Archive for the “Bad Science” Category

Yup, and I can prove it:  Ancel Keys had a tiny dataset — but that didn’t stop him from leaping to big conclusions.  Nina Teicholz wrote about Keys’ problematic data in the terrific book The Big Fat Surprise, and I just came across an old paper that backs her up.

The paper appeared in a 1989 edition of The American Journal of Clinical Nutrition and was (of course) based on Keys’ famous Seven Countries study.  You’ll recall that Keys supposedly recorded what people in seven countries ate and then followed their health outcomes for several years.

Here’s a description of the study’s design from the paper:

During the base-line survey 13,000 men, aged 40- 59 y, were medically examined. Information on diet was collected in random samples from each cohort by use of the record method.  Detailed data on food consumption patterns have been published only for 9 of the 16 cohorts. Therefore, the food intake data were coded once again into a standardized form by one person. Then the foods were summarized in a limited number of food groups. The average daily consumption per person of these food groups was calculated for each cohort.

So Keys had food records, although that coding and summarizing part sounds a little fishy.  Then he followed the health of 13,000 men so he could find associations between diet and heart disease.  So we can assume he had dietary records for all 13,000 of them, right?

Uh … no.  That wouldn’t be the case.

The poster-boys for his hypothesis about dietary fat and heart disease were the men from the Greek island of Crete.  They supposedly ate the diet Keys recommended:  low-fat, olive oil instead of saturated animal fats and all that, you see.  Keys tracked more than 300 middle-aged men from Crete as part of his study population, and lo and behold, few of them suffered heart attacks.  Hypothesis supported, case closed.

So guess how many of those 300-plus men were actually surveyed about their eating habits?  Go on, guess.  I’ll wait …

And the answer is:  31.

Yup, 31.  And that’s about the size of the dataset from each of the seven countries:  somewhere between 25 and 50 men.  It’s right there in the paper’s data tables. That’s a ridiculously small number of men to survey if the goal is to accurately compare diets and heart disease in seven countries.

But wait … so far we’re assuming the dietary records were accurate.  As Teicholz pointed out, Keys took one of his food-recall surveys in Greece during Lent, when religious Greeks abstain from animal foods.  I’d call that a bit of a confounding variable.  And then there’s this, directly from the paper:

In Crete the villages involved were Agies, Paraskies, Thrapsano, and Kastelli. In Corfu the villages were Ano Korakiana, Skriperon, and San Marco. About 30 men were involved in each dietary survey. However, the original 7-day records were no longer available.

No original records?!  So you dumped the study, right?

It was therefore decided to reconstruct the diets of these cohorts on the basis of results of the dietary surveys mentioned in a publication by Keys et al.

Uh … so you swapped in the results from an earlier paper.  Okay, got it.  But tell me we’re at least talking about a genuine dietary survey here.

When no information about the consumption of certain foods, eg, fruits and vegetables, was available food balance sheet data from Greece in 1961-65 were used as a substitute.

Head.  Bang.  On.  Desk.

Getting the picture?  Keys followed the health of more than 300 men from Crete.  But he only surveyed 31 of them, with one of those surveys taken during the meat-abstinence month of Lent.  Oh, and the original seven-day food-recall records weren’t available later, so he swapped in data from an earlier paper.  Then to determine fruit and vegetable intake, he used data sheets about food availability in Greece during a four-year period.

And from this mess, he concluded that high-fat diets cause heart attacks and low-fat diets prevent them.

Keep in mind, this is one of the most-cited studies in all of medical science.  It’s one of the pillars of the Diet-Heart hypothesis.  It helped to convince the USDA, the AHA, doctors, nutritionists, media health writers, your parents, etc., that saturated fat clogs our arteries and kills us, so we all need to be on low-fat diets – even kids.

Yup, Ancel Keys had a tiny one … but he sure managed to screw a lot of people with it.

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Well, lookie here … turns out canola oil may help people with type 2 diabetes control their glucose levels. At least that’s the conclusion from a study reported in Science Daily with the rah-rah headline Canola oil may be an oil of choice for people with type 2 diabetes:

Canola is Canada’s oil and new research from St. Michael’s Hospital suggests it should also be one of the oils of choice for people with Type 2 diabetes. Dr. David Jenkins, head of the hospital’s Clinical Nutrition and Risk Factor Modification Centre, compared people with Type 2 diabetes who ate either a low glycemic index diet that included bread made with canola oil, or a whole wheat diet known to reduce the risk of cardiovascular disease.

His study, published today in the journal Diabetes Care, found that those on the canola bread diet experienced both a reduction in blood glucose levels and a significant reduction in LDL, or “bad,” cholesterol.

Even more exciting, he said, was the finding that the canola bread diet seemed to have the most significant impact on people who needed help the most — those whose HbA1c test measuring blood glucose over the previous two or three months was highest.

Well, that’s it, then. Time to call all your friends and relatives with type 2 diabetes and tell them to stock up on canola oil so they can go on that canola bread diet. Clearly some specific property in an oil chemically extracted from rapeseeds helps control diabetes.

On the other hand, maybe we should take a peek at the study first. Here’s part of the abstract:

The study was a parallel design, randomized trial wherein each 3-month treatment was conducted in a Canadian academic center between March 2011 and September 2012 and involved 141 participants with type 2 diabetes (HbA1c 6.5%-8.5% [48-69 mmol/mol]) treated with oral antihyperglycemic agents. Participants were provided with dietary advice on either a low-GL diet with ALA and MUFA given as a canola oil-enriched bread supplement (31 g canola oil per 2,000 kcal) (test) or a whole-grain diet with a whole-wheat bread supplement (control). The primary outcome was HbA1c change.

Hmmm … economics professor Thomas Sowell (author of The Vision of the Anointed) once wrote that when students in his classes declared this-or-that to be good or bad, he always replied with “Compared to what?” Seems to me this study didn’t compare canola oil to any other fats or oils; it compared two rather different diets, one of which happened to include canola oil. So I found the full study. Here are some quotes from that:

The study was a parallel design, randomized trial wherein each 3-month treatment was conducted in a Canadian academic center between March 2011 and September 2012 and involved 141 participants with type 2 diabetes (HbA1c 6.5%-8.5% [48-69 mmol/mol]) treated with oral antihyperglycemic agents. Participants were provided with dietary advice on either a low-GL diet with ALA and MUFA given as a canola oil-enriched bread supplement (31 g canola oil per 2,000 kcal) (test) or a whole-grain diet with a whole-wheat bread supplement (control). The primary outcome was HbA1c change.

The study followed a randomized, parallel design with two treatment arms of 3 months duration as follows: 1) a low-GL diet with a canola oil–enriched bread provided as a supplement (test) or 2) a high wheat-fiber diet emphasizing whole-wheat foods (control).

The dietitians and participants could not be blinded …

I understanding blinding a group of dieticians wouldn’t get past the ethics committee, but couldn’t we at least poke them in the eye?

… but equal emphasis was placed on the potential importance of both diets for health.

Okay, so no placebo effect. Both groups were told they were going on a good diet.

The test diet included 4.5 slices of canola oil–enriched whole-wheat bread (500 kcal/day) provided as a supplement. The supplement delivered 31 g canola oil or 14% of total dietary calories of a 2,000-kcal diet. The control diet included 7.5 slices of whole-wheat bread without canola oil per day (500 kcal).

A little math tells us the canola oil provided 280 of the 500 calories in the bread. In other words, the canola bread was 56% fat by calories, or 62 fat calories per slice. We can also determine that the canola bread contained 111 total calories per slice. The wheat breads I looked up online also contain 3-4 grams of protein per slice, so let’s figure 3.5 * 4 cals/gram = 14 protein calories … now subtract here, divide there, roll a set of dice, count on our fingers … I’m getting a figure of 8.78 carbs per slice on the canola bread. Multiplied by 4.5 slices per day, that’s 39.5 carbs from the canola bread.

The commercial whole-wheat breads I looked up contain around 12 carbs per slice. Multiplied by 7.5 slices per day, that’s 90 carbohydrates. So that’s a good guess as to what the control group was consuming as carbohydrates from bread. Now if only we had an idea about the non-bread portions of the two diets …

Dietary advice on the test diet emphasized low-GI foods, including legumes, barley, pasta, parboiled rice, and temperate-climate fruit, as outlined in previous studies. For the control diet, participants were instructed to avoid white-flour products and replace them with whole-wheat breakfast cereals, study breads, brown rice, and so forth.

Boy, if I didn’t know better, I’d say the canola-bread diet was designed to result in both a higher fat intake and a lower carbohydrate intake, and hence a lower glycemic index than the control diet.

By design, the test diet resulted in significantly greater increases in MUFA and ALA intake and corresponding lower carbohydrate intake, and hence GL, relative to the control diet.

I see. So what this study actually demonstrated is that replacing calories from refined carbohydrates with calories from fat results in better glucose control. And yet the headline in Science Daily was about the wonders of canola oil, and the study’s conclusion was:

A canola oil–enriched low-GL diet improved glycemic control in type 2 diabetes, particularly in participants with raised SBP …

I’m thinking the canola oil itself had nothing to do with it. The answer to Sowell’s question (“Compared to what?”) is that compared to a diet that includes bread and cereal, a fattier diet with a lower glycemic index is better for diabetics.  Perhaps canola oil got such a special mention because of this fact, which appeared at the bottom of the Science Daily article:

This research was funded by the Canola Council of Canada, Agriculture and Agri-Food Canada, Loblaw Companies, and the Canada Research Chairs Program.

For the record, I don’t know if canola oil has any harmful effects on humans. There are internet articles claiming canola oil will cause a slew of health horrors, but I don’t find those articles convincing. Perhaps canola oil has a neutral effect on health. But I don’t consume the stuff for two reasons:

One, the whole pitch for canola oil is that it’s mostly monounsaturated, like olive oil – i.e., it’s very low in artercloggingsaturatedfat! Well, heck, even TIME magazine has come around to admitting that there’s no need to avoid saturated fat. (Check out this TIME video on that subject.) So at best, canola oil is an answer in search of a problem.

Two, this is how it’s made:

I’d rather not consume a fat that has to be bleached and de-odorized before it reaches a state we could charitably call “not disgusting.” Coconut oil, butter, bacon grease, beef tallow, chicken fat – they all taste great without any industrial processing. And if you replace the refined carbohydrates in your diet with any one of them, you’ll probably end up with better glucose control.

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Six months ago or so, I wrote a couple of posts praising a two-part series titled The Heart of the Matter, which ran on ABC Catalyst in Australia. I also embedded videos of the episodes that ABC Catalyst had put on YouTube. Part one of the series questioned the Lipid Hypothesis, and part two questioned the benefits of statins.

If you click the play button for the video embedded in this post now, you’ll get a message that the video doesn’t exist. That’s because ABC Catalyst bowed to pressure from the Statin Empire and agreed to pull the videos.

The excuse was that the program violated the network’s journalist standards. (Yes, I know … these days journalistic standards is almost as oxymoronic as government assistance.)

I sincerely doubt the program violated ABC’s standards. I suspect it was more of a case of someone from the network being sat down and given an updated version of this speech from the 1976 movie Network – which, if anything, seems more relevant now than when it was released.

I could go through the excuses the network offered for its cowardly cave-in point by point, but I don’t have to. Dr. Malcolm Kendrick already did. Here are a few paragraphs from a lengthy post I urge you to read in its entirety:

As an important aside, I find it fascinating that the committee accepted that there is no ‘definitive proof’ that saturated fats cause heart disease. Check.

Yet, in a complete rupture of logic, the report stated that the ‘National Heart Foundation believe there is enough good quality evidence to recommend a diet low in saturated and trans-fats.’

Well, if there is enough good quality evidence, there must be, by definition, definitive proof. Either one statement is correct, or the other. They cannot both be, as they are mutually contradictory. This I am afraid is the level of thinking that goes on here. As expected, there is no criticism of the National (Australian) Heart Foundation for recommending a diet for which where is no ‘definitive proof.’ ‘It’s okay, they believe there is enough good quality evidence, and they are good chaps. So that is good enough for me.’

This is the usual kowtowing to the experts. If the roles had been reversed, Catalyst would have been crucified for promoting dietary advice based on nothing at all. Yet, the NHF are completely let off the hook with this pathetic statement.

‘Notwithstanding the lack of definitive proof, mainstream medical organisations such as the National Heart Foundation (NHF) believe there is enough good quality evidence to recommend a diet low in saturated and trans fats.’

Hang your heads guys. What is sauce for the goose should also be sauce for the gander.

There was another part of the report where the judgment is so weird that I cannot understand it. I defy anyone else to understand it either. You can read the whole report if you wish, and see what you think.

It seems to be saying that stratifying risk in primary prevention of heart disease is something that is contentious, but a lot of doctors believe in it, so it should have been mentioned. Something with no evidence to support it, that happens to be believed in by a number of doctors, should be presented as what….the truth? That bit is bonkers. It seems they thought they should say something, but descended into gibberish.

ABC Catalyst isn’t the only organization to retreat recently after being attacked by the Statin Empire. The British Medical Journal did likewise with a report of statin side-effects. Here are some quotes from an article in The Australian:

Patients have been urged not to shy away from statins after a key claim about potential harm caused by the cholesterol-lowering drugs was withdrawn.

The British Medical Journal has accepted that research that claimed that 20 per cent of patients on statins suffered side-effects was flawed. That claim, which was likened to scaremongering over the MMR jab, has been retracted after the journal accepted it was the result of errors not spotted by researchers, peer reviewers or editors.

Author John Abramson, of Harvard Medical School had used the claim about higher rates of muscle pain, tiredness and diabetes to raise concerns over more widespread use of statins.

The error the researchers failed to spot is the unwritten rule that you’re not allowed to criticize statins in medical journals. Billions of dollars depend on that rule being vigorously enforced.

BMJ editor-in-chief Fiona Godlee said the journal was making a public retraction “so that patients who could benefit from statins are not wrongly deterred from starting or continuing treatment because of exaggerated concerns over side-effects”.

Yes, indeed, let’s not have patients suspecting the muscle pain they’re experiencing is caused by statins. Much better for The Statin Empire if doctors attribute the muscle pain to old age or some other cause and prescribe a painkiller – as my mom’s doctor did. In what was apparently a matter of pure coincidence, however, I talked my mom into giving up the statins and her mysterious muscle pains vanished soon after.

The paper the BMJ is retracting concluded that the rate of statin side-effects is around 20%. The researcher who (ahem) corrected the data in the BMJ paper says that according to his research, only about 1% of people on statins experience adverse side-effects. That conclusion, of course, is based on data provided by the manufacturers of statins, who routinely 1) don’t publish studies with negative outcomes and 2) refuse to release raw study data to independent researchers, even for the positive studies. I wouldn’t expect their data to show anything other than a very low rate of side-effects.

However, there was a study conducted a couple of years ago that calculated the rate of side-effects by (how’s this for a wacky idea?) checking the records of patients from two large medical centers. As an article on the NPR site explained:

With one-quarter of adults over age 45 taking cholesterol-lowering statin drugs, it figures that more than a few people would have trouble sticking with the program.

More than a few, actually. A big new study of statin use in the real world found that 17 percent of patients taking the pills reported side effects, including muscle pain, nausea, and problems with their liver or nervous system.

That’s a lot higher than the 5 to 10 percent reported in the randomized controlled trials that provided evidence for regulatory approval of the medicines.

This study, which was published in Annals of Internal Medicine, looked at more than 100,000 people who’d been prescribed statins from 2000 through 2008 at two academic medical centers.

About two-thirds of people with side effects quit taking statins. All in all, half of all the people who been prescribed the drugs quit them at last temporarily. Twenty percent quit for more than a year.

So in a real-world setting, 17 percent of the patients on statins reported nasty side-effects. Twenty percent of the patients quit taking statins for more than a year. Darned if that doesn’t sound eerily similar to the 20 percent figure cited in the BMJ paper – which the BMJ later decided to yank.

Those are likely older patients, by the way.  Three years ago, I wrote a post about a study showing that 72 percent of professional athletes on statin therapy ended up dumping the drugs.  Why?  Because while a middle-aged desk jockey may not notice if he gets a little weaker thanks to statin-induced muscle damage, a professional athlete will notice right away.  His livelihood depends on it.

So what’s the BMJ’s fear here, exactly? That people will become too aware that statins might cause muscle pain and other side-effects? Isn’t that better than being too unaware that a drug can cause damage to your muscles and nerves?  For Pete’s sake, medical organizations think nothing of warning everyone to cut back on salt, even though only a tiny fraction of the populations is salt-sensitive.  They’ll tell me not to smoke cigars because my risk of developing mouth cancer will climb from 1 in 10,000 to 2 in 10,000 (thus doubling my risk!!)  Seems to me they have a rather different standard for warning people about hugely profitable drugs that can make you weak and foggy-brained.

I suspect someone at the BMJ got the same updated version of the speech from Network that caused ABC Catalyst to tuck its tail and lick the master’s hand.

Let’s not be pessimistic, though. These incidents may be the Statin Empire’s version of the Battle of the Bulge – a last-gasp attempt to turn the tide of a war they’re going to lose eventually. In case you didn’t read it, here’s another quote from Dr. Kendrick’s post:

As a disclosure of interest, I did help the programme’s producer and presenter, Dr Maryanne Demasi, with questions and background information whilst she was putting the Catalyst programs together. I tried to give her as much factual information as possible. The day after the programmes came out, I wrote her this e-mail on 31st October 2013:

Maryanne,

Just seen part II. Brilliant, well done…….. I feel a sense of pride being able, in a small way, to help you put this together.

I now hope that you are viciously attacked, because that means you have won. (And it also means that thincs has won). Be ready – I suspect the attacks have already started.

THINCS is The International Network of Cholesterol Skeptics, a group of doctors and researchers who believe anti-fat and anti-cholesterol hysteria is misguided. And while THINCS may not have won yet, I believe it (along with many other like-minded individuals and organizations) has the Statin Empire more than a little worried. That’s why the ferocious counter-attacks were launched so quickly.

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Several people asked if I planned to take apart the latest “meat kills!” study to make a big media splash.  In case you missed it, here’s part of one of the many, many articles about the study that hit the news:

A diet rich in meat, eggs, milk and cheese could be as harmful to health as smoking, according to a controversial study into the impact of protein consumption on longevity.

The overall harmful effects seen in the study were almost completely wiped out when the protein came from plant sources, such as beans and legumes, though cancer risk was still three times as high in middle-aged people who ate a protein-rich diet, compared with those on a low-protein diet.

You just know the vegan crowd loved reading those words.  But let’s keep reading:

But whereas middle-aged people who consumed a lot of animal protein tended to die younger from cancer, diabetes and other diseases, the same diet seemed to protect people’s health in old age.

So there you have it:  meat, eggs and other animal protein will kill you until you turn 65.  Then the same foods protect your health.  Since I’m already 55, I’ve decided I’ll keep eating meat, eggs and cheese and hope I manage to hang on for another 10 years – then I’ll increase my consumption of those foods to ensure I live to age 90.

That contradiction alone – animal foods can kill you until you reach the age at which most people actually die, then protect you – should be enough to convince you this is another piece of observational garbage.

But if you want a more thorough take-down of this idiocy, Zoe Harcomb already wrote one.  Here’s a bit of it (and I’d suggest you read the whole post):

This is a direct quotation from the article (my emphasis): “Using Cox Proportional Hazard models, we found that high and moderate protein consumption were positively associated with diabetes-related mortality, but not associated with all-cause, CVD [cardiovascular], or cancer mortality when subjects at all the ages above 50 were considered.”

i.e. when we looked at the 6,381 over 50 year olds there was not even an association with protein intake and all-cause mortality, or CVD mortality, or cancer mortality.

There was a relationship with diabetes mortality and protein intake, but the numbers were so tiny (one death from diabetes in one group) that this was not considered important.

And that could have been the headline – “There is no association between protein intake and mortality” – but then there would be no headline.

One of those animal-protein foods that will kill you until you turn 65 and then save your life is the humble egg.  I recently received an article about the importance of a nutrient that eggs provide:  choline.  Here are some quotes:

Choline plays a role in multiple physiological systems from all cell membranes to the function of organs like the liver. Choline produces a neurotransmitter involved in memory storage, muscle control and many other functions.

For more than five decades, nutrition science has known that choline is an important compound in the body. However, because humans have the ability to synthesize choline and our diets generally contain significant amounts of choline, it has been difficult to de­finitively show that choline is needed in the diet.

One of the first clear indications that the body does not make choline quick enough to meet the body’s own needs was recently demonstrated. When healthy men were fed a diet which was adequate in all known essential nutrients but very low in choline, the men developed liver damage. This indicates that even though the body can make choline, there is a dietary requirement as well.

Foods especially rich in choline include beef liver, with about 450 milligrams per 3 ounce serving, and eggs, with about 280 milligrams per egg.

So according to the latest observational nonsense, animal foods will kill you until you turn 65 … but at the same time, clinical research shows that choline is an essential nutrient, and the richest sources of choline are beef liver and eggs.

I vote we ignore the observational nonsense and eat our eggs.  That won’t be a problem here on the mini-farm.  Now that the chickens in our second flock have started laying, they’re producing more eggs than we can consume.  I took this picture a week or so ago to demonstrate.

Then a couple of days ago, it occurred to Chareva to check the top level of the barn, which required climbing a ladder.  This is what she found.

Another 60 eggs or so.  Fortunately, with the cool weather, they’re still quite edible.  Oh, and Sara will be taking delivery of 25 chicks soon as part of a 4-H project.  So now she and Alana and Chareva are planning to open an egg stand by the road.

And I’ll keep eating eggs and other sources of animal protein way beyond age 65.

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I apologize for the lengthy delay in posting and answering comments.  It was a strange and sometimes stressful week with virtually zero time for blogging.

I finally had some free time over the three-day weekend, which we used to solve a couple of issues around the ol’ farmstead.  The first issue involved a runaway dog.  Well, not exactly a runaway dog, but a loose dog.  I was looking out the kitchen window on Saturday and thought, Hmmm, that’s a big animal poking around at the edge of forest back there … almost as big as one of my Rottweilers.  Hey, wait a minute!

Yup, it was our dog Misha, running happy and free, waaaay outside the backyard fence.  Nobody had left a gate open, which meant she was jumping the fence.  Most of the fencing is 48 inches tall, and she can’t jump that.  But over on the side yard, there’s a long section that’s only 40 inches.  There’s also a section that was apparently caved in a bit by a tree at some point, and it’s even shorter.

The long-term plan is to fence in the entire property, but we’re not ready to make that investment yet, so we needed a quick and easy (and inexpensive) solution.  Chareva remembered that she’d used a cow panel to make the hoop part of the portable chicken coop and thought cow panels would be tall enough to keep Misha from exploring the countryside and possibly deciding to explore the highway full of fast-moving vehicles.

I’ll be the first to admit it wasn’t the most aesthetic solution, but what the heck, the existing fence isn’t a charmer anyway.  That’s one of the reasons we plan to get all-new fencing someday.  The cow panels were easy to strap to the existing fence, and so far they’ve kept Misha from doing another remake of The Great Escape.

The other issue we solved was getting across the creek without requiring balance or long-jumping skills to avoid stepping into muddy water.  The shortest route from the house to the chicken coop and the garden is across the creek.  During dry months, it’s easy to just step over it.  But for several days after a good rain, crossing the creek requires either a decent long jump or stepping on big rocks that may or may not be slippery.  I’ve had my foot slip off a rock and plunge into the muddy water enough times to expand my vocabulary of four-letter words.

To keep our feet dry when the creek swells after a rain, I figured we needed something 12 feet long.  I thought a steel bridge with handrails would provide a charming touch, but didn’t find the price on 12-foot steel bridges charming in the least.  So we decided to just go buy $100 worth of wood at Home Depot and make a bridge ourselves.

For the base of the bridge, we bought 4×4 beams.  For the surface, we bought 12-foot planks that are just under an inch thick and cut them into 3-foot sections.

Chareva likes this picture because (according to her) I look like a boy pulling his wagon.


She suggested pre-drilling holes before attaching the planks with 2-inch wood screws.  While putting together the portable chicken coop, she apparently had a bad experience trying to drill long screws directly into the wood.   I replied that in the interest of time and efficiency, I’d like to try drilling the screws directly first.

When I pushed the drill down and the screw head ended up flat against the plank, she said, “Huh … I guess you’re stronger than I am.”  And here I thought – you know, with our workouts at the gym and all – she already knew that.  Nice when a construction project clarifies your wife’s opinions of your abilities.  She also told me several times how happy she was to see me building a bridge from scratch.  I get that … my dad never did anything with tools, I never did anything with tools until we moved to the farm, and all the years she knew me in Chicago and Los Angeles, she never saw me take on a project more complicated than hanging a picture.

I thought we’d probably have to prop up at least one beam with rocks or paving stones, but nope.  With a little moving and shoving and adjusting, we found a spot where the bridge settled in nicely, with no tilting or rocking.  I celebrated with a round of disc golf, patting myself on the back a bit each time I used the bridge to cross the creek.

Meanwhile, the girls have decided it’s a great perch for watching crawdads.

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Okay, they’re not exactly beasts and they haven’t exactly been released, but our 18 chicks are now living outside in the portable coop Chareva constructed.  The one real design flaw was the wheels (assuming, of course, you consider not staying in place and not rolling to be a flaw).  So we attached a chain to the coop, then I made like a donkey and dragged it behind me to the field behind our house.  Not a bad workout for the legs.

Chareva made two final modifications to the coop, both for security purposes.  She found that with her makeshift cord latch, she could easily push the door in several inches – which means a raccoon could do likewise – so she attached a couple of better latches, one high, one low.  Now the door doesn’t push in.

After a couple of readers warned us about predators digging underneath the bottom rails, she made a floor out of 2 x 4 fencing.  We hope that’s enough to discourage a raccoon from tunneling into the coop while still allowing the chickens to peck and scratch.  Time will tell.  When she builds her next coop, Chareva will attach fencing to the underside first.  It wasn’t an easy task doing a retrofit job.

The chicks cowered inside their cardboard box for a bit after the move, then began exploring the coop.  Soon they were pecking the ground like crazy.  I hope that means they’re eating ticks.  If they turn out to be enthusiastic tick-eaters, I’ll happily raise as many chickens as we can handle.

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