Impact of a low-carbohydrate, high-fat diet on gut microbiota. | The poor, misunderstood calorie

Impact of a low-carbohydrate, high-fat diet on gut microbiota. | The poor, misunderstood calorie

NPR recently reported on a study where the participants ate either a meat-based, fiber-free ketogenic diet or a vegetarian diet and had their gut microflora analyzed.  The low carbohydrate diet was much higher in fat, and as such, increased the prevalence of a microbe involved in fat digestion.  “Bilophilia.”  The article focused on this one and cited a 2012 study where Bilophilia was associated with intestinal inflammation… however, the ketogenic diet increased the levels of Bacteroides and decreased Firmicutes.  These are the two that brought the whole gut microbe-obesity connection into the spotlight.  The microbiome in obese mice is characterized by low Bacteriodetes and high Firmicutes. Fecal transplants from obese mice to lean mice causes them to gain weight.  Little is known about Bilophilia relative to Bacteriodetes & Firmicutes, and I suspect the focus was on Bilophilia because the authors wanted something negative to say about a meat-based, fiber-free ketogenic diet, and that 2012 mouse study suggested Bilophilia could be their answer.

Obesity alters gut microbial ecology (Ley et al., 2005)
This study shows increased Firmicutes & decreased Bacteriodetes in genetically obese mice but not their lean siblings.  This is important because microbes are usually inherited from Mom and are common among littermates.  Apparently, genetic obesity overrides both.
An obesity-associated gut microbiome with increased capacity for energy harvest (Turnbaugh et al., 2006)

This one shows decreased Bacteriodetes & increased Firmicutes in obesity.  This is also the study that shows microbial transplantation from obese to lean mice causes weight gain (with no change in food intake).  Oh yeah, and by “microbial transplantation,” they mean wiping the poop of a fat mouse all over a skinny one.  Yes, that’s how they do it.

Human intestinal microbiota composition is associated with local and systemic inflammation in obesity (Verdam et al., 2013)

This study shows decreased Bacteriodetes & increased Firmicutes is associated with obesity and inflammation in humans.

Firmicutes associated with human obesity here, too.  Sorry, everyone’s favorite Lactobacillus acidophilus is a Firmicute.  Bifidobacteria, on the other hand, is not. #Bifidobacteria.

Diet rapidly and reproducibly alters the human gut microbiome (David et al., 2013)
The current study.  The animal-based, high fat, very low carb, fiber-free ketogenic diet induced a microbial shift that correlates with leanness in humans, and causes leanness in mice.  This is what should’ve made headlines, not Bilophilia.

Dietary information was buried in the supplemental files, but great data presentation:

Calories and macro’s show that the animal-based diet was indeed, ketogenic:


And if you still think 126 grams of protein is too many for ketosis, ffs:
The diet only lasted 4 days; that’s not a disadvantage because diet-induced microbial changes occur within 1-2 days and remain stable.


This study is interesting because it tested two widely differing diets.  Critics will say we can’t know what caused the changes because there were too many variables.  To them, I say this: those studies will come; that doesn’t make this one useless or uninteresting. 

Also, I don’t care much for Firmicutes or Bacteriodetes; they’re obviously not the answer to obesity… the tone of the news reports and article itself just didn’t sit well with me.


Atlantic: Lies, Damned Lies, and Medical Science | e-Patients.net

Atlantic: Lies, Damned Lies, and Medical Science | e-Patients.net

Atlantic: Lies, Damned Lies, and Medical Science

There’s an extraordinary new article in The Atlantic, “Lies, Damned Lies, and Medical Science.” It echos the excellent article in our Journal of Participatory Medicine (JoPM) one year ago this week, by Richard W. Smith, 25 year editor of the British Medical Journal: In Search Of an Optimal Peer Review System.

oPM, Oct 21, 2009: “….most of what appears in peer-reviewed journals is scientifically weak.”
Atlantic, Oct. 16, 2010: “Much of what medical researchers conclude in their studies is misleading, exaggerated, or flat-out wrong.”

JoPM 2009: “Yet peer review remains sacred, worshiped by scientists and central to the processes of science — awarding grants, publishing, and dishing out prizes.”

Atlantic 2010: “So why are doctors—to a striking extent—still drawing upon misinformation in their everyday practice?”

Dr. Marcia Angell said something just as damning in December 2008 in the New York Review of Books: “It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine.” (Our post on Angell is here.)

What’s an e-patient to do?? How are patients supposed to research if, as all three authorities say, much of what they read is scientifically weak?

More problematic, what’s an e-patient to do when doctors commonly insult them, saying “You don’t know how to research – stick to peer reviewed journals”? You know what reaction patients get when they question those journals? Commonly, doctors’ eyes roll. Both are reasons why we’ve covered this subject forever. See our category Understanding Statistics.

I haven’t read the full Atlantic article yet, but today it was the buzz of Twitter.  I’ve asked for a post by Peter Frishauf, who authored a great commentary on Smith’s article last year: Reputation Systems: A New Vision for Publishing and Peer Review. Stay tuned.

Atlantic: Lies, Damned Lies, and Medical Science | e-Patients.net

Atlantic: Lies, Damned Lies, and Medical Science | e-Patients.net

Atlantic: Lies, Damned Lies, and Medical Science

There’s an extraordinary new article in The Atlantic, “Lies, Damned Lies, and Medical Science.” It echos the excellent article in our Journal of Participatory Medicine (JoPM) one year ago this week, by Richard W. Smith, 25 year editor of the British Medical Journal: In Search Of an Optimal Peer Review System.

oPM, Oct 21, 2009: “….most of what appears in peer-reviewed journals is scientifically weak.”
Atlantic, Oct. 16, 2010: “Much of what medical researchers conclude in their studies is misleading, exaggerated, or flat-out wrong.”

JoPM 2009: “Yet peer review remains sacred, worshiped by scientists and central to the processes of science — awarding grants, publishing, and dishing out prizes.”

Atlantic 2010: “So why are doctors—to a striking extent—still drawing upon misinformation in their everyday practice?”

Dr. Marcia Angell said something just as damning in December 2008 in the New York Review of Books: “It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine.” (Our post on Angell is here.)

What’s an e-patient to do?? How are patients supposed to research if, as all three authorities say, much of what they read is scientifically weak?

More problematic, what’s an e-patient to do when doctors commonly insult them, saying “You don’t know how to research – stick to peer reviewed journals”? You know what reaction patients get when they question those journals? Commonly, doctors’ eyes roll. Both are reasons why we’ve covered this subject forever. See our category Understanding Statistics.

I haven’t read the full Atlantic article yet, but today it was the buzz of Twitter.  I’ve asked for a post by Peter Frishauf, who authored a great commentary on Smith’s article last year: Reputation Systems: A New Vision for Publishing and Peer Review. Stay tuned.

Fraud and science Part 1 & 2: Petulant Skeptic

Petulant Skeptic: Fraud and science

07 January 2011

Fraud and science

Everyone else is writing about it, so I may as well too. Everyone is reporting that not only does the MMR vaccine not cause autism, but the data purporting to show that it did was fraudulent.

While everyone seems terribly outraged by this, they also seem to be treating the whole thing as some sort of crazy anomaly -- the scientific equivalent of that high school reunion your wife couldn't go to and where you had a bit too much to drink and the (still) hot girl you pined for long ago is now impressed at what you've become and somehow you end up with her panties in your luggage. I mean, why tell your wife? It'll turn both your lives upside down, hurt everyone involved, and it was just a once in a lifetime confluence of alcohol, chance, and reminiscence...

Except that isn't the truth and everyone knows it. While it's not tenable to deploy the mutaween to the thousands of high school reunions in this country, it does seem feasible that we come up with a better accounting system in the world of science (and retractions in particular). At present the editors of surgical journals seem to have no problem telling Retraction Watch that the reason a paper was retracted is, "None of your damn business."

This is why some context is important. The media treating this Wakefield debacle as though it's of singular import casts a shadow that obfuscates the huge number of articles that ought to be retracted. For those too lazy to click that link the authors speculated that between 10,000 and 100,000 unretracted ought to be. (Ah, but maybe their own is among them? Shut up.)

Oh, but this Wakefield thing is just a fluke. Most of those crappy journal articles don't actually hurt people. Right? Right???

Wrong. Let me tell you the story of Werner Bezwoda (as if to emphasize my point, he doesn't even have a Wikipedia page). Back in the 1980s doctors had come up with a new theory for cancer treatment. Well, it wasn't really a new theory, it was just the extension of an old one to an unfathomable degree. The limiting factor on chemotherapy effectiveness at the time was the patient's bone marrow. If you destroyed all of the bone marrow cells (along with the cancer cells) your patient invariably died (although not from cancer). Medicine being what it is, doctors decided, well we need to destroy the bone marrow to kill the cancer, so what we'll do is extract bone marrow from these folks, give them the super megadose (it was actually called that) chemo, and then implant the bone marrow back.

The guys at the NIH who first came up with this idea tried to set up some clinical trials to rigorously test the idea before putting it into practice. Unfortunately they were undermined by a media blitzkrieg that cast them as villains for keeping a potentially lifesaving therapy from dying cancer patients. The public outcry was sufficient that the FDA gave the whole procedure a compassionate use exemption. Public demand for the procedure was fed by our man Bezwoda, a physician claiming extraordinary results with the autologous transplantation after the super megadose chemo protocol he had developed. Clients from around the world were regularly flying down to his clinic at Witwatersrand in Johannesburg, South Africa.

As a metric for how quickly this protocol swept the scientific community, in 1993 alone there were 1,177 papers published on it. In any case, those NIH guys were stubbornly continuing with their trials (try recruiting for a randomized trial when your subjects can jump ship if they don't like their assigned lot).

Then in 1999 Bezwoda opened the annual cancer meeting in Atlanta with a presentation on his results: He found that 8.5 years after megadose chemo and transplantation 60% of his patients were alive, whereas only 20% survived in the control arm. During the afternoon session those guys from the NIH presented their results. Except that their results were, let's say, not good. In one of their studies the researchers found "not even a modest improvement," and complication rates considerably higher than the control arm.

Later in the year a team of researchers pulled together by the president of the American Society of Clinical Oncology flew off to South Africa to take a look at Bezwoda's data. Upon arrival they requested the log books for the 158 patients Bezwoda reported treating. He gave them log books for 58, and said the rest had been lost (oh to live in a world without paperwork retainment requirements). The data he did give them was horrible. One of Bezwoda's purported breast cancer patients was actually a man. The entire thing had been a sham. In essence, Bezwoda's protocol was completely fabricated and his fraud was the sole thing holding up a $4 billion industry that performed the protocol on approximately 40,000 women.

To recap: There was a new experimental procedure for treating breast cancer. The media created such a furor at its restricted use that the government was browbeaten into allowing anyone who could pay (or litigate their insurers into paying, a whole different tangent) have a completely unproven procedure. The procedure turned out to be an epic failure and the exposition thereof went almost completely unnoticed by the mainstream media. (Incidentally, in this case scientists were the ones who exposed the fraud, in the Wakefield case it took a journalist to do so).

I do not have a solution to this madness, but until we, collectively, realize that the status quo is madness we're never going to get any closer to coming up with one.

As a parting note I'm going to quote an email that was sent to Jonah Lehrer by a former academic scientist who now works for a large biotech company:
When I worked in a university lab, we’d find all sorts of ways to get a significant result. We’d adjust the sample size after the fact, perhaps because some of the mice were outliers or maybe they were handled incorrectly, etc. This wasn’t considered misconduct. It was just the way things were done. Of course, once these animals were thrown out [of the data] the effect of the intervention was publishable. 
Here we have to be explicit, in advance, of how many mice we are going to use, and what effect we expect to find. We can’t fudge the numbers after the experiment has been done… That’s because companies don’t want to begin an expensive clinical trial based on basic research that is fundamentally flawed or just a product of randomness.
Reagan famously said, "Trust but verify." That's not sufficient any more. The new maxim is closer to, "Doubt until you've figured out their incentives to lie."

08 January 2011

Fraud and science, part II

There are reports all over (they're actually just disguised pressers since that's all the journalists read) about a new study in a journal no one reads (Pharmacoepidemiology and Drug Safety; it's the fourth google result when searching its title...). That antipsychotics are being prescribed off label in ever increasing amounts with scant data to support doing so. The actual study (gated, natch) is not linked to by a single one of those articles.

It does not reflect well on the PR acumen of Science (capital S) or scientists that the article was first "published" and the presser released on a Friday. It's as though they're undermining their own cause by ensuring that no one will read this article. (What possible incentive could they have for that? See III.)

Because I'm not actually a journalist, I'm just going to tell you that the presser gives you the highlights fairly accurately and reading the article is (probably) a waste of your time (unlike real journalists, I did link you to the article itself). Here were those highlights:

  • Antipsychotic treatment prescribed during the surveyed doctors' visits nearly tripled from 6.2 million in 1995 to 16.7 million in 2008, the most recent year for which they had data. During this period, prescriptions for first-generation antipsychotics decreased from 5.2 million to 1 million.
  • Antipsychotic use for indications that lacked FDA approval by the end of 2008 increased from 4.4 million prescriptions during surveyed doctors' visits in 1995 to 9 million in 2008.
  • In 2008, more than half — 54 percent — of the surveyed prescriptions for the new-generation antipsychotics had uncertain evidence.
  • An estimated $6 billion was spent in 2008 on off-label use of antipsychotic medication nationwide, of which $5.4 billion was for uses with uncertain evidence.
  • Prescriptions for antipsychotics began dropping slightly in 2006, shortly after the FDA issued a warning about their safety.
I'm not a psychiatrist (nor, God willing, will I ever be) but this is Bezwoda all over again. An entire industry built upon some questionable assumptions and a few unproven theories has exploded into a multibillion dollar industry for pharmaceutical companies and a publication factory for grant/tenure hungry faculty members.

The difference here is that there are too many genies for us to stuff back into the bottle if and when the whole house of cards falls down. This isn't someone falsifying data and then exhorting their colleagues to follow their invented protocols. This is a bunch of psychiatrists writing prescriptions that may work with no real basis for doing so beyond "everyone else is doing it and it might work." (If this sounds a lot like homeopathy to you, you're not far off... this is Homeopathy 2.0 where we use real drugs because they cost more and require med checks.)

Incidentally, if everyone else is doing it and you aren't, have fun trying to pay your mortgage. When word gets out that you won't exhaust every option for your patients not only will the malpractice suits come raining down, the waiting room will empty out. Patients don't care how well considered your refusal to participate in this charade is, they just want to get better and it's your job to make that happen.

Why Almost Everything You Hear About Medicine Is Wrong

Why Almost Everything You Hear About Medicine Is Wrong

If you follow the news about health research, you risk whiplash. First garlic lowers bad cholesterol, then—after more study—it doesn’t. Hormone replacement reduces the risk of heart disease in postmenopausal women, until a huge study finds that it doesn’t (and that it raises the risk of breast cancer to boot). Eating a big breakfast cuts your total daily calories, or not—as a study released last week finds. Yet even if biomedical research can be a fickle guide, we rely on it.
But what if wrong answers aren’t the exception but the rule? More and more scholars who scrutinize health research are now making that claim. It isn’t just an individual study here and there that’s flawed, they charge. Instead, the very framework of medical investigation may be off-kilter, leading time and again to findings that are at best unproved and at worst dangerously wrong. The result is a system that leads patients and physicians astray—spurring often costly regimens that won’t help and may even harm you.
It’s a disturbing view, with huge im-plications for doctors, policymakers, and health-conscious consumers. And one of its foremost advocates, Dr. John P.A. Ioannidis, has just ascended to a new, prominent platform after years of crusading against the baseless health and medical claims. As the new chief of Stanford University’s Prevention Research Center, Ioannidis is cementing his role as one of medicine’s top mythbusters. “People are being hurt and even dying” because of false medical claims, he says: not quackery, but errors in medical research.
This is Ioannidis’s moment. As medical costs hamper the economy and impede deficit-reduction efforts, policymakers and businesses are desperate to cut them without sacrificing sick people. One no-brainer solution is to use and pay for only treatments that work. But if Ioannidis is right, most biomedical studies are wrong.

In just the last two months, two pillars of preventive medicine fell. A major study concluded there’s no good evidence that statins (drugs like Lipitor and Crestor) help people with no history of heart disease. The study, by the Cochrane Collaboration, a global consortium of biomedical experts, was based on an evaluation of 14 individual trials with 34,272 patients. Cost of statins: more than $20 billion per year, of which half may be unnecessary. (Pfizer, which makes Lipitor, responds in part that “managing cardiovascular disease risk factors is complicated”). In November a panel of the Institute of Medicine concluded that having a blood test for vitamin D is pointless: almost everyone has enough D for bone health (20 nanograms per milliliter) without taking supplements or calcium pills. Cost of vitamin D: $425 million per year.
Ioannidis, 45, didn’t set out to slay medical myths. A child prodigy (he was calculating decimals at age 3 and wrote a book of poetry at 8), he graduated first in his class from the University of Athens Medical School, did a residency at Harvard, oversaw AIDS clinical trials at the National Institutes of Health in the mid-1990s, and chaired the department of epidemiology at Greece’s University of Ioannina School of Medicine. But at NIH Ioannidis had an epiphany. “Positive” drug trials, which find that a treatment is effective, and “negative” trials, in which a drug fails, take the same amount of time to conduct. “But negative trials took an extra two to four years to be published,” he noticed. “Negative results sit in a file drawer, or the trial keeps going in hopes the results turn positive.” With billions of dollars on the line, companies are loath to declare a new drug ineffective. As a result of the lag in publishing negative studies, patients receive a treatment that is actually ineffective. That made Ioannidis wonder, how many biomedical studies are wrong?
His answer, in a 2005 paper: “the majority.” From clinical trials of new drugs to cutting-edge genetics, biomedical research is riddled with incorrect findings, he argued. Ioannidis deployed an abstruse mathematical argument to prove this, which some critics have questioned. “I do agree that many claims are far more tenuous than is generally appreciated, but to ‘prove’ that most are false, in all areas of medicine, one needs a different statistical model and more empirical evidence than Ioannidis uses,” says biostatistician Steven Goodman of Johns Hopkins, who worries that the most-research-is-wrong claim “could promote an unhealthy skepticism about medical research, which is being used to fuel anti-science fervor.”

Even a cursory glance at medical journals shows that once heralded studies keep falling by the wayside. Two 1993 studies concluded that vitamin E prevents cardiovascular disease; that claim was overturned by more rigorous experiments, in 1996 and 2000. A 1996 study concluding that estrogen therapy reduces older women’s risk of Alzheimer’s was overturned in 2004. Numerous studies concluding that popular antidepressants work by altering brain chemistry have now been contradicted (the drugs help with mild and moderate depression, when they work at all, through a placebo effect), as has research claiming that early cancer detection (through, say, PSA tests) invariably saves lives. The list goes on.
Despite the explosive nature of his charges, Ioannidis has collaborated with some 1,500 other scientists, and Stanford, epitome of the establishment, hired him in August to run the preventive-medicine center. “The core of medicine is getting evidence that guides decision making for patients and doctors,” says Ralph Horwitz, chairman of the department of medicine at Stanford. “John has been the foremost innovative thinker about biomedical evidence, so he was a natural for us.”
Ioannidis’s first targets were shoddy statistics used in early genome studies. Scientists would test one or a few genes at a time for links to virtually every disease they could think of. That just about ensured they would get “hits” by chance alone. When he began marching through the genetics literature, it was like Sherman laying waste to Georgia: most of these candidate genes could not be verified. The claim that variants of the vitamin D–receptor gene explain three quarters of the risk of osteoporosis? Wrong, he and colleagues proved in 2006: the variants have no effect on osteoporosis. That scores of genes identified by the National Human Genome Research Institute can be used to predict cardiovascular disease? No (2009). That six gene variants raise the risk of Parkinson’s disease? No (2010). Yet claims that gene X raises the risk of disease Y contaminate the scientific literature, affecting personal health decisions and sustaining the personal genome-testing industry.
Statistical flukes also plague epidemiology, in which researchers look for links between health and the environment, including how people behave and what they eat. A study might ask whether coffee raises the risk of joint pain, or headaches, or gallbladder disease, or hundreds of other ills. “When you do thousands of tests, statistics says you’ll have some false winners,” says Ioannidis. Drug companies make a mint on such dicey statistics. By testing an approved drug for other uses, they get hits by chance, “and doctors use that as the basis to prescribe the drug for this new use. I think that’s wrong.” Even when a claim is disproved, it hangs around like a deadbeat renter you can’t evict. Years after the claim that vitamin E prevents heart disease had been overturned, half the scientific papers mentioning it cast it as true, Ioannidis found in 2007.
The situation isn’t hopeless. Geneticists have mostly mended their ways, tightening statistical criteria, but other fields still need to clean house, Ioannidis says. Surgical practices, for instance, have not been tested to nearly the extent that medications have. “I wouldn’t be surprised if a large proportion of surgical practice is based on thin air, and [claims for effectiveness] would evaporate if we studied them closely,” Ioannidis says. That would also save billions of dollars. George Lundberg, former editor of The Journal of the American Medical Association, estimates that strictly applying criteria like Ioannidis pushes would save $700 billion to $1 trillion a year in U.S. health-care spending.
Of course, not all conventional health wisdom is wrong. Smoking kills, being morbidly obese or severely underweight makes you more likely to die before your time, processed meat raises the risk of some cancers, and controlling blood pressure reduces the risk of stroke. The upshot for consumers: medical wisdom that has stood the test of time—and large, randomized, controlled trials—is more likely to be right than the latest news flash about a single food or drug.

Petulant Skeptic: Why nearly everything Newsweek writes about medicine is wrong

Petulant Skeptic: Why nearly everything Newsweek writes about medicine is wrong

29 January 2011

Why nearly everything Newsweek writes about medicine is wrong

Newsweek has an article about Dr John Ioannidis and his work discrediting many medical studies. Incidentally The Atlantic wrote about him and his work back in November as did The New Yorker in December. All of these articles highlight Ioannidis' findings that many studies are flawed, but take different approaches, and draw different conclusions from his work. Newsweek's take is by far the worst and most harmful.

In any case Newsweek informs us:
In just the last two months, two pillars of preventive medicine fell. A major study concluded there’s no good evidence that statins (drugs like Lipitor and Crestor) help people with no history of heart disease. The study, by the Cochrane Collaboration, a global consortium of biomedical experts, was based on an evaluation of 14 individual trials with 34,272 patients.
Combining this "fact" with Ioannidis' findings they go on to boldly assert: "Even a cursory glance at medical journals shows that once heralded studies keep falling by the wayside."
Lets take a look at their statin example since it characterizes the rest of the piece nicely. Newsweek tells us what the Cochrane Collaboration is, yet they omit that it does not conduct clinical studies. They conduct reviews, often in the form of meta-analyses. There's a qualitative difference between a meta-analysis and a study; studies examine real patients, meta-analyses examine data. Here is Dr Mark Crislip's explanation of why this difference matters:
The studies included in a meta-analysis are often of suboptimal quality. Many [meta-analyses] spend time bemoaning the lack of quality studies they are about to stuff into their study grinder. Then, despite knowing that the input is poor quality, the go ahead and make a sausage. The theory, as I said last week, is that if you collect many individual cow pies into one big pile, the manure transmogrifies into gold. I still think it as a case of GIGO: Garbage In, Garbage Out.

It has always been my understanding that a meta-analysis was used in lieu of a quality clinical trial. Once you had a few high quality studies, you could ignore the conclusions of a meta-analysis.
Not any longer, and not if you're Newsweek. Instead they prefer to ignore these substantive differences and merely inform us that one study has invalidated another. In fact they go so far as to make it sound as though the Cochrane review were an actual clinical study by telling us how many patients it "evaluated." In case you're wondering whether meta-analyses can be used as stand-ins for clinical trials, the NEJM published an article that explored just that:
We identified 12 large randomized, controlled trials and 19 meta-analyses addressing the same questions. For a total of 40 primary and secondary outcomes, agreement between the meta-analyses and the large clinical trials was only fair (kappa= 0.35; 95 percent confidence interval, 0.06 to 0.64). The positive predictive value of the meta-analyses was 68 percent, and the negative predictive value 67 percent. However, the difference in point estimates between the randomized trials and the meta-analyses was statistically significant for only 5 of the 40 comparisons (12 percent). Furthermore, in each case of disagreement a statistically significant effect of treatment was found by one method, whereas no statistically significant effect was found by the other.
Beyond this singular lack of understanding, Newsweek devotes many paragraphs to Ioannidis' work on statistical problems, yet only half of one sentence to the fact that his own statistical methods are controversial. In fact the sentence calling his methods controversial is buttressed by Newsweek telling us of Ioannidis' childhood genius and that his mathematical arguments are "abstruse"; evidently this complexity and his childhood genius were sufficient to convince the author of his accuracy and ought to be enough for the readers as well. (Handy rule of thumb: When not reading a profile you encounter a cute vignette from someone's childhood, the author is using it to paper over a logical deficiency.)

Indeed Newsweek spends a paragraph on Ioannidis' work discrediting statistical techniques (formerly) used in genetic attribution of disease and fails to tell us how that relates, at all, to medical studies. Indeed, they mention that it matters to the results genotyping companies give their customers, but how it relates to the article's thesis is ignored. This is the same as me telling you, "There are many problems with Mitsubishi automobiles" then spending a paragraph telling you about the dismal quality control conditions at Mitsubishi's television factories. It's the same aspersion by association and implication nonsense that I have written about before.

Perhaps the worst offense of all is that the article's central thesis is, "Everything you hear about medicine is wrong." Except that all of their reasons for discarding previously held findings are... new findings. Here they are telling us about vitamin E, "Two 1993 studies concluded that vitamin E prevents cardiovascular disease; that claim was overturned by more rigorous experiments, in 1996 and 2000." This is like a conspiracy theorist telling you that you can't trust anything a government official says and then quoting Robert Gibbs to evidence his opinion.

Don't get me wrong, there are plenty of problems with how modern science and medicine interact. Near the top of that list, though, are articles just like this. Consider that Newsweek has published literally dozens of articles about medical studies that have not met the article's central criteria:
[M]edical wisdom that has stood the test of time—and large, randomized, controlled trials—is more likely to be right than the latest news flash about a single food or drug.
That Newsweek has the gall to publish a poorly reasoned article decrying the hype over recently released medical results without addressing, or even mentioning, their own habit of doing precisely that is a problem. A larger problem, though, is that the editors of Newsweek are blind to the hypocrisy of hyping Ioannidis' findings in an article about how often such findings turn out to be wrong.


Dr William E.M. Lands, American nutritional biochemist - world's foremost authority on essential fatty acids

"Dr William E.M. Lands (born July 22, 1930) is an American nutritional biochemist who is the world's foremost authority on essential fatty acids. Lands graduated from University of Michigan in 1951 and served on the faculty there from 1955 to 1980. He then moved to University of Illinois (1980-1990) and subsequently the National Institutes of Health (1990-2002), where he served as the Senior Scientific Advisor to the Director of the National Institute on Alcohol Abuse and Alcoholism.
Lands is credited for discovering the beneficial effects of balancing the effects of excess omega-6 fatty acids with dietary omega-3 fatty acids. The effect of essential fatty acids on formation of hormones is documented in his book, "Fish, Omega-3 and Human Health." University of Michigan's Department of Biological Chemistry endowed a Lectureship in honor of William E.M. Lands."

30 grams of protein within 30 minutes of waking - The 30 in 30 Experiment

The 30 in 30 Experiment

I’ve started a new experiment. This time I will be testing an idea from Tim Ferriss. Upon waking I will consume 30 grams of protein within 30 minutes. In the book The 4 Hour Body, Ferriss mentions how this trick helps accelerate fat burning.

By starting the day off with a high dose of protein, Ferriss has found that it has an appetite suppressing effect which results in an easier path to fat loss. 4HourLife has some ideas on how to get those 30 grams. For me, even though I think whey protein is the one of most hyped overrated supplements, I bought some to make this experiment easier.

The 4-Hour Body: An Uncommon Guide to Rapid Fat-Loss, Incredible Sex, and Becoming Superhuman
The 4-Hour Body: An Uncommon Guide to Rapid Fat-Loss, Incredible Sex, and Becoming Superhuman by Timothy Ferriss

This experiment is a radical change for me. I’ve never started my day off immediately with food. In the past few years, I’ve gone hours before consuming calories. Besides seeing if the 30-30 method could control my appetite, I also selected this experiment because it will help me be morning compliant with an idea from the Ray Peat crowd. They warn against consuming coffee on an empty stomach as it can trigger stress hormones.

I started this experiment on Friday September 20th. Way too soon to tell if it is having an effect. I’m only interested in losing 10 pounds. Unless I get a negative response, which I don’t expect, I’ll keep this experiment going for at least 60 days.

I wonder how well the 30-30 plan works for the last 10 pounds? Has anyone experimented with it? I’d especially like to hear from those that normally would skip breakfast.


Ketones inhibit fat synthesis - Kindke's Scrap Notes

Kindke's Scrap Notes: Ketones inhibit fat synthesis

Metabolite regulation of nucleo-cytosolic trafficking of carbohydrate response element binding protein (ChREBP): role of ketone bodies.

Without going into all the technical details, here's the punchline....
 These observations show that ketone bodies play an important role in regulation of ChREBP activity by restricting ChREBP localization to the cytoplasm, thus inhibiting fat synthesis during periods of ketosis.

ChREBP is a transcription factor that is activated by increased glucose levels, and ChREBP increases synthesis of enzymes like fatty acid synthase that are responsible for lipogenesis.

Anyway what this paper implies is that high ketone levels will inhibit glucose induced lipogenesis.  I think potentially if your in ketosis this could probably mean that you can eat carbs for 1-2 days while stimulating only very limited lipogenesis. Basically the ability of carbs to cause fat gain should be curbed by high ketone levels. ( in theory ). However ofcourse repeated carb feeding will eventually kill your ketone levels and this will allow ChREBP to frontload its lipogenic power.

Now, who knows the answer to this question....... lets say you eat some carbohydrate, you activate ChREBP and it subsequently causes your cells to manufacture some fatty acid synthase enzymes. Now, how long do these enzymes sit around for? Whats their half life?

From the paper it seems oleate and linoleate also appear to be quite good at inhibiting ChREBP.

Oleic acid

From Wikipedia, the free encyclopedia
Fatty acids (or as their salts) do not often occur as such in biological systems. Instead fatty acids like oleic acid occur as their esters, commonly the triglycerides, which are the greasy materials in many natural oils. Via the process of saponification, the fatty acids can be obtained.

Triglycerides of oleic acid compose the majority of olive oil, although there may be less than 2.0% as free acid in the virgin olive oil, with higher concentrations making the olive oil inedible.[citation needed] 

It also makes up 59-75% of pecan oil,[3] 61% of canola oil,[4] 36-67% of peanut oil,[5] 60% of macadamia oil, 20-85% of sunflower oil (the latter in the high oleic variant),[6] 15-20% of grape seed oil, sea buckthorn oil, and sesame oil,[2] and 14% of poppyseed oil.[7] It is abundantly present in many animal fats, constituting 37 to 56% of chicken and turkey fat[8] and 44 to 47% of lard.
Oleic acid is the most abundant fatty acid in human adipose tissue.[9]

Linoleic acid

From Wikipedia, the free encyclopedia
Linoleic acid (LA) is an unsaturated omega-6 fatty acid. It is a colorless liquid at room temperature. In physiological literature, it has a lipid number of 18:2 cis,cis-9,12. Chemically, linoleic acid is a carboxylic acid with an 18-carbon chain and two cis double bonds; the first double bond is located at the sixth carbon from the methyl end.[3]

Linoleic acid belongs to one of the two families of essential fatty acids. The body cannot synthesize linoleic acid from other food components.[4]

The word "linoleic" comes from the Greek word linon (flax). Oleic means "of, relating to, or derived from oil of olive" or "of or relating to oleic acid" because saturating the omega-6 double bond produces oleic acid.

Some medical research suggests that excessive levels of certain omega−6 fatty acids relative to certain omega-3 fatty acids, but likely in conjunction with exogenous toxins, may have negative health effects.


Autoimmune Panel: Wahls, Ballantyne, Jaminet, & Gray - Perfect Health Diet | Perfect Health Diet

Autoimmune Panel: Wahls, Ballantyne, Jaminet, & Gray - Perfect Health Diet | Perfect Health Diet

This is probably the most important and interesting podcast I’ve had the privilege of being part of: an expert panel on Recovering from Autoimmune and Neurodegenerative Diseases.
The panel was arranged by Whitney Ross Gray of Nutrisclerosis, who has recovered from Multiple Sclerosis with an ancestral diet rich in animal foods.
The expert panelists were:
  • Terry Wahls, M.D., who has famously recovered from Multiple Sclerosis on an ancestral diet rich in plant foods, and is now leading a clinical trial studying ancestral diets as treatments for M.S.
  • Sarah Ballantyne, Ph.D., who blogs at The Paleo Mom. Sarah suffered from an autoimmune disease, lichen planus, as well as other ailments, and healed them (and lost 120 pounds) with an ancestral diet.
  • Paul Jaminet, Ph.D. I had a chronic disease with neurological symptoms that overlapped with M.S., but it turned out to be an infectious disease and cleared with antibiotics. However, this could not be diagnosed until after I’d made considerable progress addressing it through an ancestral diet, which became the Perfect Health Diet.
Questions were solicited beforehand from patients suffering from autoimmune and neurodegenerative diseases, and in an hour and forty minutes we covered many fascinating topics.
I think the combination of personal experience recovering from chronic diseases, and scientific and medical expertise, made for an exceptionally useful conversation. If you are interested in these diseases – or just in how to be healthy, since the methods that address these conditions are generally beneficial for anyone’s health – take a listen.
My thanks to Whitney for organizing the discussion, Carl for hosting it, and Terry and Sarah for making a great panel.

Dietary Fiber - Most claim About It That are a Myth | Mark's Daily Apple

Dietary Fiber Is Bad for Sex – That’s the Only Claim About It That Isn’t a Myth | Mark's Daily Apple

brancerealToday’s article is a guest post from Konstantin Monastyrsky of GutSense.org. In keeping with the mission statement of Mark’s Daily Apple to investigate, discuss, and critically rethink everything we’ve assumed to be true about health and wellness, I like to periodically give credible researchers who are challenging conventional wisdom the opportunity to share their insights and findings here. It’s a great way to open a dialogue on topics that deserve challenging. Like fiber, for instance. Everyone knows that fiber is good for you, right? Well, let’s find out what Konstantin—a guy who’s spent an incredible amount of time researching this topic—thinks about this truism. Enter Konstantin…
Does dietary fiber contain anything of nutritional value? No, it doesn’t. Zero vitamins… Zero minerals… Zero protein… Zero fat… Nothing, zilch, not even digestible carbohydrates. Why, then, is it considered a healthy nutrient? As the story goes, you can thank Dr. John Harvey Kellogg for that:
“Dr. Kellogg was obsessed with chastity and constipation. True to principle, he never made love to his wife. To “remedy” the sin of masturbation, he advocated circumcision without anesthetic for boys, and mutilation of the clitoris with carbolic acid for girls. He blamed constipation for “nymphomania” in women, and lust in men, because, according to Kellogg, impacted stools inside one’s rectum were stimulating the prostate gland and the female vagina into sexual proclivity.” [link]

To fix these “ailments,” Dr. Kellogg was prescribing a coarse vegetarian diet along with 1 to 3 ounces of bran daily, and mineral oil with every meal. As any nutritionist will tell you, the decline of libido and infertility are among the very first symptoms of malnutrition prevalent among ardent vegans. And in this particular case, extra bran and mineral oil were “enhancing” damage by blocking the assimilation of nutrients from an already meager diet.

And what was Dr. Kellogg’s rationale for prescribing mineral oil? Well, because so much fiber was enlarging stools, intense straining was required to expel them. The oil was used as a lubricant to reduce pain caused by straining, and to prevent bloody anal fissures inside the anal canal.

However, the ultimate fame and money came to Dr. Kellogg not from crusading against sex, but from ready-to-eat morning cereals after he found that baking bran into cereals proved to be incredibly profitable for Kellogg Company. From that point on, it took another sixty years or so of relentless brainwashing to turn what once used to be a dirt-cheap livestock feed into a premium health food.
Well, that’s an old story, and I can understand if you doubt it—it sounds too incredulous to be true! So, let’s debunk fiber’s mythology with facts and science. Here we go, one myth at a time:

Myth #1: For maximum health, obtain 30 to 40 g of fiber daily from fresh fruits and vegetables.

Reality: Here is how many fresh fruits you’ll need to eat throughout the day in order to obtain those 30 to 40 grams (1-1.4 oz.) of daily fiber: fruit
As you can see, that comes to five apples, three pears, and two oranges. A small apple contains 3.6 g of fiber and 15.5 g of sugars. A small pear—4.6 g and 14.5 g; and a small orange—2.3 g and 11.3 g, respectively (USDA National Nutrient Database; NDB #s: 09003; 09200; 09252 [link]).

These ten small (not medium or large) fruits will provide you with 36.4 g of indigestible fiber and a whopping 143.6 g of digestible sugars, or an equivalent of that many (ten) tablespoons of plain table sugar! spoons
And that‘s before accounting for all the other carbs consumed throughout the day for breakfast, lunch, dinner, and from snacks and beverages.

So ask yourself this question: even if you are a 100% healthy 25-year-old muscle-bound athlete, would you ever ingest that much sugar willingly? Well, maybe under the influence of a controlled substance or torture…

But that’s exactly what’s being recommended for “health purposes” to children and adults. It‘s not surprising that so many Americans are suffering from the ravages of diabetes and obesity—a moderately active adult can utilize no more than about 200 grams of carbohydrates per day without encountering a scourge of the inevitable obesity, prediabetes, or diabetes.

The ratio of digestible carbohydrates (sugars) to fiber in vegetables, cereals, breads, beans, and legumes is, on average, similar to fruits. Thus, no matter how hard you try to mix’n’match, you’ll be getting harmed all the same.

Please do note that if you are healthy, active, and normal weight, there is nothing wrong with consuming fruits and vegetables in moderation. The point of this section is to impress on you that it is NOT OK to binge on fruits to ingest recommended daily intake of fiber.

This myth—that fruits and vegetables are the best source of dietary fiber—is probably the most pervasive and damaging of all. If 30 grams of fiber is what you’re really after, you’re better off getting it from supplements. These, after all, have almost no digestible carbs. But, then, of course, you run into those other persistent falsehoods…

Myth #2: Fiber reduces blood sugar levels and prevents diabetes, metabolic disorders, and weight gain.

Reality: That’s a blatant deception. If you consume 100 g of plain table sugar at once, the blood absorbs all 100 g of sugar almost as soon as it reaches the small intestine, where the assimilation takes place. If you add 30 g of fiber into the mix, the fiber may extend the rate of sugar assimilation into the blood, from, let‘s say, one hour to three.

But at the end of those extra three hours the blood will still absorb exactly the same 100 g of sugar—not an iota more, not an iota less. If you are a diabetic, the only difference will be that you‘ll require more extended (long-acting) insulin for type 1 diabetes, or larger doses of medication for type 2 diabetes in order to deal with slow-digesting sugars, and your blood glucose test will not spike as high after the meal.

But you‘re fooling no one but a glucose meter. In all other respects, the damage will be all the same, or even worse. And that‘s even before taking into account the negative impact of fiber on the digestive organs, or hyperinsulinemia and triglycerides on the heart, blood vessels, and blood pressure.

Myth #3: Fiber-rich foods improve digestion by slowing down the digestive process.

Reality: Fiber indeed slows down the “digestive process,” because it interferes with digestion in the stomach and, later, clogs the intestines the “whole nine yards.” The myth is that it can be good for health and the digestive process.

Here is what you get from delayed digestion: indigestion (dyspepsia), heartburn (GERD), gastritis (the inflammation of the stomach‘s mucosal membrane), peptic ulcers, enteritis (the inflammation of the intestinal mucosal membrane), and further down the chain, constipation, irritable bowel syndrome, ulcerative colitis, and Crohn‘s disease.

All this, in fact, is the core message of Fiber Menace: fiber slows down the digestive process! And slow digestion is ruinous for your health. Don‘t mess with fiber unless your gut is made of steel!

Myth #4: Fiber speeds food through the digestive tract, helping to protect it against cancer.

Reality: Not true. In fact, this claim directly contradicts the claim that fiber-rich foods slow down the digestive process. For a reality check, here’s an excerpt from a college-level physiology textbook that reveals the truth:
“Colonic Motility: Energy-rich meals with a high fat content increase motility [the rate of intestinal propulsion]; carbohydrates and proteins have no effect.”
R.F. Schmidt, G. Thews; Human Physiology, 2nd edition. 29.7:730 [link]
This, incidentally, is why low-fat diets and constipation commonly accompany each other. And don’t count on getting any cancer protection from fiber, either. That‘s yet another oft-repeated deception.

Myth #5: Fiber promotes a healthy digestive tract and reduces cancer risk.

Reality: Not true. Here’s what doctors-in-the-know have to say on the subject of the colon cancer/fiber connection:

Lack of Effect of a Low-Fat, High-Fiber Diet on the Recurrence of Colorectal Adenomas
“Adopting a diet that is low in fat and high in fiber, fruits, and vegetables does not influence the risk of recurrence of colorectal adenomas.”
Arthur Schatzkin, M.D et al. The New England Journal of Medicine; [link]
The excerpt below comes, of all places, from the Harvard School of Public Health:

Fiber and colon cancer
“For years, Americans have been told to consume a high-fiber diet to lower the risk of colon cancer—mainly on the basis of results from relatively small studies. Larger and better-designed studies have failed to show a link between fiber and colon cancer.”
Fiber: Start Roughing It [link]
Not convinced yet? Well, here is even more damning evidence from the U.S. Food and Drug Administration:

Letter Regarding Dietary Supplement Health Claim for Fiber With Respect to Colorectal Cancer
“Based on its review of the scientific evidence, FDA finds that (1) the most directly relevant, scientifically probative, and therefore most persuasive evidence (i.e., randomized, controlled clinical trials with fiber as a test substance) consistently finds that dietary fiber has no [preventive] effect on incidence of adenomatous polyps, a precursor of and surrogate marker for colorectal cancer; and (2) other available human evidence does not adequately differentiate dietary fiber from other components of diets rich in foods of plant origin, and thus is inconclusive as to whether diet-disease associations can be directly attributed to dietary fiber. FDA has concluded from this review that the totality of the publicly available scientific evidence not only demonstrates lack of significant scientific agreement as to the validity of a [preventive] relationship between dietary fiber and colorectal cancer, but also provides strong evidence that such a relationship does not exist.”
U. S. Food and Drug Administration – Center for Food Safety and Applied Nutrition Office of Nutritional Products, Labeling, and Dietary Supplements; [link]
Alas, the story doesn’t end there. Adding insult to injury, Chapter 10 of my book entitled Fiber Menace, “Colon Cancer” cites studies that demonstrate the connection between increased fiber consumption and colon cancer. Also, countries with the highest and lowest consumption of meat are compared. Not surprisingly, the countries with the lowest consumption of meat and, correspondingly, the highest consumption of carbohydrates, including fiber, have the highest rate of digestive cancers, particularly of the stomach.

Myth #6: Fiber offers protection from breast cancer.

Reality: A blatant, preposterous lie. According to the recent massive study jointly conducted by the U.S. Center for Disease Control and Prevention, the Ministry of Health of Mexico, and the American Institute for Cancer Research, it’s the opposite: women with the highest consumption of carbohydrates, and, correspondingly, of fiber, had the highest rates of breast cancer:

Carbohydrates and the Risk of Breast Cancer among Mexican Women
“In this population, a high percentage of calories from carbohydrate, but not from fat, was associated with increased breast cancer risk.”
Isabelle Romieu, et al; Cancer, Epidemiology, Biomarkers & Prevention; 2004 13: 1283–1289. [link]
Although this study has singled out carbohydrates as the culprit behind various cancers, where there’s smoke, there’s also fire: carbs and fiber are as inseparable as Siamese twins, as I have already explained in Myth #1.

Myth #7: Fiber lowers blood cholesterol levels, triglycerides, and prevents heart disease.

The myths about fiber’s role in coronary heart disease (CHD) and the management of elevated cholesterol have their roots in some dubious research, which culminated in “reduced mineral absorption and myriad of gastrointestinal disturbances” after the study participants were given supplements containing a mixture of guar gum, pectin, soy fiber, pea fiber, and corn bran along with a low-fat and reduced cholesterol diet.

The total reduction of LDL cholesterol after 15 weeks was from “7% to 8%”. As any cardiologist will tell you, the reduction of “bad” cholesterol from, let’s say, 180 to 166 mg/dL (-8%) is completely meaningless. Besides, if you cause someone to have a “myriad of gastrointestinal disturbances” in the process, that person is more likely to die prematurely from malnutrition and cancer than of stroke or heart attack.

Even then, this marginal reduction of cholesterol had little to do with fiber, and everything to do with the reduction of dietary fats. LDL cholesterol happens to be a major precursor to bile. The moment a person is placed on a low-fat diet, their cholesterol level drops because their liver no longer needs to produce as much bile.

In addition, intestinal inflammation caused by soluble fiber blocks the ability of bile components to get absorbed back into the bloodstream, further lowering the cholesterol level. This is as basic as the physiology of nutrition gets, and it makes the whole claim of a fiber-cholesterol connection a deliberate con.

There is another dimension to the con used to “prove” fiber‘s role in reducing cholesterol. Most of the studies on fiber’s cholesterol-lowering effect—particularly psyllium—used The American Heart Association’s (AHA) Step 1 diet.

The Step 1 diet is high in carbohydrates and low in fat by design, with less than 10% of total energy derived from saturated fat. During clinical studies among people using the Step 1 diet without added fiber, their total cholesterol fell by 8%, LDL cholesterol fell by 6%, and HDL cholesterol fell by 16%.
In other words, the Step 1 diet on its own, without any extra fiber and/or digestive side effects, demonstrates an almost identical drop in cholesterol as with added fiber. In legalese, this particular “coincidence” is called fraud, plain and simple.

So one fraud more, one fraud less…what‘s the worry, if my cholesterol goes down?
Well, there is a legitimate worry, at least, according to this respected source:

Problem with American Heart Association “Step 1″ diet
“Although the AHA Step 1 diet decreased total and LDL cholesterol levels in this group of women, it decreased HDL cholesterol by an even greater proportion. In women, a low HDL cholesterol concentration is a stronger independent predictor of cardiovascular disease risk than is elevated total cholesterol or LDL cholesterol. Therefore, women who follow AHA guidelines for lowering their serum cholesterol may actually be increasing their risk of heart disease”
Alan R. Gaby, M.D. Townsend Letter for Doctors and Patients [link]
Amazingly, back in 2001, the AHA replaced the Step 1 diet with the Step II, TLC, and ATP III diets [link], which are even more restrictive in terms of fat, and even more permissive in terms of carbohydrates.

And don’t get me started on triglycerides… First, nothing raises triglycerides as profoundly as a high-fiber diet does, because, paraphrasing the smoke-fire cliché, where there’s fiber, there’re carbohydrates, usually eight to ten times as much.

This fact—the more fiber you consume, particularly from natural sources, the higher your level of triglycerides from carbohydrates intake—has been dodging Dr. Dean Ornish [link] one of the most prominent proponents of a high-carb/high-fiber diet.

Second, once inside the colon, fiber itself gets fermented by intestinal bacteria. Among the byproducts of bacterial fermentation are short-chain fatty acids—butyrate, acetate, and propionate. Most of these fatty acids get assimilated directly into the bloodstream to provide energy.

According to the Dietary Reference Intakes manual “current data indicate that the [energy] yield is in the range of 1.5 to 2.5” calories per each gram of consumed fiber [link]. If you aren’t starving, the absorbed fatty acids unused for energy get metabolized by the liver into triglycerides for further storage as body fat.

Granted, a few calories here, a few calories there, may not seem like a lot. Still, if you are consuming 30 to 40 grams of fiber daily plus whatever “hidden” carbohydrates you are ingesting unknowingly along with processed food, it all adds up to epidemics of obesity, diabetes, and heart disease.

Myth #8: Fiber satisfies hunger and reduces appetite.

Reality: When the scientists from the Human Nutrition Research Center on Aging at Tufts University decided to look at this dubious claim, here is what they have found out:

Fermentable and Nonfermentable Fiber Supplements Did Not Alter Hunger, Satiety or Body Weight in a Pilot Study of Men and Women Consuming Self-Selected Diets
“Despite the large total intakes of FF [fermentable fiber - ed.] and NFF [non-fermetable fiber - ed.] supplements, there were no significant changes in body weight or fat during consumption of either type of fiber, even among the subjects with higher BMI.”
The Journal of Nutrition [link]
And as you keep digging deeper, you soon realize that consuming too much fiber may actually contribute to obesity. Because fiber rapidly absorbs water and expands in the stomach up to five times its original size and weight, it indeed pacifies the appetite for a short while.

Unfortunately, while faking satiety, expanded fiber also stretches out the stomach‘s chamber, and each new fill-up requires progressively more and more fiber to accomplish the same trick. Lo and behold, in order to reduce its capacity and “speed up” satiety, surgeons suture the stretched-out stomachs of obese individuals or squeeze them with a bridle (LAP-BAND©). A complete opposite of what fiber does.

Myth #9: Fiber prevents gallstones and kidney stones.

Reality: I‘ve seen several observational studies that claim fiber can prevent gallstones. It isn‘t true. It‘s common knowledge that diabetes and obesity are consistently associated with higher risk for gallstones, and both of these conditions are the direct outcome of excessive consumption of carbohydrates, and correspondingly, of fiber. Beyond these few studies, there isn‘t a shred of physiological, anatomical, clinical, or nutritional evidence that connects gallstone formation with fiber consumption.

Here‘s an excerpt from Fiber Menace that sheds further light on the gallstone-fiber connection:

Fiber’s affect on the small intestine: Not welcome at any price
Gallstones are formed from concentrated bile salts when the outflow of bile from the gallbladder is blocked. […] before they can form, something else must first obstruct the biliary ducts. Just like with pancreatitis, that “something” is either inflammatory disease or obstruction caused by fiber.

Women (in the West) are affected by gallstones far more than men, because they are more likely to maintain a “healthy” diet, which nowadays means a diet that is low in fat and high in fiber. Since the gallbladder concentrates bile pending a fatty meal, no fat in the meal means no release of bile. The longer the concentrated bile remains in the gallbladder, the higher the chance for gallstones to form (from bile salts).
Fiber Menace, page 25 [link]
Just as with gallstones, kidney stones are also common among people who suffer from diabetes and obesity, because excessive consumption of carbohydrates increases the excretion of urine, changes its chemistry, and predisposes to kidney stones.

To investigate this myth further, I consulted PubMed, a service of the National Library of Medicine, which is the most thorough compendium of medical research. I reviewed eighty-one articles published between 1972 and 2005 (the year I was researching my book) that mention the words “fiber” and “kidney stones”. Not a single one of them connected kidney stones to fiber consumption, while several specifically pointed out that an increased consumption of carbohydrates is one of the major contributing factors.

One article suggested that a diet free of digestible carbs, but containing fiber, makes urine composition less stones-prone. You don‘t have to be Dr. Watson to deduce that fiber—an indigestible substance—can‘t materially affect urine chemistry, because what can‘t get digested also can‘t reach the kidneys. Besides, it wasn’t the presence of fiber that did the “trick,” for those investigators, but the reduction in digestible carbohydrates.

Myth #10: Fiber prevents diverticular disease.

For a while, it was difficult to disprove this absurdity by appealing to common sense. So I devoted a whole chapter in Fiber Menace to explaining why fiber CAUSES diverticular disease. Thank God, I am no longer alone in this thinking:

Fiber Not Protective Against Diverticulosis
Contrary to popular medical wisdom, following a high-fiber diet has no protective effect against developing asymptomatic diverticulosis, according to a colonoscopy-based study presented at the 2011 Digestive Disease Week (DDW) meeting (abstract 275). In fact, the study showed that patients who ate more fiber actually had higher prevalence of the disease.
Gastroenterology and Endoscopy News, July 2011, Volume: 62:07 [link]
Fiber May Not Prevent Diverticular Disease
For decades, doctors have recommended high-fiber diets to patients at risk for developing the intestinal pouches, known as diverticula. The thinking has been that by keeping patients regular, a high-fiber diet can keep diverticula from forming. But the new study suggests the opposite may be true.
WebMD, January 23, 2012 [link]
A High-Fiber Diet Does Not Protect Against Asymptomatic Diverticulosis
A high-fiber diet and increased frequency of bowel movements are associated with greater, rather than lower, prevalence of diverticulosis. Hypotheses regarding risk factors for asymptomatic diverticulosis should be reconsidered.
Gastroenterology; Volume 142, Issue 2, Pages 266-272.e1, Feb. 2012 [link]
The only problem with all of the above research is that it may take another six to eight years to tell people what I was telling them eight years ago: if you wish to protect your gut from diverticular disease, keep fiber out of it.

Myth #11: Fiber is safe and effective for the treatment and prevention of diarrhea.

Reality: Actually, it’s the complete opposite—fiber, particularly soluble, is the most common cause of diarrhea in children and adults. That’s why it’s recommended as a laxative to begin with. The idea of fiber as a preventive treatment for diarrhea is one of the most preposterous and harmful fiber-related frauds.

Soluble fiber is widely present in fruits, vegetables, laxatives, and processed foods, such as yogurt, ice cream, sour cream, cream cheese, soy milk, non-dairy creamers, preserves, jellies, candies, cakes, snack bars, canned soups, frozen dinners, sauces, dressings, and endless others.

It’s always expertly concealed from scrutiny behind obscure names such as agar-agar, algae, alginate, β-glucan, cellulose gum, carrageen, fructooligosaccharides, guaran, guar gum, hemicellulose, Irish moss, kelp, lignin, mucilage, pectin, oligofructose, polydextrose, polylos, resistant dextrin, resistant starch, red algae, and others.

These inexpensive industrial fillers are added as stabilizers and volumizers to practically all processed foods, because they hold water, maintain shape, and fake “fattiness.” Besides, they are cheaply bought by the ton, and are resold retail by the gram for immense profit.

Once inside the body, these fiber fillers remain indigestible, hold onto water just as tight, and prevent absorption. This property—the malabsorption of fluids—lies behind soluble fiber‘s laxative effect: under normal circumstances a very limited amount of fluids enter the large intestine. When their amount exceeds the colon’s holding capacity, you get hit with diarrhea.

In other words, the term “laxative” is just a euphemism for a “diarrheal” agent. If you overdose on a fiber laxative, you’ll end up with diarrhea. If you “overdose” on fiber from food, you’ll end up with exactly the same diarrhea. But since fiber in food can’t be measured as reliably as fiber in capsules, wafers, or powders, it’s much easier to “overdose” the latter fiber and cause severe diarrhea.

Besides, fiber is even more offensive than synthetic laxatives, because the byproducts of its fermentation cause intestinal inflammation, flatulence, bloating, and cramping—just as described in medical references:

Malabsorption Syndromes
Colonic bacteria ferment unabsorbed carbohydrates into CO2, methane, H2, and short-chain fatty acids (butyrate, propionate, acetate, and lactate). These fatty acids cause diarrhea. The gases cause abdominal distention and bloating.
Gastrointestinal Disorders; The Merck Manual of Diagnosis and Therapy [link]
The diarrheal effect of soluble fiber is particularly harmful for children, because their smaller intestines need lesser amounts to provoke diarrhea. According to the Centers for Disease Control and Prevention:

The Management of Acute Diarrhea in Children
…diarrhea remains one of the most common pediatric illnesses. Each year, children less than 5 years of age experience 20-35 million episodes of diarrhea, which result in 2-3.5 million doctor visits, greater than 200,000 hospitalizations, and 325-425 deaths.
Centers for Disease Control and Prevention [link]
These figures are from 1992, the latest statistic I could find. It must be much worse today because fiber is so much more prevalent. And if you analyze the most basic facts, you’ll understand immediately why this travesty is taking place. Consider this:

A single adult dose of Metamucil®—a popular fiber laxative made from psyllium seed husks—contains 2 g of soluble fiber in 6 capsules [link]. One apple, one orange, and one banana—not an unusual number of fruits a child may eat throughout the day—contain a total 4 g of soluble fiber, or an equivalent of 12 capsules of Metamucil for a much larger adult.

And that’s on top of all the juices, cereals, yogurts, ice creams, candies, cakes, and all other processed food consumed on the same day, all loaded with fiber as well. No wonder that “diarrhea remains one of the most common pediatric illnesses” in the United States, and there is an acute shortage of pediatricians nationwide.

Myth #12: Fiber relieves chronic constipation.

I left this myth for last because it is the most pervasive. For the same false reasons that people believe in the cleansing prowess of fiber, everyone and their uncle also believes that fiber relieves constipation.
Not quite true. According to the experts from the American College of Gastroenterology’s Functional Gastrointestinal Disorders Task Force, all legitimate clinical trials “…did not demonstrate a significant improvement in stool frequency or consistency when compared with placebo.” [link]

In plain English, it means fiber is no better at relieving constipation than a sugar pill. Indeed, how could it be, when fiber causes constipation in the first place! Again, I describe the exact reasons behind the fiber-constipation connection in Fiber Menace.

Even The Merck Manual of Diagnosis and Therapy, the very first book your doctor consults when needing up-to-date medical advice, has recently changed their tune regarding fiber, clearly the outcome of my work.

“Fiber supplementation is particularly effective in treating normal-transit constipation but is not very effective for slow-transit constipation or defecatory disorders” [link]

In plain English, it means the following: “Fiber supplements will catapult healthy people into a loo because of their laxative effect. But for anyone with a history of chronic constipation, they don’t work.”

Finally, consider the stern warnings, that accompany Metamucil, a fiber supplement made from psyllium: riteaid
So not only do fiber supplements not work for most people with chronic constipation, but they may also make them ill. Probably not ill enough to kill their libido as Dr. Kellogg originally intended, but imagine enjoying sex with your partner while being bloated and flatulent courtesy of extra fiber in your morning cereals.

That doesn’t describe a health food, does it?

Learn More About Fiber Menace at GutSense.org