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You seem to be thinking of mild depression or even subclinical sadness

No, counseling is equally ineffective against major depression.

The last hundred years or so of medical research specifically tests for effectiveness VS a placebo, so it's not like people are just shooting in the dark here. (To throw you a bone, medications don't seem to be very effective against mild depression.)

The best supported counseling method, CBT, is no better than placebo for depression. Consider this metaanalysis Particularly look at figure 4 and see how the error bars for the effect size of CBT on depression overlaps the Y axis for every disorder except PTSD.

CBT is a well supported treatment for anxiety, not depression. No other form of therapy is well supported for anything at all. SSRIs, like you say are only effective in major depression. For those of us with mild depression, there is no well supported mainstream treatment at all.

Also, stop getting your medical knowledge from TV, it's wrong

Stop getting your medical information from salesmen (aka psychologists), it's wrong. These people have a vested interest in delivering you services, whether or not they're any help to you. A combination of confirmation bias on their part, and the placebo effect on your part fools both of you.

IMO, the real solution to depression, major and minor, is ketamine. It's safe, it's FDA approved, it's out of patent, and it's effective within hours and lasts for a week with one treatment. The only problem is you have to go through the entire battery of SSRIs, MAOIs, tricyclics and atypicals before they'll let you try something quick, easy, safe, and effective.

A study measured arousal (by measuring penile circumference) in exclusively heterosexual men in response to various kinds of pornographic image. They found a clear correlation between homophobia and homosexual arousal.

So yes, other AC is a fag.

Damn, pasted wrong URL. Hate it when I do that.

http://projectreporter.nih.gov/project_info_description.cfm?aid=8070026&icde=12211723

I haven't! The NY Times review is pretty gripping, though, and it sounds like it has a lot of great anecdotes buried in it. I'll see if I can pick it up some time.

Generally I try to avoid using the word 'environment' in these sorts of discussions, because it often brings to mind images of a static forest or workplace or something—I prefer 'experience,' since that can also encompass personal revelations. Undoubtedly your "genes * environment" formula is what I'd generally endorse. Genetic factors will always necessarily impact human intelligence; as a trivial proof of this, consider that the gene HAR1F is one of the major differences between humans and chimpanzees, and is expressed in the brain. Hereditary mental disorders also attest to this.

That being said, it's almost certain that because of assortative mating, at least some of our expectations about intelligence being tied directly to the influence of genes is rubbish; people in the dating pool segregate themselves according to intelligence much like they segregate themselves according to income (and possibly with some correlation), so right there you have many confounding factors about approaches to child-rearing, social environment, and so on. Go back to the middle ages, or even just the beginning of the century (all of the participants in this study were born in the UK or Norway in the 20s and 30s—nice work, guys) and the meaningless correlation is even more prominent. Wikipedia is quick to provide a citation for 'IQ scores have been shown to be associated with [...] parental social status'.

Sometimes I feel like bioinformatics is a really unintelligent field for this very reason: just as their biologist mentors once looked for a single gene that could explain everything about a chemical pathway, we now look for a set of genes that can explain everything about human behaviour. It's staggeringly irresponsible and a colossal waste of money, especially in the hands of behavioural psychologists.

...anyway.

Too little emphasis is placed on personal drive, ambition, and desire, and I'm happy to hear that Shenk focused on this. I found it a little shocking that the Times reviewer felt it was necessary to point out that many people lack the ability to motivate themselves to this extent. I think the major cause of this shortage of motivation might be a consequence of over-socialization in childhood: if you never have to think for yourself, it's going to be harder to learn how. Mob mentality seems like an easy enough scapegoat.

Another bit that's recently been ruffling things up is the discovery that the genome in brain cells is unstable. Were Shenk's book a couple of years newer, it undoubtedly would have mentioned this, at least in passing. In a strange way (that cheats the semantics of the question) the 'nature' of the brain itself may very well be able to change due to 'nurture.' The changes, however, can't be passed on, so it's not really the same thing.

their end goal is to use red blood cells as a vehicle for drug delivery

Now they'll have probable cause if the K9's detect that you have red blood cells.

- sarcasm off.

In all seriousness, gold nano particles are being explored medically in some pretty freakin' cool ways - to kill cancer by heating the gold with light, kill cancer by heating the gold radio waves in places where light can't reach and targetted delivery of chemotherapy.

their end goal is to use red blood cells as a vehicle for drug delivery

Now they'll have probable cause if the K9's detect that you have red blood cells.

- sarcasm off.

In all seriousness, gold nano particles are being explored medically in some pretty freakin' cool ways - to kill cancer by heating the gold with light, kill cancer by heating the gold radio waves in places where light can't reach and targetted delivery of chemotherapy.

Naturally my analogy was an exaggeration, and like most analogies has its flaws. But I do understand stem cells; I'm currently doing a PhD in biology that relates to stem cells and differentiation. I'm certainly aware of the potential that stem cell-based therapies have, but they ought to be done in a controlled and experimentally-validated manner, not just injecting some cells into humans and hoping they help. They might be beneficial - this needs to be properly studied - but they might do nothing, or even risk causing other pathologies or even cancer.

This gives some thoughts on the subject, and this is a recent review article on the risks associated with various therapies.

The grandparent didn't say we eat meat because we evolved to, he said we eat meat because our body is configured to eat meat. To make an absurd analogy, just because we evolved to breath oxygen doesn't mean we have to breath oxygen, or even that we should.

In other words, a naturalistic argument would be that we should eat meat because we evolved to and have always done so. The GP argued that we should eat meat because that's what our bodies are built to do. Such an argument implies it's healthier to do so, but it's not incontrovertible (supported - yes, proven - no).

If you want a more formal example, look at our lipoprotein enzymes. They work much better with saturated ("animal") fats, leading to larger LDL sizes. Unsaturated fats lead to smaller LDL sizes. High levels of either are bad, but the smaller ones get stuck in blood vessels more easily, counteracting the benefit of lower absolute levels. Hence the probable reason why traditional Eskimo diets (99% meat) lead to lower cardiovascular disease than modern diets, and why the Atkins diet works. (Meat-derived omega fats, and such also have an effect.)

Saturated Fat is an interesting topic to compare to AGW. There's a lot more scientific controversy (e.g. the last big meta-analysis) but public consensus. The science behind the two is similarly difficult to study. In nutrition, you can't do randomized controlled clinical trials in humans for 30-40 years to measure the health effects, just as you can't do direct RCTs in climatology. So, the science isn't terribly strong behind either, hence why there's controversy. Plus they're both overly-politicized.

1) Shorter protection time than expected indicating boosters are required

(See: http://www.ncbi.nlm.nih.gov/pubmed/22423127 for example)

and

2) Emergent bacterial strains with modified surface antigens being selected due to evolutionary pressure (gasp!) from the acellular vaccine

(See: http://www.ncbi.nlm.nih.gov/pubmed/22416243 for example)

If you want to understand the science, go to the scientific literature. Not 'naturalnews.com'...

1) Shorter protection time than expected indicating boosters are required

(See: http://www.ncbi.nlm.nih.gov/pubmed/22423127 for example)

and

2) Emergent bacterial strains with modified surface antigens being selected due to evolutionary pressure (gasp!) from the acellular vaccine

(See: http://www.ncbi.nlm.nih.gov/pubmed/22416243 for example)

If you want to understand the science, go to the scientific literature. Not 'naturalnews.com'...

Several people have commented on patsolve (which I wrote) and FreeCellSolver (Shlomi Fish).
The "patsolve-3.0" link that was mentioned was broken, I have updated it. You can find it here:

http://kurage.nimh.nih.gov/tomh/public_html/archives/patsolve-3.0.tgz

FYI, searching the entire game tree for game number 11982 takes .7 seconds on a 3 GHz machine.

I have difficulty with the millions of years in the vacuum of space being irradiated by gamma rays (that we use to sterilize things now). Bacteria will not survive hundreds to thousands, much less millions of years on Earth! How long does it take bacteria to die on your kitchen counter/door knob, etc? Usually minutes to hours. Only certain kinds of spore forming bacteria can survive dessication (drying out) even.

May I suggest: http://www.ncbi.nlm.nih.gov/pubmed/18225667 "One of the most important aspects of the problem of life transfer in the cosmic space is the resistance of microorganisms to high-temperature heating during the launch and entry into the atmosphere. The high-temperature limits of the survival of microorganisms were studied under conditions modeling the laungh from the Mars and the landing on the Earth. Two strain of E. coli K12 exposed to short heating pulse were studied in order to tind out if they could resist high temperature while being in the desiccated state. The procedure was performed in vacuum. It was found that a fraction of bacteria survive heating pulses up to 250 degrees C in vacuum, while similar heating at normal atmospheric pressure leads to the total sterilization of samples."

Actual article for the journal Cancer referred to by the OP's news site is here as a pdf:

http://onlinelibrary.wiley.com/doi/10.1002/cncr.26625/pdf

Read it yourself-- not outlandish and makes a good case for the methodology used.

Also, I encourage you to look at other studies that are related as I think you might be interested. For example, the following says nothing about whether radiation in bite-wing x-rays is dangerous, rather it explores the question "what is the most effective technique for patient treatment" (my wording not theirs):

http://www.ncbi.nlm.nih.gov/pubmed/22103270

Research is a good thing. Research applied is a very good thing. Results of research ignored because "this is how we do it" and "it's really not dangerous anyway you silly scardy cat" is a very sad and potentially dangerous thing. Note-- not directed at jd, this is just my observation (okay, frustration) of how it sometimes "is" in the real world.

Here are a handful, there are lots:
http://www.sciencedirect.com/science/article/pii/S1750946710000498
http://bmo.sagepub.com/content/31/3/264.short
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7610.1985.tb01641.x/abstract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1310767/

And so on. The list goes on and on really, there are literally hundreds of studies on IQ and how to improve it. IQ scores as a metric of pure cognitive ability divorced from education is just fundamentally debunked, and actually has been for some time.

But it's not a small difference - sucrose digests slowly in the small intestine

No, the difference is not significant. This has been known since at least 1966.

"...paired experiments demonstrated the same absorption rates of these monosaccharides from sucrose as from an equivalent glucose-fructose mixture. Hence, hydrolysis does not appear to be rate limiting in the process of sucrose absorption, and the individual absorption rates for glucose and fructose may define the rate of the disaccharide absorption process."

First off, thanks for your links. It's nice to have informed discussion.

There is a good analysis and discussion of this issue here:
http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/

There's a lot of text about dose-dependent, but the problem is clearly in the dosage, as Lustig says in his talk. For example:

"In the single human study I'm aware of that linked fructose to a greater next-day appetite in a subset of the subjects, 30% of total daily energy intake was in the form of free fructose [12]. This amounts to 135 grams, which is the equivalent of 6-7 nondiet soft drinks. Is it really that groundbreaking to think that polishing off a half-dozen soft drinks per day is not a good idea? Demonizing fructose without mentioning the dose-dependent nature of its effects is intellectually dishonest. Like anything else, fructose consumed in gross chronic excess can lead to problems, while moderate amounts are neutral, and in some cases beneficial [13-15]."

My answer to his question is, yes, it is groundbreaking when you compare the mechanisms of fructose to that of alcohol. We know it's not good to binge on alcohol, yet parents think nothing about feeding their kids sodas or fruit juices, sugary cereals, and dessert as part of a day's meal. We've put vending machines that serve sugary junk food in our schools.

All this while what used to be known as adult-onset diabetes is now commonly found in young people. Chalking this up as a lack of exercise and excess calories when their is a clear metabolic mechanism that is dose dependent, just like alcohol, sounds dangerously naive and stubborn.

Prof Jennie Brand-Miller, one of the leading researchers on the relationhips between diet and diabetes has expressed great dismay at Lustig's claims:

http://www.theaustralian.com.au/news/health-science/war-over-sweet-nothings/story-e6frg8y6-1226261140744

I can't access it. It looks to be pay-walled, or at least login-walled and bugmenot doesn't work.

As for correlations(which a lot of the anti-sugar and anti-HFCS crowd place emphasis on), here's an interesting paper showing sugar consumption has declined during the past three decades in Australia and yet there has been a similar rise in metabolic problems as seen in the U.S.:
http://www.ncbi.nlm.nih.gov/pubmed/22254107

Interesting. I'll have to look at it in more detail, but one thing that strikes me right off the bat is that they don't talk about the rates of diabetes or metabolic syndrome, only obesity.

This would appear to indicate that the substance in question does not occur in tobacco nectar, nor anywhere else in nature:

"The invention of imidacloprid, the most important neonicotinoid insecticide, was initiated by replacement of the framework of nithiazine with an imidazolidine ring."

There has been some research into the use of nanoparticle delivery systems for treatment of glioblastoma multiforme, a brain tumor which is often both aggressive and difficult to treat conventionally. Here is an example that met with some success.

yet they still pout off 28-45db, and emit a frequency around 200hz.

Three are several reviews on pubmed.

http://www.ncbi.nlm.nih.gov/pubmed?term=wind%20turbines

What a crappy video. It only prov3es that some things are louder then wind turbines. BIG FUCKING DEAL.

Better?
http://www.ncbi.nlm.nih.gov/pubmed/21682397

You should do a little research before calling other people retarded.

http://www.ncbi.nlm.nih.gov/pubmed/21682397

Actually, the noise the make causes stress as well as sleepless nights. Something that has been seen more and more as usage near populations go up.

http://www.ncbi.nlm.nih.gov/pubmed/21959113

http://www.ncbi.nlm.nih.gov/pubmed/22122963

http://www.ncbi.nlm.nih.gov/pubmed/21682397

Certainly worth the effort of doing better studies. The tighter the controls, the more pronounced the effect seems to becomes.

Well within plausible range, unlike wi-fi and cellphones 'allergies'. Which have been proven to be solely in the head of the person making the claim.

Actually, the noise the make causes stress as well as sleepless nights. Something that has been seen more and more as usage near populations go up.

http://www.ncbi.nlm.nih.gov/pubmed/21959113

http://www.ncbi.nlm.nih.gov/pubmed/22122963

http://www.ncbi.nlm.nih.gov/pubmed/21682397

Certainly worth the effort of doing better studies. The tighter the controls, the more pronounced the effect seems to becomes.

Well within plausible range, unlike wi-fi and cellphones 'allergies'. Which have been proven to be solely in the head of the person making the claim.

Actually, the noise the make causes stress as well as sleepless nights. Something that has been seen more and more as usage near populations go up.

http://www.ncbi.nlm.nih.gov/pubmed/21959113

http://www.ncbi.nlm.nih.gov/pubmed/22122963

http://www.ncbi.nlm.nih.gov/pubmed/21682397

Certainly worth the effort of doing better studies. The tighter the controls, the more pronounced the effect seems to becomes.

Well within plausible range, unlike wi-fi and cellphones 'allergies'. Which have been proven to be solely in the head of the person making the claim.

Your basic clams end up with like 110,000 times the radioactivity of the surrounding seawater, because all they do, all day long, is filter seawater.

The two long-lived isotopes which might be significantly concentrated are Strontium-90 and Cesium-137.

About 70-80% of ingested strontium is excreted; the remainder is generally absorbed into biochemical pathways where it replaces Calcium. Thus it will primarily be found in the bones of vertebrates and the shells of creatures like clams and isopods. The bioaccumulation in things like clams will tend to be comparatively lower in the "edible tissue", and certainly nowhere near "110,000 times" the surrounding water. The flesh will exhibit some elevated levels of Strontium, but a significantly lower elevation than bone/shell material.

Cesium is slightly more problematic, because it tends to be absorbed into chemical pathways which use Potassium, and thus will be found throughout the body in blood and other tissues. However studies have found that concentration factors range from ~2 to ~35x the concentration of surrounding waters for that, as well.

At the dilution levels we're talking about for this material, you'd have to be more concerned about "bioaccumulation" of the radioactive potassium that occurs naturally in seawater, which represents a much larger proportion of the background radiation dose than any of the materials released, at the concentrations they're present. Realistically, these materials low enough concentrations that you would have to eat nothing but clams harvested from just off the Fukushima coast 3 meals a day for years for there to be any significant increase in your chances of health problems.

They are pretty similar, since the only purpose of the digital exams may be your doctor's amusement

http://www.ncbi.nlm.nih.gov/pubmed/20948525

Results showed that the total sugar content of the beverages ranged from 85 to 128% of what was listed on the food label. The mean fructose content in the HFCS used was 59% (range 47-65%) and several major brands appear to be produced with HFCS that is 65% fructose. Finally, the sugar profile analyses detected forms of sugar that were inconsistent with what was listed on the food labels. This analysis revealed significant deviations in sugar amount and composition relative to disclosures from producers. In addition, the tendency for use of HFCS that is higher in fructose could be contributing to higher fructose consumption than would otherwise be assumed.

There's a very good, highly readable article about ocean acidification from 2007 in Science. If you have access to a subscription, you can see the article here.

If you don't have access to a subscription, you can find lots of research about ocean acidification in the freely-accessible pubmed central database. this article looks like it gives a good overview of ocean acidification.

The short answer is that the pH of the ocean has changed measurably since the industrial revolution, and the current pH is far outside the values that have been historically observed. Even based on conservative estimates of future CO2 emissions, it looks like hydrogen ion concentrations in the ocean (remember pH is a log scale) will more than double by 2100. Ocean acidification has a number of impacts on the marine environment, but most notably it increases dissolution of the CaCO3 deposits that make up coral reefs and decreases the rate at which new shells and reefs can be formed.

There's a very good, highly readable article about ocean acidification from 2007 in Science. If you have access to a subscription, you can see the article here.

If you don't have access to a subscription, you can find lots of research about ocean acidification in the freely-accessible pubmed central database. this article looks like it gives a good overview of ocean acidification.

The short answer is that the pH of the ocean has changed measurably since the industrial revolution, and the current pH is far outside the values that have been historically observed. Even based on conservative estimates of future CO2 emissions, it looks like hydrogen ion concentrations in the ocean (remember pH is a log scale) will more than double by 2100. Ocean acidification has a number of impacts on the marine environment, but most notably it increases dissolution of the CaCO3 deposits that make up coral reefs and decreases the rate at which new shells and reefs can be formed.

The suicide rate in these places is shocking.

You lost all credibility right there. There's plenty to criticize about Apple, the suicide rate at a contractor's factories is not one of them.

The Foxconn worker suicide rate (1.5 per 100,000 at its worst, in 2010) is lower than the general Chinese population (22.23 per 100,000).

It is lower than New York (6 per 100,000), which itself is over half the national average (11 per 100,000).

It is lower than US soldiers soldiers (20 per 100,000 as of 2008), which was already an 80% jump over the rate in 2004.

It is lower than suicide rates at both MIT and Harvard (10.2 and 7.4 per 100,000, respectively, from a 2001 report). That's right, MIT and Harvard students are PAYING to be there, and their suicide rate is higher than Foxconn workers.

What are you doing about those shocking numbers? Who are you holding to account and starting online petitions to boycott?

The only thing shocking about the suicide rate of Foxconn workers is that people like you keep thinking it bolsters your argument. Hint: it does the exact opposite, if only you'd thought to analyze it for one minute.

I will go half way with you on editing: let's keep "recognized" where it is, but we adopt your "but it's never been demonstrated [conclusively]." I invite you to read this paper, and look at page eight of this. We can say with good certainty that genetic effects alone are probably insufficient to explain the entire autistic problem, as cases are still going up—it's not just a matter of more sensitive diagnostics (this is in TFA.) All that's left to do is to invoke Conan Doyle, and use some good old-fashioned Holmesian abduction: the environment looks pretty damn suspect.

Citation needed.

The environment as an etiologic factor in autism: a new direction for research. (2000)

Autism, Brain, and Environment. (2006)

ASD-CARC Genetics and Environments Studies. (2007 or so.)

Nurture over nature (page 8). (2011)

No it hasn't. late clamping increase jaundice risk. A risk worth taking if you are in an iron poor community. Otherwise don't do it. Jaundice can cause brain damage, among other things. Even in the iron poor community, the statistical difference is much about noise. Meaning, more study is needed.

When did asking for someone to show there data make them Nazis? Are we suppose to just let people like you continue to spread lies? I, for one, will not do that. SO you can keep making your ad hom attack, but I will not stop trying to get people to see accurate information and be able to find good data.

http://www.ncbi.nlm.nih.gov/pubmed/18591323

A few minutes, sheesh.

That's not a theory. It's a wild ass guess based on the naturalistic fallacy.

The current data shows this:
Late clamping (>60 seconds) increase iron but also increase jaundice risk.

SO, if you are iron poor, then late clamping may be worth the jaundice risk.
If you are not iron poor, then late clamping has no gain and still carries the jaundice risk.

http://www.ncbi.nlm.nih.gov/pubmed/18591323

That is a cochrane review. Since it is a review of the literature, it is a good place to start. Reviews aren't always the best place to make policy from. Depending on method a size of available data to review.

oh, and while people relate jaundice to 'just yellow skin' it can actual cause liver and brain problems.

http://www.ncbi.nlm.nih.gov/pubmed

there you go, search. Be sure the study has good controls, blinded and has significant results, and has been repeated.

Google "Jaundice", which can be a result of dumping too much blood into the kid.

That's the carp you hear from doctors who are unwilling to change the way they have always done things..
It's just that there is no study showing that. On the contrary. While there is no significant increase of jaundice, delayed clamping might lead to healthier babies a few months later and might give the baby a boost right after birth.

The effect of timing of cord clamping on neonatal venous hematocrit values and clinical outcome at term: a randomized, controlled trial.

Delayed Cord Clamping in Very Preterm Infants Reduces the Incidence of Intraventricular Hemorrhage and Late-Onset Sepsis: A Randomized, Controlled Trial

Late vs Early Clamping of the Umbilical Cord in Full-term Neonates

My suggestion:
read up on delayed cord clamping (decent sources, like parent-to-be-books from your local library written by MDs and maybe medical journals) and include it in your birth plan. With the money saved from cord blood banking buy something like this binary Infant Bodysuit

Here's a reference:
http://www.ncbi.nlm.nih.gov/pubmed/22089242
search for "umbilical anaemia"

This. Dunno about other fields, but it's pretty routine these days in bioinformatics and biostatistics for authors to post their data either as supplemental material with the article or on their departmental web site. The problem is that the format for the data they post is generally "whatever format I have it in at the moment" -- if your lab chooses to keep everything in Excel, that's your business, but it's no fun for the rest of us. Microarray data all goes into GEO or ArrayExpress these days, but even there the file specifications are much looser than they should be; and of course microarray data, as important as it is, is only one small portion of the bioinformatics data universe.

"Some researchers have suggested that drinks containing higher alcohol concentrations are more deleterious per gram of alcohol than drinks with lower alcohol concentrations. The evidence for this hypothesis, however, is weak and inconclusive (Doll et al. 1999)." Source: http://pubs.niaaa.nih.gov/publications/arh25-4/263-270.htm

I'll try to resume some data in this message.

Vitamin D supplementation was found in years-long, randomized interventional trials, to slash cancer incidence - by, for example, 77%. ( http://www.ajcn.org/content/85/6/1586.short [ajcn.org] , http://jnci.oxfordjournals.org/content/98/7/451.short [oxfordjournals.org] ) Even mechanisms of action are known ( http://www.sciencedirect.com/science/article/pii/S0960076010001822 [sciencedirect.com] , http://onlinelibrary.wiley.com/doi/10.1002/ijc.24762/full [wiley.com] , http://www.ncbi.nlm.nih.gov/pubmed/20936945 [nih.gov] ), althought not all are fully understood.

Vitamin D RDA was 200 IU, which is a joke, almost the same thing as nothing. Specially if we consider the human body will produce 10.000 IU in a 15-minute tropical noon-day sun full-body exposure ( http://0101.nccdn.net/1_5/3a0/1e8/00e/Cannell-Vitamin-D-study.pdf [nccdn.net] The FDA was faced with this new Vitamin D pleiotropic effects, and given that the RDA was old and obviusly innadequate, it asked the IOM (Institute of Medicine) to review it. They dismissed a Vitamin-D -cancer connection in a completely biased, and non-scientific report, cherry picked some articles, ignored many articles. It shocked the vitamin-D research community, as this link is more than clear. ( http://onlinelibrary.wiley.com/doi/10.1002/jbmr.328/full [wiley.com] , http://brn.sagepub.com/content/13/2/117 [sagepub.com] ). The committee had conflicts of interest, and deliberately suppressed the favourable studies ( http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8225367 [cambridge.org] , http://www.prnewswire.com/news-releases/today-the-food-and-nutrition-board-has-failed-millions-111112159.html [prnewswire.com])

It's interesting to note that people in the committee were hand-picked to have conclicts of interest and are developing vitamin D analogs (that work the same way, but are patenteable), so their best interest is to keep natural vitamin D the lowest level possible. Like Glenville Jones, from Cytachroma, developing CTAP101, a medicine to treat vitamin D insufficiency. Or Hector F. DeLuca, that has 101 patents of vitamin D analogs. Or J. Christopher Gallagher, working for GlaxoSmithKline, that develops Sirilux, a vitamin D analog to treat psoryasis. There are other to cite, but you got the point.

Links or it didn't happen.

I'll try to resume some data in this message.

Vitamin D supplementation was found in years-long, randomized interventional trials, to slash cancer incidence - by, for example, 77%. ( http://www.ajcn.org/content/85/6/1586.short , http://jnci.oxfordjournals.org/content/98/7/451.short ) Even mechanisms of action are known ( http://www.sciencedirect.com/science/article/pii/S0960076010001822 , http://onlinelibrary.wiley.com/doi/10.1002/ijc.24762/full , http://www.ncbi.nlm.nih.gov/pubmed/20936945 ), althought not all are fully understood.

Vitamin D RDA was 200 IU, which is a joke, almost the same thing as nothing. Specially if we consider the human body will produce 10.000 IU in a 15-minute tropical noon-day sun full-body exposure ( http://0101.nccdn.net/1_5/3a0/1e8/00e/Cannell-Vitamin-D-study.pdf
The FDA was faced with this new Vitamin D pleiotropic effects, and given that the RDA was old and obviusly innadequate, it asked the IOM (Institute of Medicine) to review it.

They dismissed a Vitamin-D -cancer connection in a completely biased, and non-scientific report, cherry picked some articles, ignored many articles. It shocked the vitamin-D research community, as this link is more than clear. ( http://onlinelibrary.wiley.com/doi/10.1002/jbmr.328/full , http://brn.sagepub.com/content/13/2/117 ). The committee had conflicts of interest, and deliberately suppressed the favourable studies ( http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8225367 , http://www.prnewswire.com/news-releases/today-the-food-and-nutrition-board-has-failed-millions-111112159.html)

It's interesting to note that people in the committee were hand-picked to have conclicts of interest and are developing vitamin D analogs (that work the same way, but are patenteable), so their best interest is to keep natural vitamin D the lowest level possible. Like Glenville Jones, from Cytachroma, developing CTAP101, a medicine to treat vitamin D insuficiency.

Or Hector F. DeLuca, that has 101 patents of vitamin D analogs. Or J. Christopher Gallagher, working for GlaxoSmithKline, that develops Sirilux, a vitamin D analog to treat psoryasis. There are other to cite, but you got the point.

You seem to be confusing the issue of reporting on a released study versus original reporting or research.

. . . that much doubt means it's not even worth considering. When they eliminate all those doubts and get within 6-sigma I'll consider it.

Do let me know when the FDA begins approving double blind randomized studies of illegal drugs on minors, won't you?

Ditto your sciencedaily (which is about as reliable as the Daily Mail) - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360494/ [nih.gov] - in fact there are hundreds more reliable studies than the crap you're posting, which aren't even from reliable sources.

Well, maybe this will be more to your liking? It is also several years more recent than the one you quote.

Bullous lung disease due to marijuana - Respirology. 2008 Jan;13(1):122-7.

CONCLUSIONS: Marijuana smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function. In subjects who smoke marijuana, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers.

Emphysema and secondary pneumothorax in young adults smoking cannabis - Eur J Cardiothorac Surg. 2007 Dec;32(6):834-8. Epub 2007 Oct 10.

CONCLUSIONS: In case of emphysema in young individuals, marijuana abuse has to be considered in the differential diagnosis. The period of marijuana smoking seems to play an important role in the development of lung emphysema. This obviously quite frequent condition in young and so far asymptomatic patients will have medical, financial, and ethical impact, as some of these patients may be severely handicapped or even become lung transplant candidates in the future.

Smoked marijuana as a cause of lung injury - Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

You seem to be confusing the issue of reporting on a released study versus original reporting or research.

. . . that much doubt means it's not even worth considering. When they eliminate all those doubts and get within 6-sigma I'll consider it.

Do let me know when the FDA begins approving double blind randomized studies of illegal drugs on minors, won't you?

Ditto your sciencedaily (which is about as reliable as the Daily Mail) - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360494/ [nih.gov] - in fact there are hundreds more reliable studies than the crap you're posting, which aren't even from reliable sources.

Well, maybe this will be more to your liking? It is also several years more recent than the one you quote.

Bullous lung disease due to marijuana - Respirology. 2008 Jan;13(1):122-7.

CONCLUSIONS: Marijuana smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function. In subjects who smoke marijuana, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers.

Emphysema and secondary pneumothorax in young adults smoking cannabis - Eur J Cardiothorac Surg. 2007 Dec;32(6):834-8. Epub 2007 Oct 10.

CONCLUSIONS: In case of emphysema in young individuals, marijuana abuse has to be considered in the differential diagnosis. The period of marijuana smoking seems to play an important role in the development of lung emphysema. This obviously quite frequent condition in young and so far asymptomatic patients will have medical, financial, and ethical impact, as some of these patients may be severely handicapped or even become lung transplant candidates in the future.

Smoked marijuana as a cause of lung injury - Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

You seem to be confusing the issue of reporting on a released study versus original reporting or research.

. . . that much doubt means it's not even worth considering. When they eliminate all those doubts and get within 6-sigma I'll consider it.

Do let me know when the FDA begins approving double blind randomized studies of illegal drugs on minors, won't you?

Ditto your sciencedaily (which is about as reliable as the Daily Mail) - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360494/ [nih.gov] - in fact there are hundreds more reliable studies than the crap you're posting, which aren't even from reliable sources.

Well, maybe this will be more to your liking? It is also several years more recent than the one you quote.

Bullous lung disease due to marijuana - Respirology. 2008 Jan;13(1):122-7.

CONCLUSIONS: Marijuana smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function. In subjects who smoke marijuana, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers.

Emphysema and secondary pneumothorax in young adults smoking cannabis - Eur J Cardiothorac Surg. 2007 Dec;32(6):834-8. Epub 2007 Oct 10.

CONCLUSIONS: In case of emphysema in young individuals, marijuana abuse has to be considered in the differential diagnosis. The period of marijuana smoking seems to play an important role in the development of lung emphysema. This obviously quite frequent condition in young and so far asymptomatic patients will have medical, financial, and ethical impact, as some of these patients may be severely handicapped or even become lung transplant candidates in the future.

Smoked marijuana as a cause of lung injury - Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

You seem to be confusing the issue of reporting on a released study versus original reporting or research.

. . . that much doubt means it's not even worth considering. When they eliminate all those doubts and get within 6-sigma I'll consider it.

Do let me know when the FDA begins approving double blind randomized studies of illegal drugs on minors, won't you?

Ditto your sciencedaily (which is about as reliable as the Daily Mail) - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360494/ [nih.gov] - in fact there are hundreds more reliable studies than the crap you're posting, which aren't even from reliable sources.

Well, maybe this will be more to your liking? It is also several years more recent than the one you quote.

Bullous lung disease due to marijuana - Respirology. 2008 Jan;13(1):122-7.

CONCLUSIONS: Marijuana smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function. In subjects who smoke marijuana, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers.

Emphysema and secondary pneumothorax in young adults smoking cannabis - Eur J Cardiothorac Surg. 2007 Dec;32(6):834-8. Epub 2007 Oct 10.

CONCLUSIONS: In case of emphysema in young individuals, marijuana abuse has to be considered in the differential diagnosis. The period of marijuana smoking seems to play an important role in the development of lung emphysema. This obviously quite frequent condition in young and so far asymptomatic patients will have medical, financial, and ethical impact, as some of these patients may be severely handicapped or even become lung transplant candidates in the future.

Smoked marijuana as a cause of lung injury - Monaldi Arch Chest Dis. 2005 Jun;63(2):93-100.

Abstract
In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.

Your go.com link is bullshit - "They acknowledged some limitations, including the use of self-reported data, the lack of adjustment for a family history of psychosis, and possible bias from selected recall" - that much doubt means it's not even worth considering. When they eliminate all those doubts and get within 6-sigma I'll consider it.

Ditto your sciencedaily (which is about as reliable as the Daily Mail) - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360494/ - in fact there are hundreds more reliable studies than the crap you're posting, which aren't even from reliable sources.

Your oddly angry and needlessly insulting response aside, what I was referring to were sources for willow bark metabolism vs aspirin. After a 20 second Google search, I find you're wrong about willow bark's metabolism and you're wrong about their having the exact same active constituents. http://www.ncbi.nlm.nih.gov/pubmed/21226125 Sounds like willow bark has anti inflammatory mechanisms outside the small amount of salicylic acid it contains. Anti inflammatory=Good. Maybe even more benefits than aspirin and almost definitely the same, especially if thinking of daily low dose aspirin for prevention. There are standardized versions of willow bark now, so I don't think the dosage always has to be so variable. Personally, I'd prefer to take a natural version of pretty much anything. Must stem from my (highly justified) distrust of the pharmaceutical industry.

I'm happy to read any sources you might have.

Sources for what?

Aspirin metabolism is outlined here, with a bit more here. Salicylic acid is derived from willow bark (the name Salix from Latin for willow) and is the active form of the drug, resulting predominantly from first pass metabolism in the liver - although some also occurs in the intestine.

Or, did you want a reference for my criticism of your wooly thinking? My only source for that was your post, which I referenced and quoted. For all I know you could be usually quite sharp. If you have other examples of misinformed decisions based on warm-and-fuzzy concepts I will of course be happy to take a look.

Or, were you looking for a reference to the suggestion that taking excessive quantities of some drugs may cause ill effects? I think that's well established fact. Even your own inference that willow bark would be 'better' was based on that very idea. If we're going to accept these things have pharmacological action (which they do) it follows that inconsistent or excessive dosing is either going to limit effectiveness or cause harm. Natural products are intrinsically variable, ergo replacing aspirin with willow bark is introducing variability with the potential to limit effectiveness or cause harm.

I'm not arguing that willow bark "wouldn't work" I'm arguing against your suggestion that it would be in any way better. If you still genuinely think it would be I think the onus is on you to provide both a coherent argument why that is the case - and references to support it.

Yes heavens forbid you actually Google before replying.
http://abcnews.go.com/blogs/health/2012/03/22/obesity-might-lower-cognitive-function/
http://www.ncbi.nlm.nih.gov/pubmed/19236339

The above inflammation related.

Smart to question sources ignorant to stop researching.

"I was having a heart attack, a 100% blockage of the lower anterior decending artery. It was a killer heart attack. Without angioplasty and a stent I was dead. Cardiac intervention is corrective medicine. When you need it, you need it."

AC, I can only plead with you to look into Dr. Fuhrman's approach. It is true the article says "almost" worthless, and maybe you were someone who benefitted from a stent for a time -- although were you really informed of all your options? But if you keep eating the same way that produced the first blockage, your stent and/or arteries will block again leading to another heart attack, possibly in six months to two years time, like happened to my own father and sister. I wish I knew before my loved ones died what I know now. This paper says the median survival time for people with stents in one study was something less than six months:
http://www.ncbi.nlm.nih.gov/pubmed/18766117
"The median survival time in patients treated with metal and plastic stent was 5.9 and 4.4 months (P = 0.074), respectively. "

See also:
http://www.fatsickandnearlydead.com/

You can most likely cure your heart disease by changing your eating patterns today following Dr. Fuhrman's approach or similar, and it will bring you as much joy or more than the way you now eat:
"How to escape The Pleasure Trap !"
http://www.drfuhrman.com/library/article16.aspx

Success stories:
http://www.drfuhrman.com/success/stories.aspx/heartdisease

At least get your vitamin D level checked and try to stay away from refined starches and sugars. Idealy "make the salad the main dish" as Dr. Fuhrman says, and eats lots of fruits, vegetables, and beans.

Good luck if you happen to see this.