He has published a magnitude of articles. To see more of Dr. Rose completed his transplant hepatology fellowship at Integris-Baptist Medical Center and his gastroenterology fellowship at the University of Arkansas for Medical Sciences in Little Rock.

My interests in gastroenterology include therapeutic endoscopy. Thank you for your interest. My goal is for you to makes choices specifically suited to your own health preferences. This means you feel I have understood and addressed your concerns.

I hope you leave your appointment with a feeling that I have clearly explained your plan of care, you understand it, and it matches your own personal health goals. This goes just beyond our personal interaction and extends to our full team: Moore is a graduate of the University of Minnesota School of Medicine and has received numerous professional accolades and recognitions throughout his long and distinguished career.

He is a highly respected endoscopist with high polyp detection rates and patient satisfaction. He welcomes the opportunity to care for you and your loved ones. Pinto's practice is office-based, and he sees patients two days per week, on Mondays and Wednesdays. He is board-certified in Gastroenterology, and completed fellowships in both Gastroenterology as well as Hepatology Liver Disease. He has a special interest in all aspects of liver disease.

Gerrard-Gough brings more than 35 years of general surgery and endoscopy to the practice. He is widely respected in the community and maintains longstanding relationships with providers and patients alike. His surgical background adds depth and an extra dimension to the practice.

Lee comes to Peak Gastroenterology Associates from her practice in central Virginia. Lee is a general gastroenterologist who specializes in colon and rectal cancer screening, the evaluation and management of gastroesophageal reflux disease, inflammatory bowel disease, liver diseases, and irritable bowel syndrome. As a female physician, Dr. Lee appreciates the concerns and specific needs of the female patient. Atkins is a dangerous man promoting a highly dangerous diet. Atkins is not a scientist, how can he know anything.

Next came the terror tactics: This is all complete rubbish. Whilst it is true that a diet high in fat and protein will result in greater production of acidic residues, ketone bodies and the like, and your blood and urine will become slightly more acidic, there is not the slightest, remotest, teeny weeniest piece of evidence to support the claim that this is in any way damaging.

Not a single clinical end-point has ever been demonstrated to be affected. And if you read anything that does claim the Atkins diet is damaging, please take the time to read the small print — if you can find it.

What you will normally discover is that the level of some substance in the blood is found to be raised which may note the word may , lead to kidney damage. Perhaps those leading the Atkins attacks would care to raise their gaze up to the Innuit in Canada and the frozen north.

In years gone by they rarely ate a vegetable, any fruit or a carbohydrate molecule. They existed almost entirely on fat and protein. When they were studied before their lifestyle changed , they were found to be in exceptional health. Without, it must be added, any sign of heart disease or renal failure. But my point, the point of this column, is not to discuss whether or not the Atkins diet works. I wanted to make it clear that the attacks on Atkins are not scientific, not rational.

He, and his supporters, are being subjected to the secular equivalent of the Spanish Inquisition. The sort of attacks that Popper would have recognised for what they are.

Atkins must be destroyed to protect the mighty diet-heart hypothesis. And all of the recent articles that just seem to be springing out of nowhere about the terrible dangers of the Atkins diet are designed to do just this.

One thing that has seriously hampered research in this area is the factor that I call "terminological inexactitude". When you have spent twenty years of your life studying something, you can become somewhat of a bore on the subject.

A bold claim indeed, but I think I can sustain it. The first thing to state, however, is that there is no single cause, no one factor. If there was, it would have been discovered by now. I sometimes think that the obsession with finding the cause of a disease has seriously hampered research into this, and many other areas. There is always a sense, within science, that the answer, when you find it, should be simple, and that therefore the simplest explanation is usually correct: Another thing that has seriously hampered heart disease research is the factor that I call "terminological inexactitude.

Equally, various papers talk about atherosclerosis. If you describe atherosclerosis as thickening and hardening of the arteries, then almost all populations throughout the world suffer from the same rate of atherosclerosis. Yet, the rate of CHD between populations can vary more than fifteen-fold.

In order to understand CHD another horribly inexact term , you must be a bit more precise about what it is that you are actually talking about.

And what I am talking about are discrete, or focal, areas of arterial damage. Some people refer to them as plaques, and so that is the term I will use. Plaques are the little beauties that can narrow an artery, causing things like angina. You can have as much thickening, or hardening, or atherosclerosis of the arteries as you like.

So, what causes plaques to develop? There are two basic processes that do this. The two processes are highly interconnected.

For example, damage to the endothelium stops it from acting as an anti-coagulant surface, making it more likely for a thrombus to form over the damaged area. When a blood clot, or thrombus, forms over an area of artery wall, this is the start of plaque formation.

Repeated thrombus formation over the same spot causes the plaque to grow, and eventually it can completely block the artery. Factors that have been shown to damage the endothelium include: Factors that make the blood more prone to clotting include.

These lists are not exclusive, but they highlight the main factors. You will have noticed a great deal of overlap, which is not surprising. Why some things protect against heart disease. So, what things do protect against CHD, and how. Anti-coagulant and endothelial protection. Endothelial protection Nitric oxide synthesis. Equally, what factors cause plaques to develop? Some of them are the usual suspects: This leads to insulin resistance and raised blood sugar levels. This causes increased blood coagulability and endothelial damage.

This leads to increased levels of stress hormones in the blood. Whether or not a raised blood pressure can cause plaques to form is a moot point. One can see that a high blood pressure may cause endothelial damage, but the evidence from blood pressure lowering trials shows zero impact on the rate of death from CHD So, I think the jury is out on this one.

There are other factors that are relatively rare that directly cause CHD. This leads to increased clotting factors and also all sorts of other things that damage the endothelium. This can be a genetic condition.

Homocysteine, in high levels damages the artery wall, and increased blood coagulation. The single most important cause of CHD, however, is metabolic syndrome. This syndrome can be caused by a number of different factors: Whatever the cause, metabolic syndrome develops because of abnormal cortisol levels. The abnormal cortisol levels, in turn, cause insulin resistance cortisol is a powerful insulin antagonist. This then leads to a spectrum of metabolic abnormalities: As previously described, these factors then lead to plaque formation.

It is likely that the most common cause of metabolic syndrome is chronic stress, which creates HPA-axis abnormalities the HPA-axis is the system that controls the reaction to stress and then abnormal cortisol secretion. Populations most likely to suffer from chronic stress are those suffering social dislocation, emigration, forced relocation, etc. For this reason migrants will generally have high rates of CHD.

Also populations who have been disrupted by other populations moving in on top of them, e. In addition, populations undergoing rapid social change will suffer from CHD.

Wherever Asian immigrants move to, they suffer very high rates of heart disease. Additionally, they have a very high rate of metabolic syndrome, and high levels of cortisol secretion. And just to treat you to one quote on this: South Asians have high rates of cardiovascular disease and its risk factors.

We investigated the relationships between HPAA activity, adiposity and the metabolic syndrome….. This study demonstrated that fasting Clinical Endocrinology 58, Another important cause of heart disease is eating food under stress.

If you eat whilst under physical or mental stress, you will be producing stress hormones: These are all powerful insulin antagonists.

The antagonism from these hormones during a meal will lead to spikes of blood sugar, insulin and triglyceride to name but three factors as insulin, the anabolic hormone, battles against the catabolic stress hormones. The French spend a long time eating their meals, so they give their metabolism a chance to absorb and digest food properly, rather than set up a metabolic battleground with stress hormones.

So, there you have it, now you know what causes heart disease. And if you want to protect yourself against heart disease, do the following things: What about high cholesterol levels? Well, what about high cholesterol levels? This red-herring has thrown researchers off the scent for the last sixty years.

Only when it is abandoned as a risk factor will mainstream researchers be able to make sense of heart disease. An analysis that will make it easier for you to hack your way through the misinformation that spews forth from the great medical research machine. I have only just recovered from the idea that everyone in the whole world over the age of fifty-five should spend the rest of their lives on six different medications, all stuck together in one great big pill.

I was stimulated to look again at the concept of risk. Yet, that is not what it means at all, for this figure is a relative risk reduction figure. And a relative risk reduction means nothing, by itself.

The challenge to make an article about statistics interesting….. But maybe a little bit interesting? When you talk about a risk, you need to know the absolute risk of a thing happening. For example, the risk of getting struck by lightening. But again, that figure means nothing unless you put a time scale on it. Is this a one in five million risk over a hundred years, or one year? This is one hundred percent certain — shock claim from Astronomer. And of course, this is true. The Earth will be hit by a big Asteroid, sometime in the next three billion years or so.

I am even willing to take a bet on it. So, I must define risk in two ways, the possibility of the thing happening, and the time period during which that thing will happen. With lightening strikes, this is about a one in five million risk, over a five year period. Unless they want money to fund their Asteroid defence system.

A snip at five trillion dollars, plus VAT. What generally happens is that people inflate the risk in the following way. For example, the chances of dying of lung cancer, for a non-smoker, are about 0.

If, however, you live with a heavy smoker, your chances will increase to about 0. These figures are for illustration only. Now you can report this in two ways.

You can state that passive smoking can increase the risk of lung cancer by 0. Or, you can state that passive smoking increases the risk of lung cancer by fifty per cent. Both figures are correct.

If you are an anti-smoking zealot, then I would imagine you would prefer to highlight the second figure. The relative risk figure. And when it comes to reducing cardiovascular risk, exactly the same procedure is used in reverse. By reducing this risk to 0. In this way a 0.

Mangling statistics is easy when you know how. Anyway, now you know the difference between a relative risk and an absolute risk, and I hope this makes it easier for you to hack your way through the misinformation that spews forth from the great medical research machine.

Not that long ago, a number of people were put under general anaesthetic and had holes drilled into their skulls. These procedures carried all the risks of major surgery, yet the doctors who carried out the operations knew that they would provide no benefit.

Why was this done? It was done to satisfy the demands of the great placebo God. A strange creature that lives in a metaphysical world. A creature of belief without substance, a wraith like thing that constantly changes its shape and appears in a different guise to everyone who sees it. But surely, everyone knows that there is a placebo effect; it really exists.

Give someone a white pill with no active ingredients and it will have an impact of some sort — usually a positive impact. Everyone believes this to be true. So strong is this belief that almost all major clinical trials, wherever possible, are split in two, with one group being given an active substance, and the other group a placebo.

So we are told. Ah, the placebo effect. Yet, everyone is quite happy to accept that there is a placebo effect, without ever bothering to measure it in any meaningful way. Do you think that this would make the placebo effect more or less powerful? Has anyone ever bothered to measure this… ah, well….

Most people assume that the placebo only works if the patient thinks they are taking a real drug. Has this ever been tested, or measured? It is only the belief in the pill that works. And if there is a real placebo effect, should we not use it to treat diseases?

Or, at least, it only exists if the patient really believes that they are taking a real drug. Most mainstream doctors believe that alternative medicine works purely through the placebo effect.

Is this true… who knows? All that we really know about the placebo effect is that, in some areas, such as pain relief, patients who take a placebo report reduced pain, an effect as powerful in some people as that achieved by strong painkillers. No-one, in fact, really knows if a placebo arm is ever required in any clinical trial. It is just an article of faith.

And to look at this another way: So surely, it is important to establish the difference between taking a drug, and taking nothing — as this will reveal the absolute benefit of taking the drug in real life — even if that did include some placebo effect.

So the placebo arm offers no value, other than some data of purely academic interest. The placebo arm was required to have surgery with holes drilled in their skulls, so that they could not know that they did not have the device implanted….. I think you may be able to guess at the answer to this by now. In fact, some studies have clearly shown that there are conditions with no placebo effect at all whatever a placebo effect might actually be , e.

All this, in reality, because a placebo can reduce pain. I have never taken morphine, or heroin. But I have spoken to those who have for pain relief. Soldiers shot in combat often say that they feel no pain at all. The brain can create pain out of nothing, and also shut it off completely. So it is not exactly surprising that an inactive white pill presented as a painkiller can reduce the perception of pain, or the recollection of it, or the reporting of the recollection of it.

However, from this completely subjective and unscientific observation has sprung the assumption that there is always a placebo effect — in all conditions. Beware the dreaded placebo effect, my son. The jaws that bite, the claws that catch! Beware the Jubjub bird, and shun The frumious Bandersnatch! He took his vorpal sword in hand: Long time the manxome foe he sought— So rested he by the Tumtum tree, And stood awhile in thought.

And as in uffish thought he stood, The Jabberwock, with eyes of flame, Came whiffling through the tulgey wood, And burbled as it came! And through and through The vorpal blade went snicker-snack!

He left it dead, and with its head He went galumphing back. Come to my arms, my beamish boy! Not a disease, or a cause. We have become mesmerized by blood sugar levels — we fight to get them down — we are happy when the level is lowered.

Doctors claim when the blood sugar level falls below an arbitrary figure that the Type ll Diabetes has been treated, even cured. But what exactly have we cured? What is a disease? Here are a few definitions, culled from three dictionaries: Okay, so that counts as pretty unhelpful. I can sense a circular discussion arriving. There was a time when I thought I knew what a disease was. Then I started thinking about it, and realized that the concept of disease is horribly difficult to get a handle on.

For here we have an agent, and a set of symptoms and signs caused by that infection. But even in the case of an infection, what is the disease? If you get infected with the tuberculin bacillus you may develop TB.

But TB can affect the lungs, the gut, the lymph nodes, bone. The infective agent is the same in each case, but the disease state can vary enormously. Having TB in the lungs can lead to coughing up blood, breathlessness — death. TB in the gut can just sit there dormant, unnoticed. Is TB, therefore, always the same disease, or several different diseases caused by the same agent? We would call TB in the lungs, consumption, and TB in the guts, bowel nodularity — or something of the sort.

What becomes clearer, when you start thinking about things more deeply, is that, in general, the process of defining disease starts when doctors find an abnormality.

At this point they usually define the abnormality as the disease, unless, or until, they find a deeper underlying cause for that abnormality. Thus high blood pressure of unknown cause becomes essential hypertension, and hypertension is considered by most doctors to be a disease. Even though there must be a deeper problem that causes the blood pressure to be high in the first place.

Equally, if you find a number of interconnected abnormalities clustered together, these are quite often named as a disease after the doctor who first noticed the connections, for example: None of these doctors had the faintest idea what the underlying cause might be.

They just said that they had seen patients with this set of abnormalities. Well, it has a ring to it. The most recent example I know of is Gerry Reaven of Stanford University who noticed a number of interconnected metabolic abnormalities in patients at high risk of CHD.

A syndrome, not a disease — discuss. So you might ask where has all this has got us. The point I am trying to make here is that our definition of a disease is actually totally arbitrary. I am sure that almost everyone believes that they know what a disease is, and what it is not. But when you try to get a grip on it, you will find the concept slips away like mercury. Does it matter at all?

Which, in a roundabout way, is how we get back to diabetes. Everyone I speak to is certain that diabetes is a disease. But what is diabetes? The Greek root of "diabetes" means "siphon," and the Latin root, "mellitus," means "honey," referring to the copious voiding of sweet-tasting urine by the diabetes sufferer. From the first century a. These were descriptions of type I diabetes. Type I diabetes happens when the insulin producing cells in the pancreas are destroyed by an auto-immune process — of unknown origin.

With no insulin, the blood sugar rockets up and sugar starts to leak into the urine. Type II diabetes is primarily caused by resistance to the effects of insulin, or insulin resistance.

The different types of diabetes have gone through a number of different naming protocols. Type I used to be called juvenile diabetes, as it tended to start at an early age. Type II was called adult diabetes, for obvious reasons. Type I and type II diabetes have also been designated insulin dependent and non insulin dependent, and type A and type B.

There is another terminology kicking around called Latent Autoimmune Diabetes of Adults LADA , which describes adults who end up with auto-immune destruction of insulin producing cells. There is even another type of diabetes entirely, called diabetes insipidus. Something that you could stare at for the rest of your life and never even realize that there was anything wrong at all.

An underlying assumption is now forming in your mind, actually it has already formed, and it is this. Diabetes is a disease where the blood sugar level rises too high. I am restricting the discussion here to type II diabetes by the way.

Of course that is true. But what is the disease? The high blood sugar level? Or the underlying problem that causes the sugar to get high in the first place.

Tracking backwards in time for a moment. Next, it was discovered that in diabetes, the sugar level in the blood was also very high.

So diabetes came to mean a high blood sugar level. When Banting Best and Mcleod isolated insulin from the pancreas of cows and injected it into people with type I diabetes, their blood sugar level went down, and they recovered.

Until the insulin ran out, of course. But it was never the high blood sugar levels that killed a type I diabetic patient. In diabetes, you die because insulin is required to switch on the production of sugar receptors from within cells all around the body - other than in the brain.

With no insulin, no sugar receptors are produced, and no sugar can be absorbed from the blood. With no sugar to use for energy, the cells start to metabolise fat, and protein. One of the residues of fat and protein metabolism are ketone bodies, and these are acidic. By giving insulin they were allowing cells to manufacture sugar receptors, absorb and metabolise sugar and clear out the acidity from the blood. But because the disease, in diabetes, was a raised blood sugar level, it was just assumed that it was the lowering of the sugar that was critically important.

And even though everyone now knows that type I diabetics die of diabetic ketoacidosis, the historical baggage that comes with diabetes has proven impossible to shift. So we still define diabetes, the disease, as a high blood sugar level.

The current goal of treatment in type II diabetes is to lower the blood sugar level. Can lowering a metabolic sign really prevent mortality and morbidity? Are we treating a disease when we lower blood sugar levels? No, we are not. We are lowering blood sugar levels which is an effect, not a cause. Does this mean that lowering blood sugar levels is a waste of time….

In fact, some studies appear to show that tight blood sugar control may actually result in increased mortality. This would be surprising if we were actually treating a disease. But it is less surprising once you recognize that you are treating a metabolic sign.

I will try to finish where I started with the statement that type II diabetes is not a disease. A sign, an effect. Doctors claim, when the blood sugar level falls below an arbitrary figure, that the type II diabetes has been treated, even cured.

But what, exactly, have we cured? An annoyingly high figure on a piece of paper that comes back from the laboratory — or a disease? If you want to understand coronary heart disease, you cannot ignore the role of the humble blood clot. Up to now I have resisted writing about this area, as blood clotting is a mind-boggling and complicated area of human physiology.

In the end, however, if you want to understand coronary heart disease CHD , you cannot ignore the role of the humble blood clot. For it is now accepted by everyone involved in CHD research that the final event, the thing that kills you with CHD, is the formation of a blood clot on top of an atherosclerotic plaque. If the blood clot is big enough to completely block a critical artery, in a critical area, you will die. In the last few years medics have become increasingly expert at trying to clear these potentially fatal clots.

Aspirin is the first line of defence, then the clot busters streptokinase, or tissue plasminogen activator tPA are used. Increasingly, cardiologists get to work with thin wires and balloons, and stents, to remove the clot, prize the artery apart, and stick a metal framework to keep the artery open after unblocking it. New drugs have been developed to keep the artery patent. This is all great stuff, and many thousands of people who used to die are now being saved.

So there is no argument from anyone about the final event in CHD. It is also recognised that blood clots develop over atherosclerotic plaques on quite a regular basis without causing any symptoms at all, presumably because they are not big enough to fully block the artery. However, in these silent episodes, once the blood clot stabilises it adds to the plaque size, and can lead to greater narrowing of the artery.

And if you look at plaques closely, you can — in many plaques — clearly see bands, with each band indicating an episode of plaque growth. This is all agreed upon by almost everyone. And if you were a simple soul, like me, you might argue that if plaques grow, and eventually kill you due to clots forming on the artery wall, could this not be how they start in the first place?

This hypothesis was initially proposed by Karl Von Rokitansky in Although supporters of Rudolf Virchow may argue that he said it first. Unfortunately, therefore, I can hardly claim that this idea is either new, or mine. Can it really be that simple? Surely there must be something wrong with the hypothesis that atherosclerotic plaques are the remnants of repeated blood clots?

Where does this idea break down? But I will attempt to be a little more objective than this. After all, a critical function, perhaps the critical function of the lining of the artery the endothelium is to prevent blood clots from forming.

So how can this process actually start? A good point from my learned friend. Equally, every factor that has been identified as reducing the risk of CHD has clearly identifiable anti-coagulant activity. Which, I would vouchsafe, is pretty heavyweight proof. Is this really true? But you have to understand that there are three interconnected factors at play here that can cause a clot to form over the artery wall.

Once damaged, the endothelium stops acting as a non-stick anti-coagulant surface. Indeed, if the endothelium is stripped away, it exposes the middle layer of the artery, the media, to the blood, and the media releases the most powerful pro-clotting factor known to man: The second factor is how pro-coagulant the blood is itself.

There are a multitude of clotting factors in the blood. Increase a pro-coagulant factor, and you increase the chance of clots forming.

The third factor is the structure of the blood clot itself. Some clots are wobbly and weak; others are very tough, and difficult to break up. For example, incorporated into all blood clots is a substance called plasminogen.

This is an enzyme which, when activated, chops the clot into pieces. Which is why tPA — tissue plasminogen activator - is given to people having a heart attack However, if you have a high level of Plasminogen activator inhibitor — 1 PAI — 1 in the blood, plasminogen is less effective at breaking the clot up. So, you have to look at three basic factors: Bearing this in mind, I think it is interesting to run through a few factors known to alter the risk of CHD, and see how they fit: Smoking creates free-radicals in the blood, these reduce nitric oxide NO synthesis in the endothelium, and NO is the single most powerful anti-coagulant factor in the body.

Smoking also has pro-coagulant effects in the blood; it raises fibrinogen levels. It also has endothelium damaging effects. Ethanol, in moderate doses, reduces free-radical synthesis, reduces clotting factors, such as fibrinogen, and reduces the blood clot toughness.

However, excess alcohol consumption creates rebound platelet stickiness platelets are hugely important in blood-clotting. Moderate drinking protects against CHD, heavy drinking is a risk factor. A high blood sugar level leads to increased free-radical synthesis, see above. Not surprisingly, haemophilia reduces blood coagulability. Statins have strong anti-coagulant effects, they stabilise plaques and increase NO synthesis.

Aspirin reduces the stickiness of platelets see alcohol. Platelet aggregation is the first step in blood clotting. Omega-3 fatty acids have strong anti-coagulant effects in the blood. Physical, or psychological stress causes the release of the stress hormones: I am a little ambivalent about this risk factor. However, it is possible to see how high pressure, and turbulent blood flow, could strip away a layer of endothelium, exposing the blood to the media, and thus factor VII, thus stimulating a blood clot to form.

However, the clinical trials on blood pressure lowering are very unconvincing when it comes to a correlation between the degree of blood pressure lowering and the prevention of CHD.

HDL has strong anti-coagulant effects. T his is a complex pathway. When platelets start to stick together, they release free radicals. Free radicals oxidise LDL. Oxidised LDL is a powerful blood clotting factor. If you wish to, it is possible to link every single factor known to have an impact on CHD rates to one of three effects: Now that is another story altogether.

But if enough people think I am making all of this up, then I will provide a series of references from prestigious journals to support every single fact that I have presented.

Perhaps it is too obvious for anyone to see it. To quote a riddle that my son came home with the other day: What is greater than God More evil than the devil The poor have it The rich need it If you eat it you will die.

The pro and anti-fat battle seems to be raging in the colonies, with people hurling data of mass destruction at each other with great vigour. As usual, I find that "truth is the first victim in any war. A number of people have written, asking me to comment on the Gary Taubes-Michael Fumento battle.

What do I think, what is true? Over on this side of the pond, most people have never heard of Taubes or Fumento, or Dr Aktins. But the pro and anti-fat battle seems to be raging in the colonies, with people hurling data of mass destruction at each other with great vigour.

So what is the truth? Who is right, the pro or anti-fat lobby? The question, in the case of Taubes vs. Because they are extremely lipid soluble, cannabinoids accumulate in fatty tissues, reaching peak concentrations in 4—5 days. They are then slowly released back into other body compartments, including the brain.

Within the brain, THC and other cannabinoids are differentially distributed. High concentrations are reached in neocortical, limbic, sensory and motor areas. THC is highly lipophilic and initially taken up by tissues that are highly perfused, such as the lung, heart, brain, and liver. Drug Testing and Analysis: Handbook of Experimental Pharmacology. Journal of Experimental Botany. Journal of Analytical Toxicology. Disposition of Toxic Drugs and Chemicals in Man 9th ed.

Archived from the original on Archived from the original on 19 June Journal of Natural Products. Multidisciplinary Association for Psychoactive Substances. Efficacy and safety of medical marijuana in selected neurologic disorders: Cochrane Database of Systematic Reviews 2: Cannabinoid receptor modulators cannabinoids by pharmacology List of: Recreational and medical applications rights Industrial applications. Autoflowering cannabis Cannabis indica ruderalis sativa Difference between C.

Medical cannabis History Timeline Religious and spiritual use Chalice. Cannabis in pregnancy Dependence Effects of cannabis Long-term Endocannabinoid system Impaired driving.

Adult lifetime use by country Annual use by country. Return to class B Uruguay: Decriminalization of non-medical use Rescheduling per the Controlled Substances Act. Cannabis political parties List of British politicians who have acknowledged cannabis use List of US politicians who have acknowledged cannabis use. ADPF Gonzales v. United States thermal imaging Leary v. Medical and recreational uses. Calea zacatechichi Silene capensis. Coffee break Coffeehouse Latte art Tea house. Abuse Date rape drug Impaired driving Drug harmfulness Effects of cannabis Addiction Dependence Prevention Opioid replacement therapy Rehabilitation Responsible use Drug-related crime Fetal alcohol spectrum disorder Long-term effects of cannabis Neurotoxicity Overdose Passive smoking of tobacco or other substances.

Alcohol legality Alcohol consumption Anabolic steroid legality Cannabis legality Annual use Lifetime use Cigarette consumption Cocaine legality Cocaine use Methamphetamine legality Opiates use Psilocybin mushrooms legality Salvia legality. Diphenidine Ephenidine Fluorolintane Methoxphenidine. Dextrallorphan Dextromethorphan Dextrorphan Racemethorphan Racemorphan.

Iamges: anabolic primer pill

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Her philosophy as a physician is to serve as an empathetic guide for patients as they navigate through their GI and liver problems, and provide them with as much information as possible to make educated decisions about their care. But even in the case of an infection, what is the disease? In addition to this, the 0.

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Or, at least, it only exists if the patient really believes that they are taking a real drug. However, with regard to unquestioned dogma, things are much the same today. Actually, that is not true.

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