Recommended Gateway Pages

Phrma's Tobacco Science Exposed--a list with links

Four families of block busters

HEART  --  CARDIOVASCULAR TOPICS:

Anticoagulants prevent ischemic events and embolism, I covered only warfarin and Plavix and compared them to aspirin.  The benefits of aspirin (more in healthful choices section) based on very extensive research of the literature has caused me to conclude that all those with a significant risk of ischemic event should be taking aspirin (325 mgs, and  uncoated for better absorption), and not the low dose to which over 80% become tolerant in the first year.  The same applies to those at high risk for an embolism.  The risk of ulcer is double from 2% to 4%, but if the cause, H. pylori, were treated, it would go down to near 2% (see section on PPIs).  The many health benefits of aspirin is why pharma through their KOLs oppose its use (see section below on aspirin.

If I had an MI or pulmonary embolism I would take 4 aspirins with water, and another 4 I would crush and take sublingually for quick absorption.  For a stroke because of a 15% chance that it is hemorrhagic, I would not take aspirin.  

Arrhythmia drugs, long term studies show that they promote arrhythmia, in Bad Pharma Supra Prof. Goldacre (pages 133-34, The CAST Trial) recounts how they were once prescribed following a MI, and this caused a minimum of 100,000 excess deaths.  Arrhythmia is over treated with drugs that are worse than nothing at all.  An August, 2017 BMJ article recounts how often an EKG is used to justify drugs for patterns which aren’t indicative of a significant risk of a blood clot or fatal fibrillation.    

Atherosclerosis: Since atherosclerosis is the result of an inflammatory process, pharma’s claims that oxidative damage to LDL causes an inflammation response and then based on looks of atheroma claims it is mainly cholesterol.  Contrary plaque contains only 7 to 27% an amorphous mix with some of it being cholesterol, based on autopsy studies, while 66% was fibrous—this has been known for over 100 years.  Pathogens within the artery walls through an immune cause response the plaque.[1]  Endothelia dysfunction is a causal factor. 

Cardiovascular disease & MI, covers a long list of what is taught that benefits pharma’s interest, and also includes a section on what is the major cause for the formation of plaque is bacteria within the artery walls that causes an immune response. Imaging and thus procedures are not done on the high risk atheroma:  “Older plaque is stable and unlikely to cause a medical emergency, though, for example, it can cause stable angina.  Most MIs occur with less than 50% and typically at locations with about 20% stenosis (narrowing), prior to sudden lumen closure resulting in an MI” Wiki 2014.  Bypass and angioplasty are done on coronary arteries with occlusion of over 70%. 

Cholesterol myth and at  id5, relies upon Prof. Uffe Ravhskov and D Adams articles, and others published elsewhere on my site; their articles show that there is no causal relation between serum cholesterol , LDL, triglycerides, saturated fats, and cardiovascular disease. Mere association does not prove causality.  Pharma through scientific fraud has created a fake cause and “proves” slight benefit from cholesterol lowering drugs. 

Endothelial dysfunction is a systemic pathological state of the inner lining of the blood vessels (endothelium) which increases the risk for cardiovascular disease.  Insulin resistance leading to defective collagen, reactive chemicals in the blood including fructose affect these gatekeeper cells functions.  Rancid fats and glycation affect the cell membranes, and the stress from malignant hypertension are other major causal factors.[2] 

Hypertension is not a disease but a sign of an underlying atherosclerosis and inflammatory response,[3] or a sign of kidney disease.  Hypertension drugs do not significantly reduce risks associated with CVD, because lowering blood pressure doesn’t undo existing cardiovascular disease (CVD), kidney disease or reduce the rate of formation of new plaque—the exception is malignant hypertension, above 180.  Hypertension most times is signs of atherosclerosis (hard, calcified, clogged arteries); in response the heart pumps harder to get an adequate supply of blood and thus oxygen to the brain and other organs as needed.  Lowering blood pressure with drugs that have neuroleptic effects reduces quality of life, cognitive functions, and functions of organs and tissues throughout the body by reducing blood and oxygen; and the side effects create new conditions. 

High salt (sodium) diet appreciable raises blood pressure.  As Dr. Fung explains with reference, salt contributes at most to a 5% increase in blood pressure—and its dietary history.  Moreover sodium has several vital functions including lower the risk for  gout, obesity and diabetes; and it is tightly regulated by the kidneys.  Failure is a way to persuade the patient to take drugs.

LDL is the bad form of cholesterol.  LDL has besides transporting triglycerides and cholesterol to areas of growth and repair a second function of neutralize toxins excreted by bacteria[4].  One location of transport is to the tunica media of the artery walls where pathogens have caused an immune system response.    

Lipid hypothesis, hypercholesterolemia when lowered does not reduce the rate of ischemic events: 1) high serum cholesterol is not causal for heart attacks; 2) cholesterol is only a minor constituent of atheromas; 3) LDL and its contents of cholesterol and triglycerides in atheroma are a result of a response to inflammation and they are actively transported by endothelial cells on the artery walls to promote the healing process. 

Niacin under attack, in a very high dose which causes the unpleasant flush, thus 1.5 to 3 grams per day is recommended.  Another way pharma reduces competition.  Since cholesterol is produced by the liver at night, giving cholesterol lowering drugs during the day serves to increase the dose, costs, and side effects, and thus is contrary to the needs of the patient.   

Physical interventions, bypass surgery, angiogram various ablations, and angioplasty they are not effective because the plaque that leaks and causes ischemic events is fresh young, with occlusion under 50%, typically about 20%.  It doesn’t show up on imaging, moreover, there is no way of know, if it did, which one would leak to cause an MI.  Bypass and angioplasty can reduce or cure angina, however, other claims are sales pitches.  But these procedures are done to extend life in the real-world population; they don’t.  Various common interventions such as coronary angioplasty, thrombolysis, and bypass surgery at best to benefit only a small select subgroup of patients.[5] “The 60 hospitalizations prevented by CABG required 555 hospitalization for the CABG procedure, not a great trade-off!” Oxford Journals. Cardiac catheterization has issues such as “ restenosis which occurs in over 30% to 50% of angioplasties by month 6; 4) cancer from high exposure to x-rays during the 1 hour procedure; 5) “Thrombosis within a stent causing myocardial infarction and death.”  See section 20 for the longer list, at.   Anthony Colpo, The Great Cholesterol Con has chapters where he goes over the evidence.  Some of that can be found at healthfully and longer version has details about the procedures, side effects, and failure rate, and much more. 

Statins  To lower cholesterol profile and LDL which is the end product of the HGM-CoA reductase pathway also called the mevalonate pathway not only reduces its end product cholesterol (typically about 40%) it also reduces a number of other important bioactive products including CoQ10 (ubiquinones) an essential enzyme in the production of ATP in the Krebs cycle, and the production of a number of other essential compounds including the sterols (steroid alcohols), heme A, dolichols, prenylated proteins, a number or precurcer molecules DMAP, IPP, and others, and by lowering cholesterol it lowers the precursor for the synthesis of the sex hormones, vitamin D, and all steroid hormones including cortisol, digestive bile that aids the absorption of fat molecules as wells as the fat soluble molecules vitamin A, D, E, and K, and cholesterol is 30% of cell membranes and modulates membrane fluidity. Statins reduce quality of life for the elderly: a large Canadian study had 75% dropout by 2 years, and 80% in a NJ study.  See my summary paper for more details including how statins increases the risk for heart failure. Since the side effect reporting has been given to pharma; we can’t know the extent of pathologies or all of them.

Radiofrequency ablation (RAF) and other physical interventions--such as AC or pules of DC current--is a medical procedure in which part of the electrical conduction system of the heart, tumor, or other dysfunctional tissue is ablated using the heat generated from medium frequency radio frequency.  The use is justified by a surrogate outcome of change pattern on a graph rather than lives extended. In a 2015 review article on RAF, it was safe and effective; however there were inclusion of studies showing much greater risks, that this conclusion of safe, given the bias of industry, is likely wrong.[6]  I would take the conservative path and let the heart heal natural rather than injury heart tissue through ablation.    

CANCER:    

Cancer: Pharma promotes the 6 mutation theory, mutations which account for the properties of a cancer, and for which they have hundreds of poisonous drugs based on that theory.  Of late pharma has taken an interest in the defective mitochondria as a cause for cancer, but not as the cause, but as a downstream event. Otto Warburg and others hold that the damage to the mitochondria which results in them becoming non-functional, and this is the initiating event that makes a cell cancerous.   This disabling of the mitochondria is the way a tumor avoids apoptosis[7], thus this step is essential.  Metabolism must now occur in the cytosol in an anaerobic process called “lactic acid fermentation”. This anaerobic process produces only about 1/15^th the amount of ATP per molecule of glucose metabolized in the mitochondria does in the Krebs (citric acid) cycle.  This process typically results in an indolent tumor, and often fails to meet the criteria of invading adjacent tissue.[8] The rare swap of DNA of these precancerous cells with a macrophage results in a line of cells that are not attacked as foreign when the cancer cells spread to other tissues and rapidly reproduce as though they were growing new tissue as when wound healing occurs.  So turned on there is a high rate of glycolysis to promote the “needed” cell proliferation.  Driven by the low rate of production of ATP from lactic acid fermentation, the cancer is in most cases a glucose hog. 

In 2007 I started to doubt the 6-mutation theory and believed that probably stem cell were the cause of metastatic cancer, in 2011 I switched to pluripotent cells, both being able to cause a precancerous cell to rapidly reproduce and evade the immune system—one event was more likely than six.  In 2015, I read articles on starving cancer as part of my continuing research on cancer, and a year later a seminal article on the role of macrophages which swap genes with a tumor cell.  I learnt that anaerobic metabolism is believed to be the way cancer cells avoid apoptosis and the gene swap with macrophages enables the tumor cells to evade the immune system as cancer spreads to different tissues.  The evidence for this is beyond the scope of this paper, however, posted at my website is some of the articles that argue for the Warburg hypothesis. 

Starving cancer -- Warburg Hypothesis:  In its drive to maximize profits, pharma ignores the defective metabolism of cancer cells since it promotes both fasting and ketogenic diet as a way to control and/or destroy cancer.  In 1924 by Otto Warburg, Nobel Laureate, discovered that most cancer cells have shut down their mitochondria due to gross abnormalities, thus the cells cannot metabolize fats,[9] and rely upon glucose metabolized anaerobically; and they can also metabolize glycine, but there isn’t enough available  glycine alone to sustain cancer cells.  Fasting is anti-angiogenic, anti-inflammatory, and pro-autophagy and pro-apoptotic.  With fasting and later augmented by a ketogenic diet most cancer cells cannot obtain enough ATP for growth, and survival.  This often results in tumor shrinkage, remission, and sometimes a cure.  Around the beginning of this millennium the biology behind the Warburg observation became “a hot item”; unfortunately, the main focus is on developing drugs to augment existing chemotherapy.  Starving cancer instead of standard chemo therapy is not on their radar.  Not surprisingly regulatory bodies are not funding or approving clinical trials that without chemo starve cancers through fasting and a ketogenic diet—see Prof. Thomas Seyfried.  Nevertheless over 1,000 cases are referenced in the medical literature.

Chemotherapy in most cases targets a factor of rapidly reproducing cells such as mitosis or angiogenesis which slows, or sometimes stops the growth of cancer.  This approach not only harms the cancer cells but other rapidly reproducing cells through the body such as intestinal endothelial cells, hair cells, and immune system cells.  Therefore the therapy must be administered intermittently and for a limited time.  The negative health consequences limit their application. 

Target Therapy “blocks cancer growth of cancer cells by interfering with specific targeted molecules need for carcinogenesis and tumor growth rather than by simply interfering with all rapidly dividing cells (e.g. with traditional chemotherapy)” Wikipedia. Sounds good but the wedge of difference is very thin; it is marketing rhetoric.  There has been some success (namely Gleevec for chronic myelogenous leukemia).  The Target therapies for a few types of cancer (leukemia, lymphoma, and testicular cancer) have not been translated into success for the common adenocarcinoma because of fundamental differences.  Unfortunately, new therapies are marketed as target therapy, like new and improved Tide laundry soap.  However, the net results are cures or major extension of life for adenocarcinoma are lacking.  Pharma is a marketing machine, and complex molecular biological explanations are commonly used.  The war on cancer started under the Nixon administration has been a failure that pharma has profited from.   

Survival and hope’s hypothesis:  In the UK, NICE, which makes drug decision for the NIH, has repeated refused to include in their formulary drugs which are both expensive and extend life of terminal patients an average of 3 months or less.  Budget constrains is the reason.  Too often the word survival is used when in fact it means life extension.  Only a few chemotherapies can cure terminal cancer or extend the average life of a terminal patient a year longer than best current treatment.     

Sunshine and cancer:  claims that sun causes not just the benign Basal and squamous cell skin cancers, but also the 40% deadly melanoma, a claim that goes back to 1975.  Another example of pharma’s expanding the results:  the early study was done on squamous cell skin cancer; the reverse is the case for melanoma.  The advice as to limit sum exposure it turns out is not in the interest of people but pharma because the sun is needed to activate vitamin D, and with low vitamin D the risk for an  assortment of conditions significantly increased – link to seminal article 2017. 

Cancer treatments that follow the guidelines:, very few types of chemo can cure metastatic cancer can be cured by chemotherapy.  Thus chemo doesn’t prevent a stage 1-3, chemotherapy from becoming metastatic. Giving chemotherapy to a person who through excision or radiation has been cured based on the possibility that that some cancer cells might be missed and the chemo will destroy those cells is marketing crap.  If the chemo can’t cure stage IV, then it won’t destroy any remaining cancer cells missed.  Shrinking a tumor short term doesn’t equate to extended life since often the most aggressive cancer cells have survived. Chemo at best might lengthen a few months the time before that patient is diagnosed with metastatic cancer, but at the same time all those for whom excision has produced a cure, their lives have been shortened, and their health and quality of life compromised--see chemobrain, and.  A reasonable guestimate would be that such pointless treatment shortens life an 4 years on an average.  I know of no long-term study of the survival of stages 1, 2,&  3 for prostate, breast, or colon cancer that compares chemo to no treatment.  The dearth of studies is evidence that those diagnosed with non-metastatic as a group benefit.   See Cameron and Pauling trial of terminal patients comparing an untreated group to those given vitamin C.  In Scotland in the 1970s terminal colon cancer patients normally are not given chemo.  Pauling and Cameron in a trial that compared 10 gram iv infusion of vitamin C and later orally to the standard no treatment.  Their protocol extended life 5 times longer than those who had no therapy.  The subsequent 2 Mayo clinic trials were hatchet jobs that deliberately deviated from the Cameron and Pauling protocol, including skipping the infusion and using chemotherapy which harms the immune system. In Scotland other hospitals had been using similar Vitamin C treatments, and Abram Hoffer, a Canadian researcher, had very significantly improved upon the Scottish protocols by adding several more vitamins (Cameron and Pauling, Cancer and Vitamin C, 1993 p 142-144).   The science behind how ascorbate damages cancer cells has been updated recently.  If I had cancer I would limit treatment to excision, or if inoperable to having the cancer irradiated, and refuse chemo unless it was one which would have a significant cure rate for terminal patients and/or extend their life on an average by over two years as compared to the best earlier treatment.  I would then take mega dose of vitamin C and 2 grams of aspirin, do extended fast (see Warburg below) and go on a ketogenic diet.  In deciding to refuse chemo, I would consider in my determination the 32% positive bias found for neuroleptic drugs (see next section, Cherry Picking, below and NEJM article).  I am not recommending others violate clinical guidelines or their doctor’s recommendations.  

Hormonal therapy: 

Mega dose of ascorbate:

Dementia (neurodegenerative diseases)  

There are 6 common neurodegenerative diseases:  Alzheimer’s disease (AD, about 50% of cases), Lewy body, ALS, Parkinson’s disease, vascular dementia, alcohol-related dementia, and frontotemporal dementia with its typical loss of over 70% of spindle neurons. For the sake of simplicity, and because of an every growing number of AD cases (July 2017 BMJ article stated that AD is the leading cause of deaths in the UK for women and second leading for men), I am focusing on AD.  The insightful question raised supra on the CAWD applies:  “Why is AD/dementia virtually unknown among the elderly aboriginal peoples on their traditional diet?” [10]--well almost unknown.[11]  Since all dementias are associated with our high fructose diet, a tentative extension of the biology behind AD and how to lower risk, the findings and prevent are likely applicable to those other types of dementias.  

There is hard evidence supporting the starting role of fructose.  Fructose causes glycation, ROS (reactive oxygen species), IR, and fatty liver, and thus their complex contributor factors.[12]   The delay in onset is likely associated with the age related reduction in ATP, thus a reduction in cerebral metabolism and cellular repairs.  Studies of the elderly have found as earlier markers for the progress both reduction in cerebral metabolism and damage from ROS (reactive oxygen species) caused by glycation[13] see also.  Insulin resistance is strongly associated with AD.  Since AD is part of the age-related package of conditions associated with the high fructose western diet, I believe that fructose is the major cause through glycation, IR, and fatty liver—causal factors missing among those who are life-long on a low sugar diet, such as the Japanese, Okinawans, Chinese, Polynesians, and the Kitavans (off the cost of New Guinea) though they all eat diets high in easily digestible carbs.     

Downstream biological changes are not particularly relevant to the prevention because they are signs, not causes.  However, some signs suggest ways to prevent AD.  Pharma’s business model is to treat the signs; thus most research dollars are spent on signs and ameliorating drugs.[14]   Though I have not put up healthfully.org/r a summation paper on AD, this is the current area of research, what follows is the same pattern of dietary causes and healthful interventions. 

Journal evidence support that AD is strongly associated with oxidative damage and diminished rate of metabolism in the brain.  “Oxidative stress with AD… is manifested by damage to proteins, lipids, and nucleic acids as well as RNA,” at 2001.  The second major contributing factor is the decline in the brain’s metabolic rate, to which oxidative stress is a cause.  Reduction in functions promotes the accumulation of Bata amyloid and tau protein in the dendrites.[15]  Third major cause is the diminished activity of the neurotropic factors (NTFs) as a result of the first two:  the repair and cleanup systems aren’t functioning very well.  Details of these causes have been worked out, for example the diminished ability of lysosomes to remove tau protein and beta amyloid.  Beta amyloid accumulates in the mitochondria of AD patients and diminishes its enzymatic activity of respiratory chain complexes and thus oxygen consumption and.   

  Contributing to the reduction in the house-keeping process is the wide use of sedatives.  They are marketed as panaceas for emotional problems, mild to moderate pain, muscle relaxants, hypertension, COPD, premenstrual syndrome, and so on.  To this I would add the statins since they block the conversion of HMG-CoA to mevalonic acid (the melavonate pathway), thus statins reduce CoQ10 by about 40%, and CoQ10 is an enzyme used in the production of ATP.  This reduction in ATP is particularly pathogenic in the elderly because of their already reduced production of ATP.   By the age of 65, a reasonable estimate for those taking one or more of these drugs that cause sedation would be over 75%.[16]  Prof. Peter Gotzsche[17] with a much shorter list of sedative drugs found that among the Dutch by the age of 75 had averaged 6 years on them.[18]   I have search for and failed to find population studies on this likely association of sedatives with AD.     

Alcohol is a water soluble sedative, and it associated with Wernicke-Korsakoff’s syndrome and alcohol-related dementia.  One causal mechanism is as a neurotoxin possible due to thiamine deficiency; others add B12 and zinc deficiency.  Olson 1998 estimates that one-fourth of the dementia population has alcohol related problems. These effects fit the pattern of drugs that affect neurotransmitters or lower the brains ability to engage in cellular maintenance such as by reducing the production of ATP, they are causal for dementia.  

The association of AD with diabetes is 3 fold (a much greater rate if only the elderly on insulin were counted) entails issues with the production of collagen (describe in the above section on metabolic syndrome).  A number of journal articles implicate collagen IV involvement and other collagens  (collagens XVIII, VI & XXV) in the pathogenicity leading to AD.  As speculated earlier, by extension insulin resistance is likely to affect the production of collagen and therefore a much larger population than diabetics are at   increased risk.[19]  IR has also been found through elevated insulin and thus elevated IGF-1 (insulin like growth factor one) to increase the risk of AD.  Since diabetics are insulin resistance their IGF-1 is also elevated and this would in part account for their increased risk.  The list of downstream causes is longer; therefore, I am not attempting to catalogue them all. 

 Another important contributing factor is the reduction in the use of things that lower the risk for AD. Major ones include the reduction in the post-menopausal use of HRT (estradiol with progesterone from a compounding pharmacy offers the most protection, while Prempro the least).  Over the last hundred years there has been a steady decline in testosterone levels-- testosterone is also neuro-protective.  Aspirin, like the major sex hormones, is neuro-protective and like them has been shown to very significantly lower the risk for AD.  Aspirin was for over 4 decades been the leading NSAID, now it is seventh, and most of its sales is for the very low dose (under 130 mg) and often enteric coated.  Low does though developing tolerance is ineffective.  The enteric coating entails aspirin is even less effective because peak absorption is delay 5 hours, and with food an average of 8 hours.  In the gut bacteria remove the acetate group which hinders some of the salubrious functions of aspirin. 

  What I have done to lower my risk for AD is based upon neuro-protective and dietary changes to avoid CAWD.  I have cut back my consumption of sugars to an average of 20 grams a day--mainly from fruits and vegetables; cut back carbs to less than 15% of calories, and thus increased coconut oil to an average of 110 grams daily because of its conversion to beta hydroxybutyrate.  I take daily the anti-inflammatory and antioxidants:   aspirin 325 mgs uncoated, topical testosterone prepared in a compounding pharmacy, 300 mgs of CoQ10 suspended in oil, 2 grams of sodium ascorbate, and vitamin E.  I still have an exercise program, though I am in my 7^th decade:  I run an average of 5 miles, swim twice, and do weight lifting 5 hours per week.  Aerobic exercise stimulates neurotrophins.  I do intermittent fasting 6 days a week whereby I skip breakfast, and I cut back on my carbohydrates to less than 15% of calories 6 days a week.  And since the age of 33, I have reduced my intake of drugs that act upon neuron, such as alcoholic beverages to about 2 ounces yearly, marijuana to zero, and drugs by pharma to zero.  The exception is caffeine, to which my consumption average over the years about 1 cup of tea a day.  We ought to take better care of our body than our car.      

At this point I would propose that the reduction in metabolism is causally associated with a reduction in the house-keeping functions in the brain which results in the.  Likely significant environmental causes besides fructose for AD,[20] I would place first among lifestyle causes the most neuroleptic drugs that affect neurotransmitters and lower brain metabolism (cause sedation) which would include some hypertension drugs, statins through reduction in CoQ10, and most psychiatric drugs.[21]  Some others such as opioids, ethanol would at most have a weak association. 

Psychiatric Diseases and Sedatives

Pharma’s record confirms their business model driven by corporate incentives described as tobacco ethics which produces tobacco sciences; thus their pattern profiting by illness, illustrated in the above sections; it is repeated with psychiatric drugs.  The prima facie fact which proves that they promote illness is their side effect of sedation.[22] Though neuroleptic drugs are classified and marketed by pharma and their KOLs as antidepressant antipsychotic and such, they aren’t.  Drowsiness is the major side effect of 95%[23] of these drugs when they are given in effective doses; they are sedative/tranquillizers, and sedation isn’t the long-term fix.  In 98%[24] of the cases taking a sedative daily is like throwing kerosene on a fire.  Lowering cognitive functions exasperates issues.  Drugging the patient for months and years increases the frequency of relapses into major depression three fold, compared to no treatment.  The vast majority of untreated depression episodes are self-limiting, short term.  Sure if one is very sad because she had her dog put down, taking a few pills that slows the brain down and increases sleep will reduce the duration and intensity of depression.  By taking that drug for a year or more as over half the patients do increase frequency of subsequent depression episodes.  And because they are downers, few people use these drugs for a recreational high because they cause general apathy, boredom, mild depressive mood, reduced sexual function, that is why they are called “downers.  For about half who have taken the sedative at a higher dose, they will find withdrawal difficult, and many will fail to get off their drugs; this fact has contributed to pharma’s marketing decisions.  These adverse consequences of the downers are not stressed (if mentioned) in medical textbooks or heard in continuing education classes.  Pharma’s mantra is safe and effective; thus withdrawal agitation, depression, and worse are attributed to the underlying condition in the patient not the drugs that have caused it.  Man can easily be manipulated by a broken evidence base into doing harm, and their verbal response is he is doing good.

A major myth is that drugs have significantly lowered the number of inmates in mental hospitals by curing mental illness.  This was done by using the high dose to limit behavior by sedation and subsequent damage to the brain.  Critics such as Dr. Peter Breggin and by Prof. Joanna Montcrieff consider such long-term high dose treatment with drugs similar to lobotomy and shock treatment in that all 3 damage the brain, and this damage alters behavior.  But it wasn’t until government policy under the conservatives Margret Thatcher and Ronald Reagan moved the inmates to the streets and nursing homes that the numbers dropped.  This, for many of the inmates was possible because of extreme sedation through drugs such as Thorazine (Chlorpromazine); but long-term sedation is not cure, and relapses are common as was tardive dyskinesia.  The damage to quality of life  doesn’t justify the treatment. 

HARM:  The evidence of mass harm is before our eyes, just ignore what is being said and observe.  Observe over the last 6 decades the increase in numbers of mental illnesses; observe the number of bizarre murders and suicides committed by those on psychiatric drugs and the increase in peoples on social security for psychiatric disability.  “Psychiatrist Peter Breggin claims that antipsychotic drugs induce a ‘chemical lobotomy’ and cause permanent brain damage, leading to a form of drug-induced dementia (Berggin 2008).  Furthermore Breggin and others suggest that the “brain disabling effect of these drugs is not an unintended side effect, but the intended consequence of drug treatment.” Prof Moncrieff, The Bitterest Pill, p. 3-4.   This pattern of harm is similar to that caused by alcohol.  Ethanol is heavily promoted by industry as a social feel-good drug, and psychiatric drugs as happy pills (mothers little helpers-Valium) and as fixes for neurosis.  Fortunately physicians don’t give out prescriptions for ethanol or recommend it, but they do with psychotropic drugs.  The market for neuroleptic drugs has been expanded to other uses, examples:  tramadol for mild to moderate pain, Spiriva for COPD, beta blockers for hypertension, varenicline, cytisine, nortriptyline, and clonidine for  nicotine addiction, and Flexor as a muscle relaxant—all have drowsiness as a side effect and all effect neurotransmitters. Their short-term benefits[25] are minimal for a select ideal subgroup in the clinical trials; and negative if results are adjusted for pharma’s thirty plus percent positive bias (scientific fraud), and still worse if real-world population is used and tracked for years.  Like with statins, there is a chorus of academic critics, but there effectiveness in changing standard medical practice is at best minimal--for books.     

The STORM –  Unfortunately, humans are the only species that long-term deliberately changes the levels of neurotransmitters with non-nutritive substances.  Plants make neural intoxicants to keep animals away, and yeast produces ethanol as a byproduct of metabolism for a similar reason.  But humans are a social animal and relief of boredom is a strong drive.  Because of this, there is a propensity to upset nature’s complex balance of neurotransmitters; and pharma profits therefrom.  In the US 23% of women between the age of 40 and 59 are on antidepressants, years 2005-2008, NCHS Data Brief, and this is for only one psychiatric indication (for men it was 8.5%).  And though they are recommended for short-term usage, the National Health and Nutrition Survey found more than 60% are taking them for 2 years or longer, and 14% over 10 years.[26]  A Finish study (likely of higher quality) found 45% were still on them at 5 years (Gotzsche p 255-6).   Thus in addition to the legal and illegal recreational drugs with have pharma’s cornucopia. I’d guestimate that that by the age of 60 there is only 15% of adults who not on pharma’s drugs with neuroleptic effects (see some of the non-psychiatric uses above). 

For those who want to read more I have a list of books with brief evaluations—all I have read.  As mentioned before, the site has a collection of lectures and documentaries, each with a brief description and rating.  You can use the internal Google search engine to fine more journal articles.

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