Month: April 2012

Interview with a Shangri-La Dieter

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A few days ago I asked Mark Qualls, a 59-year-old truck driver who lives in Longmont, Colorado, about his success with the Shangri-La Diet, which he posted about.

How did you learn about it?

Freakonomics. When I read about you in that book, it made sense to me. The whole idea of a setpoint. I used to be an accountant. I weighed 290 pounds. I’m 6′ 2″. I lost 25 pounds when I started driving a truck. I’ve been there for almost 12 years. Around 260. I get a lot of exercise delivering groceries. I can eat anything I want but the idea of going on a diet makes me hungry. My doctor said lose a bit of weight but I just couldn’t do it.

How do you do the diet?

I use canola oil. I tried flax seed oil but it has a horrible taste. I have no problem taking the oil. I feel like I could do the oil for the rest of my life. At least 4 tablespoons per day. I don’t measure it. I have a jar by a sink at home, another in my truck. I take a sip, what seems about a tablespoon. I figure I’m getting at least 4 tablespoons per day. Some days I may get only 3 tablespoons.

What effect has it had?

I feel like I’m in control. I stopped drinking sweet tea, used to drink tons of it. For 20 years. I’ve been able to stop. I couldn’t stand drinking water. Now that’s all I drink. That’s all I’ve had for two months. The most bizarre thing to me in the world. I deliver to convenience stores. All they have is soda pop and doughntuts and all that kind of stuff. I’d stop and have a doughnut and chocolate milk. Now I can go without it. I still think about it but now I can say no.

What about weight loss?

I’m down from 255 to 229 – a little over 2 months. I don’t really try that hard. I pretty much eat what I want. On two days per week I try to eat hardly anything. Unless I almost eat nothing, I stay at the same weight. It’s not hard to do it – to eat almost nothing. Almost any time of day or night I think “I could eat something”. But then it’s okay not to. It gives you willpower – that’s how I explain it to people. Find the book and read the whole thing, I tell them. They need to understand the whole concept before they start taking oil.

Any downsides?

Eating is enjoyable to me. My mom is a great cook. My wife is a great cook. I like to eat. It’s emotionally satisfying thing to eat stuff. But when I take the oil I can not eat. Now I eat slower. To try to enjoy the little bit of food you do it. You’re not going to eat 3 more times today. I tell myself, I’m going to enjoy every bite of this cottage cheese. Because that’s all I’m going to eat today. The social part I miss. It’s a social part of your life that you don’t have any more. Most of the time I’ve gone to eat with people since I started, I go ahead and eat something because I don’t want to be a jerk about it. I still lose weight. That will be a day where I don’t lose weight when I go out to eat. To lose weight I have to have a day when I don’t eat anything. Today is a day where I told myself I want to lose 1 more pound. I ate breakfast with a friend,. There’s nobody who expects me to eat with them. My wife’s away.

How do other people react?

My wife’s a skeptic about the whole thing. She doesn’t think I can’t keep the weight off. One lady at church, she got the book right away. She’d lost 50 pounds eating 1000 calories per day. She started the oil. She’s gung ho about it. We see each other Sunday: how much did you lose this week? we ask.

 

 

Effect of Vitamin D3 on My Sleep

Seth Roberts23 Comments

I have blogged many times about biohacker Tara Grant’s discovery that she slept much better if she took Vitamin D3 in the morning rather than later. Many people reported similar experiences, with a few exceptions. Lots of professional research has studied Vitamin D3 but the researchers appear to have no idea of this effect. They don’t control the time of day that subjects take D3 and don’t measure sleep. If the time of day of Vitamin D3 makes a big difference, measuring Vitamin D3 status via blood levels makes no sense. Quite likely other benefits of Vitamin D3 require taking it at the right time of day. Taking Vitamin D3 at a bad time of day could easily produce the same blood level as taking it at a good time of day.

I too had no idea of the effect that Grant discovered. I had taken Vitamin D3 several times — never in the morning — but after noticing no change stopped. I tested Grant’s discovery by taking Vitamin D3 at 8 or 9 am. First, taking it at 8 am, I gradually increased the dose from 2000 IU to 8000 IU. Then I shifted the time to 9 am. The experiment ended earlier than I would have liked because I had to fly to San Francisco.

When I woke up in the morning I rated how rested I felt on a 0-100 scale, where 0 = not rested at all and 100 = completely rested. I’d been using this scale for years. Here are the results (means and standard errors):

Vitamin D3 had a clear effect, but the necessary dose was more than 2000 IU. If Vitamin D3 acts like sunlight, you might think that taking it in the morning would make me wake up earlier. Here are the results for the time I woke up:

There was no clear effect of dosage on when I got up. Shifting the time from 8 am to 9 am may have had an effect (I wish I had 3 more days at 9 am).

Many people have reported that taking Vitamin D3 in the morning gave them more energy during the day. I usually take a nap in the early afternoon so I measured its effect on the length of those naps:

Maybe my naps were shorter with 6000 and 8000 IU at 8 am. It’s interesting that 4000 IU seemed to be enough to improve how rested how I felt but not enough to shorten my naps.

What do these results add to what we already know? First, the large-enough dose was more than 2000 IU. (A $22 million study of Vitamin D3 is using a dose of 2000 IU.) The dose needed to get more afternoon energy may be more than 4000 IU. Second, careful experimentation and records helped, even though many people found the effect so large it was easy to notice without doing anything special. For example, these results suggest the minimum dose you need to get the effect. Three, these support the value of supplements. Many people say it is better to get necessary nutrients from food rather than supplements. However, supplements allow much better control of dosage and timing and these results suggest that small changes in both can matter. I cannot imagine this effect being discovered with Vitamin D3 in food.

Assorted Links

Seth Roberts2 Comments
  • The corruption of science by research grants. This reminds me of a BBC documentary called something like Science Under Attack. It was hosted by a Nobel Prize winner (Biology) named Paul Nurse. Part of it was about “climate change denialism”. If you don’t believe that humans are dangerously warming the planet, Nurse implied, you are somehow attacking science. When people who win Nobel Prizes cannot see that AGW is a crock, something curious has happened.
  • Edward Jay Epstein interviews DSK. “”Thank you so much for your interest in this case,” he says.”
  • Researcher discovers new treatment for her own vertigo. ” A University of Colorado School of Medicine researcher who suffers from benign paroxysmal positional vertigo (BPPV) and had to “fix it” before she could go to work one day was using a maneuver to treat herself [the usual treatment] that only made her sicker. “So I sat down and thought about it and figured out an alternate way to do it. Then I fixed myself and went in to work” and [thereby] discovered a new treatment for this type of vertigo.”

Thanks to Melissa Francis.

Assorted Links

Seth Roberts4 Comments

Thanks to Alex Chernavsky.

Merck’s Vioxx and the American Death Rate

Seth Roberts8 Comments

Ron Unz makes a very good point — that just one awful drug (Vioxx) sold by just one awful drug company (Merck) appear to have caused hundreds of thousands of deaths:

The headline of the short article that ran in the April 19, 2005 edition of USA Today was typical: “USA Records Largest Drop in Annual Deaths in at Least 60 Years.” During that one year, American deaths had fallen by 50,000 despite the growth in both the size and the age of the nation’s population. Government health experts were quoted as being greatly “surprised” and “scratching [their] heads” over this strange anomaly, which was led by a sharp drop in fatal heart attacks. . . .

On April 24, 2005, the New York Times ran another of its long stories about the continuing Vioxx controversy, disclosing that Merck officials had knowingly concealed evidence that their drug greatly increased the risk of heart-related fatalities. . . .

A cursory examination of the most recent 15 years worth of national mortality data provided on the Centers for Disease Control and Prevention website offers some intriguing clues to this mystery. We find the largest rise in American mortality rates occurred in 1999, the year Vioxx was introduced, while the largest drop occurred in 2004, the year it was withdrawn. Vioxx was almost entirely marketed to the elderly, and these substantial changes in national death-rate were completely concentrated within the 65-plus population. The FDA studies had proven that use of Vioxx led to deaths from cardiovascular diseases such as heart attacks and strokes, and these were exactly the factors driving the changes in national mortality rates.

The impact of these shifts was not small. After a decade of remaining roughly constant, the overall American death rate began a substantial decline in 2004, soon falling by approximately 5 percent, despite the continued aging of the population. This drop corresponds to roughly 100,000 fewer deaths per year. The age-adjusted decline in death rates was considerably greater.

This illustrates how Merck company executives got away with mass murder on a scale that the Khmer Rouge would be proud of. It also illustrates why I find “evidence-based medicine” as currently practiced so awful. Evidence-based medicine tells doctors to be evidence snobs. As I showed in my Boing Boing article about tonsillectomies, it causes them to ignore evidence of harm — such as heart attacks and strokes caused by Vioxx — because the first evidence of harm does not come from randomized controlled studies, the only evidence they accept. It delays the detection of monumental tragedies like this one.

What Motivates Scientists? Evidence From Cancer Research

Seth Roberts4 Comments

A friend of mine who worked in a biology lab said the grad students and post-docs joked about the clinical-relevance statements included at the end of papers and grant proposals: how the research would help cure cancer, retard aging, and so on. It was nonsense, they knew, but had to be included to help funding agencies justify their spending.

Principal investigators never say such things. Are they wiser than grad students and post-docs? Fortunately for the rest of us, actions speak louder than words. An action — actually, a lack of action — that suggests that P.I.’s know their research has little connection to curing cancer, etc., is 50 years of widespread indifference by cancer researchers to the possibility that their research uses a mislabeled cell line. For example, you think you are studying breast cancer cells but you are actually studying melanoma cells. A recent WSJ article says that the problem was brought to the attention of cancer researchers in 1966 but they have been “slow” to do anything about it:

University of Washington scientist Stanley Gartler warned about the practice [of using mislabelled cells] in 1966. He had developed a pioneering technique using genetic markers that would distinguish one person’s cells from another. Using the process, he tested 20 of the most widely used cancer cell lines of the era. He found 18 of the lines weren’t unique: They were Ms. Lacks’ cervical cancer. . . . A decade after publication of his findings Gartler attended a conference and introduced himself to a scientist. Dr. Gartler recalled the man told him, “‘I heard your talk on contamination. I didn’t believe what you said then and I don’t believe what you said now.’ “

What he meant was: I ignored what you said. Yet it costs only $200 to check your cell line. Fifty-plus years later, mislabeled cell lines remain a big problem. “Cell repositories in the U.S., U.K., Germany and Japan have estimated that 18% to 36% of cancer cell lines are incorrectly identified,” says the article. This indicates considerable indifference to the possibility of mislabeling.

If you truly wanted to cure breast cancer, would you spend $200 (out of a grant that might be $100,000/year) to make sure you were using a relevant cell line? Of course. If you were trying to cure your daughter’s breast cancer or your mother’s melanoma, would you make absolutely sure you were using the most relevant cell line? Of course. I conclude that a large fraction of cancer researchers care little about the practical value of their research.

I believe that one reason my personal science found new solutions to common problems (obesity, insomnia, etc.) is that my overwhelming goal was to find something of practical value. I wasn’t trying to publish papers, impress my colleagues, renew a grant, win awards, and so on. No doubt many cancer researchers want to cure cancer. But this 50-year-and-not-over chapter in the history of their field suggests that many of them have other more powerful motivations that conflict with curing cancer.

Thanks to Hal Pashler. Hal’s work on “ voodoo neuroscience” is another instance where the guilty parties, I believe, knew they might be doing something wrong but didn’t care.

Assorted Links

Seth Roberts1 Comment

Thanks to Peter Spero and Hal Pashler.

Why We Touch Our Mouths So Much: Evidence From Ants

Seth Roberts2 Comments

In a recent post I proposed that we touch our mouths so much to transfer germs from our hands to our immune system. It’s an early warning system. The full sequence is: 1. Hands. 2. Skin around mouth. 3. Tongue (lick lips). 4. Tonsils (immune system). Forewarned is forearmed: exposure to a tiny amount of Germ X makes you much more likely to survive exposure to a large amount of Germ X.

Ants have a similar early-warning system, says a new study described here.

Cremer and her colleagues began by investigating how nestmates encountering an infected ant acted. They infected Lasius neglectus ants with Metarhizium anisopliae, a fungus that sticks to the insects’ outer cuticles and causes infection only after it has worked its way into the body, which takes a day or more. The researchers then placed infected or non-infected ants in a box with five nestmates, and watched what happened. . . . Ants without the spores were groomed at a constant rate over 5 days, while Cremer saw a spike in grooming of the fungus-infected ants in the first day or two of infection, suggesting that the pathogen was prompting a behavior change in the nestmates.

The grooming was protective:

But even though they’d been exposed, only 2 percent of nestmates died from fungal infections, even though half of the initially infected ants, which had been dipped in solvent with M. anisopliae spores, died within 5 days. When ants were exposed to a dose of fungus expected to cause a 2 percent death rate, Cremer’s group saw an increase in antifungal activity, suggesting that this low level of infection was indeed enough to stimulate a protective immune response.

Earlier studies had shown what is called “social immunization” (“a protection of naive individuals of a colony after social contact to exposed individuals”) among insects. This study was about how social immunization happens.

After I thought of this explanation of mouth touching, I became much less concerned about contact with sick people. I hadn’t known about social immunization.

Do Sonograms Cause Autism? A New Study

Seth Roberts7 Comments

A new paper (“Are Prenatal Ultrasound Scans Associated with the Autism Phenotype? Follow-up of a Randomised Controlled Trial” by Yonit K. Stoch, Cori J. Williams, Joanna Granich, Anna M. Hunt, Lou I. Landau, John P. Newnham and Andrew J. O. Whitehouse) takes another look at the results of a randomized trial started in 1989. Half the mothers were given one ultrasound during their pregnancy, the rest got five. This study gave a questionnaire sensitive to autism-like traits to the now-grown-up children. This is potentially more sensitive than binary (yes/no) assessment because the questionnaire has about 50 questions.

Here is the entire abstract:

An existing randomised controlled trial was used to investigate whether multiple ultrasound scans may be associated with the autism phenotype. From 2,834 single pregnancies, 1,415 were selected at random to receive ultrasound imaging and continuous wave Doppler flow studies at five points throughout pregnancy (Intensive) and 1,419 to receive a single imaging scan at 18 weeks (Regular), with further scans only as indicated on clinical grounds. There was no significant difference in the rate of Autism Spectrum Disorder between the Regular (9/1,125, 0.8 %) and Intensive (7/1,167, 0.6 %) groups, nor a difference between groups in the level of autistic-like traits in early adulthood. There is no clear link between the frequency and timing of prenatal ultrasound scans and the autism phenotype.

Parrish Hirasaki pointed out to me that when the study was done the intensity of ultrasounds was eight-fold less than now. Here’s what the paper says about this:

Technological advancements over the past two decades have led to considerable improvements in ultrasonographic capabilities, with corresponding increases in acoustic output.

Did you read that and realize the intensities have increased by a factor of eight? Neither did I. Such a big difference in intensity means the results are not serious evidence — contrary to what the abstract implies — against the idea that sonograms are now causing autism.

More Asked about the failure to make clear the difference in intensity, the corresponding author, Andrew Whitehouse, replied:

The parameters of the ultrasound scans were reported clearly in the Methods section, and we refer to several other articles that include a description of the USS administered in this cohort. We are also very clear in the Discussion when we state that “the current study was not designed to investigate the use of [modern] instruments”.

I disagree. So what if the parameters of the ultrasound scans were reported clearly in the Methods section? That’s not the issue. The issue is failure to make clear the huge intensity difference between the ultrasounds they studied and modern ultrasounds. Saying that “the current study was not designed to investigate the use of [modern] instruments” does not make clear at all (much less “very clear”) how much modern ultrasounds differ from the ultrasounds actually studied. Any study can put caveats like that at the end. Yet few studies are as irrelevant as this one to the question they claim (in the title, abstract and introduction) to help answer.

Cod Liver Oil Best Taken in Morning?

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Is it better to take cod liver oil in the morning than at other times of day? Kim Øyhus’s experience suggests that:

Each mid winter and summer I tend to lose my feeling of when it is day or night, especially if I am in the northern parts of Norway, or if the weather is dark clouds for a long time, which often happens. So sorry, no statistics, just my sense of being unhinged from the diurnal cycle.
Taking 1-2 spoons of cod liver oil in the morning got me back to this rhythm in about 3-5 hours. It even works for fixing my diurnal rhythm after partying to sunrise, but only after a day’s rest.

I have posted many times about the value of taking Vitamin D3 in the morning.