Bought bigger tent and smaller clothes

Seems like I’m going in opposite directions – well, I am but for different reasons.

When I first went cabin-fever crazy here I just grabbed all my old backpacking stuff and threw it in the car and headed south. Turns out I was seriously under-equipped, at least where a car and gasoline move the load. So I bought a new tent, but still thinking more like a backpacker got the smallest and lightest one from REI, but went for the heavier poles since the car would be carrying the load. Worked fine for a while, but older and a little less flexibility getting in and out of small backpacking tent is not so easy, esp. in the middle of the night which is at this age a bit more likely. So I wanted something a bit larger, but was concerned not to get something so large I couldn’t put it up myself. So I compromised on a 5-person (ha, would require really small persons) tent that I’ll so know whether I manage on my own.

But on the way out of Bass Pro some shorts were calling my name and then I realized my size isn’t going to get much smaller (near my minimum planned weight) and actually having clothes that fit (and snugly at that) would be a good short- and long-term constant reminder of even relatively small increases. Snug pants in the future means a return to fasting, not buying new pants. I was fairly surprised, then when I decided to try a shirt that down three sizes fits, but the real shock came in buying long pants, given I could fit the same dimensions as my college age. Now I don’t believe it – I’ve heard women’s clothes are bigger for the dress size than they used to be and I’ll bet the pants I bought today have undergone the same size inflation and are probably actually at least the next size up (IOW, 38″ is now the “new” 36″). Of course not being much of a clothes person I forgot about shrinking after first wash, but I joked any shrinkage in the clothes is a new incentive for yet more shrinkage in me.

So bigger tent for one reason, smaller clothes for a different (and better) reason. Now I just hope it’s been hot in Wyoming and some of that snow is disappearing.

 

Human cloning is not the bogeyman – 2

In my previous post I mentioned what I labeled as a silly book (How to Defeat Your Own Clone), but now that I have a copy I’m finding it interesting and different than I expected. With a lot of humor the authors are trying to explain the science and debunk some of the mystery of human cloning. I haven’t finished the book yet (the biology bits I already knew), but it has provoked my own thoughts.

First off all, reproductive cloning is totally misunderstood by the public, shaped more by fantasy books and pop culture and the largely irrelevant “moral” debate. The simple bit is this: your genome (the only thing you share with your clone) is only a small part of who you are. Your clone may have the same genes, but: a) will be a person in every meaning of that word, and, b) it won’t be you, in fact it may be very different from you, and, c) it’s not your property to do with as you please, it is legally and realistically a complete independent being that has the right to do as it wishes.

Are you your genes? No I don’t mean, simply, the nature vs nurture issue. I mean identity. Is your personality in your genes? (maybe a little) Is your knowledge, your experience in your genes? Absolutely not.

Let’s start with the biology. Unless you are cloned at a very young age your clone will not have the same birth mother. While cloning may be in our near-term future, an artificial womb (incredibly complex biology to synthesize) will not. That means whatever woman you get to be the surrogate birth mother is going to heavily influence the baby that is born. Prenatal environment is hugely important for shaping the embryogenesis process and it’s will be very different for your clone. And in the early growth, after live birth, will also very much affect your clone as it grows. By the time it’s 18 it will have been exposed to a totally different developmental path and it will be different, not to mention quite a bit younger than you. Your clone will be less the same as you than an identical twin (also exactly you at the genome level) would be due to these many biological factors.

But the social and history will play a huge role. Each of us has had pivotal events in our life. When my parents decided to move to a drastically different location that had a major impact on me. My clone not only wouldn’t be born in the same place (or same time) but it’s not going to grow up in the same places. The Vietnam War had a huge impact on me, changing my career, changing who I married, changing where I lived later in life. My clone would have completely different experiences and would be shaped entirely by their life experience, not mine. It will grow up in a different timeframe (just think about the other subject of this blog, social media: I experienced none of it, my clone would be immersed in it and changed by it). I’ve worked in other countries that were even the enemies of the U.S. at the time I was born; my clone might grow up in one of those countries or be employed by a company in one of them or marry someone from one of them. So while my parents couldn’t imagine the “global” life I’ve lived, I can’t imagine the even more global life my clone would live. Like many of my generation JFK had a huge effect on me; my clone might have been influenced by George W. Bush! Our identity is shaped by our experience, not our genes, and so my clone would be at least as different than me as any other child I might have had.

People think clones will know the same things, enjoy the same activities, be good (or bad) at the same things as we are, but they won’t. Memories and even most of personality and identity is stored in neurons, not DNA. My clone could never know the same things I do and would probably find most of my experience as silly as I feel about much of my parents experience. My clone would chuckle at the things I like and I’d be wondering about how the new generation is so crazy. You and your clone are not even likely to be friends and in fact might really dislike each other. So why do you think you’d have any special affinity with your clone?

So cloning is just a somewhat different way of having children, but with the same set of consequences as we experience with our children. Despite our influence they are their own person and their relationship with us will be what it will be, not something somehow special due to being our clone.

I don’t know quite how popular culture got off on such fear of clones. Assuming cloning actually works right, there is no difference between a baby born of the old-fashioned biological process and a clone. So I’m the product of the scrambled and merged chromosomes of my parents and my clone has my chromosomes (although importantly, the book pointed out, not exactly the same ones I was born with since the DNA in my adult cells is not precisely the same as my own embryonic DNA). Twenty-three chromosomes are twenty-three chromosomes, no matter how they got assembled. And also imagine not-much-later enhancements to cloning: a) why does my clone have to have just my genome, why not scramble it a bit with chromosomes from others, b) and what about embryonic gene replacement; I’m probably predisposed to some disease, wouldn’t I like my clone to have some better genes, where possible, c) will my clone perhaps get better nutrition than I did and so have fewer adipose cells to fight with later in cell, and, so forth. By the time we can clone, we’ll be able to alter the embryo, and that technology will only improve with time, offering more opportunity to “optimize” the person that is produced. And don’t tell me, if you’re willing to clone, you won’t also invest even more in positive outcomes for your clone.

When IVF first happened it shocked popular imagination but now it’s so routine who even knows who is a “test tube” baby (just that term shows how poorly the public understood IVF). If cloning works it will someday be the same as IVF, a non-event, just an alternative way to make a baby. The resistance to IVF, primarily religious, was quickly swept aside because reproduction is too important to parents to deny them what they seek. Can any authority really tell parents they can’t reproduce just because they have some defect in their natural process? No, parents demanded and got that right with IVF. And they’ll get it with cloning. Imagine the story of Lance Armstrong. At a very young age (before any children) he was diagnosed with testicular cancer. In his book he describes the total weird circumstances of being told he had a likely fatal condition and then being sent to a private room with a bottle and skin magazines to make the last sperm sample he’d ever do. So imagine he already had several children and then lost his ability to make more, would anyone deny him cloning one of the existing children, or himself, or his wife, or any other willing person? Parents will face circumstances where the only option they have for reproduction is cloning and they’re going to take it. And why not? What is that difference than any other method of getting twenty-three + one (and it’s interesting to think that my clone might have two X’s, not my Y, and why not?)

The moral issue, I think, resolves down mostly to safety, esp. in the earliest days. AFAIK Dolly suffered from shortened telomeres and thus doomed to a shorter lifetime. Now, when that could happen to a human, a human to whom you’re very connected, that is not something we’d wish on our offspring. And the crude zap and shake-and-bake method of creating the embryo is a brutal mechanical process (at the molecular level) and some DNA break seems entirely possible (or even a missing or irreparably damaged chromosome, remember that one cell only has one set, it will be vital they’re intact). Or perhaps we can’t reverse all the epigenetic programming of the DNA with the cloning process. Or mixing a different set of mitochondria with my DNA might be a bad combination. Or my adult cell that is the source of the clone’s DNA has already had one of the DNA “hits” that is further along the way to cancer. There are tons of potential “mistakes” that can happen and the being we create is a person, and condemning them to a bad life (due to some damage the process causes) is an obvious moral no-no. As it is, making a baby is a crapshoot, but at least we can just blame random bad luck if something goes wrong. When we consciously and artificially create a new person and it has problems due to the technology that created it obviously we will blame ourselves and others. Certainly the religinuts have it easier, because any mistakes that happen in the natural process they get to blame on god, but in an artificial process it’s on us! So we have to get it right. We don’t even get it right on animals today, so it’s unthinkable to do reproductive cloning until the technology is actually far more reliable than the old-fashioned process.

But beyond that, so what? What is the moral issue? That we’ll offend god (if god really exists then somehow I suspect he’d just break the process). Is it supreme human conceit and arrogance that we “play god”? Come on, when those zillions of sperm seek out an egg after a little frisky activity, do you really think it’s any more than random luck which one finds the egg first? (If you think otherwise, then explain why males need so much sperm, one should do nicely if it were divinely inspired).

No, it’s not a moral issue – it’s a power issue. Religion has always existed in ignorance. When thunder and lightning were mysterious, naturally god (not Maxwell’s equations) did it. And it was the shaman who got to tell us this and thus held power over our lives. Today religious institutions consume vast amounts of our resources, simply because we let them. And what do they deliver in return? Nothing but superstition and fear and bigotry. No, science is not a threat to god (who could squash it like a bug if she chose); science, especially reproductive science, is a threat to men (and mostly men in the continuing misogyny of most churches). The power (and pursese) of our mystics, seers, revelators, shamans, priests, and televangelists is diminished, not any omnipotent being you wish to hypothesize.

So don’t let religinuts scam us in this area any more than they try to scam us in all the other reproductive areas (abortion, birth control) or gun control or tax policy or what books we can read. All the fear about cloning (or Plan B) or whatever is artificially created and instilled in us just to hand over power (and blame) to others. It’s harder to think we’re responsible for our own lives than merely to assign that responsibility to something we can’t even define much less prove exists, BUT, that’s life, get over it! It’s your job (and your clone’s job) to live your life, not someone else. Don’t let the impoverished science of ancient goatherds drive policy and your rights today.

 

 

Human cloning is not the bogeyman

The announcement that scientists have done a sufficient amount of creating a human clone to grow the blastocyst to sufficient number of cell divisions to extract stem cells has created the predictable reaction from the mythology-based community. According to them a “red line” has been crossed and now all sorts of mischief will erupt, despite the fact this development did not create an embryo capable of uterial implantation and thus embryogenesis (no designer babies yet, folks).

For me this entirely predictable (but courageous, due to the hostility that will be heaped on the scientist who hopefully have bodyguards to protect them from relignuts) is not that big a deal, although a source of stem cells other than from a naturally fertilized egg may re-open the much-needed embryonic stem cell research. But the reaction seems to me to have two interesting flaws and internal contradictions.

On face value the idea that life begins at conception is nonsense. It is also not biblical (come on, believers, quote me any verse from your ancient books of myths that even knows what an embryo is!). It is just the unwise pronouncement used to object to birth control which is just a cover for the religinuts objecting to sex. The idea is totally unscientific and obviously false (what is human life, surely not three cell divisions). The contradictions of this silly POV have been pointed out over and over. With technology any cell has the potential of becoming a new life, so therefore whenever we rub our skin and knock off a skin cell, or bleed a little, we’re committing murder – come on, how stupid is that (plus absolutely not enforceable).

So really the relignuts object to this because it disproves their interpretation. Did god have to come breathe life into this clone or did scientific processes produce it? That is what really scares them. If they can claim that someone a sky-being directs reproduction then they can claim dominance over humanity, which is what they want. If reproduction is possible solely by the act of man, one more argument for god of the gaps is gone. But I think they also realize, just as happened with IVF (In-Vitro Fertilization) people’s desire to control their reproductive process without intervention by religious authorities is simply too strong. Yes, they’re probably right, there will be human cloning some day and their yelling and screaming isn’t going to stop it (even the Repugs can’t control the entire world). And when that day arrives yet another brick from their crumbling edifice is removed.

But even for those who aren’t driven by religious fanaticism have been well manipulated to believe that somehow cloning is some awful thing (even bad SciFi thrillers to sell that idea). So, nutjobs, tell me, exactly, what is morally and/or ethically wrong with it?

Now, poorly done with possible bad outcomes, cloning is a fearsome thing to try and screw up. So hopefully before somebody does it we’ll know a lot more about cloning (the shake-and-bake techniques they use now are way to crude). Once that cloned bunch of cells takes its first birth, it is human, and if it is screwed up by clumsy lab technique and thus sentenced to a miserable, yes, that is clearly an ethical screwup. Or, growing the embryo large enough to extract an organ and then kill, yep, that crosses a red line that any sensible person would have. But that’s the point. We don’t need some antique and antiquated POV, only accepted by a fraction of humanity to guide us. Like any other moral code we are perfectly capable of developing this one on our own (and an ancient book full of scientific mistakes is not a guide, except for an angry god who loves genocide and incest).

But once the real moral issues are resolved and the scientific process is good enough, so what if a clone is produced. A clone is still just a bunch of cells, not a fully formed human being with memories and history. Exactly what is different than blending two sets of chromosomes than using just one to then have exactly the same process.

The book, A Clone of Your Own, did a nice job of exploring these issues. There really is no reason to be afraid of cloning (as with this silly book that appeared in my Amazon search, at least based on the scary title as this book may also debunk cloning phobia). Whatever “fear” of cloning that seems to be out there is just more irrational fear of the unknown (do I really worry that someone will steal one of my cells to clone me, why me, why not themselves, and what would they accomplish if they did).

Obviously one of the thing that scares the relignuts is homosexual couples being able to reproduce (oh horrors, we’ll be overrun by LGs. With just cloning a lesbian couple could have children without any sperm donor (oh horrors, men will be obsolete). And with the aid of a baby mother (we’re impossibly far about from an actual “test tube” baby, the female reproductive system is way too complex to imitate) a gay couple could have children without the female. And then imagine the next step, figuring out a synthetic meiosis process, now LG couples could even have children with the normal DNA of two parents. But also, the human egg, definitely a limiting factor (where to get a supply) in cloning isn’t that magical. It’s just a bag of chemicals. Figure out exactly what chemicals and synthetic eggs are not beyond imagination (thus also bypassing the epigenetic programming of the egg donor). All this may take a long time but it’s entirely plausible to believe that in a century or two it’s possible.

Yes, it is a slippery slope for the religinuts. Human beings will continue to take control over their reproductive process (and, after all, isn’t that a fundamental human right?). Eventually we can wipe out the restrictions of simple originalist reproductive biology and see all sorts of potential. And, yes, someday that will include individual gene splicing and yes that means someday there will be “designer babies” (and if so, Gattaca dystopian horrors aside, what’s so wrong with that!). Parents have some bad genes of their own, possibly dooming their biological offspring to a life of misery, and this can repaired. Sure, some silly people will opt for blond hair and blues, but again, so what, what harm is done. We’re not going to breed supermen because the connection of genes to an adult person is far too complex, with most attributes being polygenic and very difficult to even understand, much less “engineer” (give or take a few more centuries).

But every step along this path, allowing human beings full control over their reproductive processes just goes a step further to removing the control of religion.

And that is really what scares them.

 

Read studies carefully

You can do it! You don’t have to be a PhD researcher or a rocket science. You merely need to read carefully and thoughtfully and perhaps occasionally look up a word or two. I say this because writers in the popular press clearly don’t read the studies they report on (or at least read them carefully). I think many, especially as appear in HuffPost, merely cherry-pick from headlines what they want to hear.

So here is a study we’ll look at a bit. Unlike many studies this is not hidden behind a paywall so you can get the entire thing. I saw a link (plus an opinionated statement of what the study said) in a HuffPo slideshow with the usual bias that your health will be wonderful if you just eat enough kale. So let’s deconstruct a bit of it.

First the full title:

A Prospective Study of the Association Between Quantity and Variety of Fruit and Vegetable Intake and Incident Type 2 Diabetes

Sounds relevant. So what is a “prospective study”? Not hard to find, here’s a reasonable definition in Wikipedia. So now you know what that is.

Next, let’s look at some of the preliminary prose in the abstract:

OBJECTIVE: The association between quantity of fruit and vegetable (F&V) intake and risk of type 2 diabetes (T2D) is not clear, and the relationship with variety of intake is unknown.

This is an important statement. These authors are claiming the that the answer to this question isn’t known. Presumably they’ve done a literature search before beginning their study so we’ll take this at face value. Note that this study was submitted for publication in 2011 AND THEREFORE statements about F&V prior to that time ARE NOT based on EVIDENCE (or else these authors wouldn’t need to do this study, except to confirm or contradict previous results). Imagine how many years nutritionists have been telling us about F&V without any evidence.

Next look at the conclusion they present in the abstract:

These findings suggest that a diet characterized by a greater quantity of vegetables and a greater variety of both F&V intake is associated with a reduced risk of T2D.

I’ve underline two words in quoted passages above: association and suggest. These are important words. Scientists, unlike pop writers, are conservative in their claims (or at least good ones are), so they don’t say their study “proved” anything, just that it suggests something. And what is the something? Causation, correlation, or assocation. An association is the weakest possible statistical connection between variables. Even correlation is stronger. Recall that correlation has been found between the length of women’s skirts and stock market prices. In short, if you crunch data enough you can find all sorts of nonsensical “correlations” (a correlation is just a simple statistical test, and in fact, correlation itself, even when the r^2 is provided doesn’t tell you very much).

Causation is what matters. If you’re going to do something, based on the outcome of a study, you want to see causation, not association, not even correlation. Causation has to take the correlation statistical analysis further and demonstrate (at some threshold value) that the correlation cannot be due to mere chance. There are standard methods of doing this and good studies will burble on about the statistical tests they did to justify their belief the correlation is “statistically significant”. But causation is much tougher, because it means you have to rule out everything else (but the correlated independent variable) AND you must confirm your results by running the null test, that is, eliminate the correlated input and determine that the outcome is completely changed. You also have to demonstrate that the variable being correlated is truly independent, i.e. it’s not just the result of something else. So, for instance, many consumers of F&V might be vegetarian and thus perhaps the correlation you’re finding is merely due to not consuming meat, not the F&V themselves. In short, causation is a very high threshold and rarely met in any nutritional studies.

But let’s go on with deconstructing this study, now that we know its goals are modest and that whatever its results, this is still not PROOF of the putative claim that F&V will prevent type 2 diabetes.

How did they do the study? Any good study will provide considerable detail on their methodology. If you don’t find that detail, discard the study. But then read, carefully, with just a little logic and commonsense what they did:

The final sample for analysis consisted of 653 incident T2D cases and a subcohort of 3,166 individuals (including 115 incident T2D cases).

This bit was reported in the HuffPo article, IMO, to try to show that the conclusion is based on a fairly significant sample size (I’ve seen other studies reported where the number of participants is a few dozen – sure, right, that will tell you something, but thousands, well, that should be enough, right?). But let’s look more closely:

From the 25,639 participants in EPIC-Norfolk at baseline, we ascertained incident cases of T2D (n = 892) and selected a random subcohort of 4,000 participants. This subcohort was representative of the entire EPIC-Norfolk cohort in terms of age, BMI, education level, physical activity level, smoking status, and total energy intake …

Something is fishy in Norfolk, folks – can you see what it is?

They claim they selected a random subsample, BUT: In the entire population of 25,639 participants there are 892 with T2D, or 1 in 29, but in their subsample of 3166 there were 115 cases, or about 1 in 27 (not quite random). But of course, the numbers of cases don’t quite add up, so something is unclear. But they excluded a bunch of people:

Of the 4,749 participants, we excluded those … with prevalent myocardial infarction stroke, or cancer were also exclude (n = 400). Oh, got rid of the sickies, eh?

those with fewer than 7 days of diary data (n = 435) or who did not return a diary (n = 15), Oh, got rid of the lazies, eh?

Now these exclusions are reasonable, but they aren’t random. But so be it, we’ve now got our 3166 people. What are we going to study about them? Recall they said “We examined the 11-year incidence of T2D“, so 11 years of studying these people, that sounds pretty good, but, here’s what they did:

In brief, participants residing in Norfolk, England, were recruited … and attended a baseline health check. Follow-up of participants constituted a postal questionnaire at 18 months, a second health check in 1998–2000, and a further postal questionnaire in 2002–2004.

Wow, twice they got a postal questionnaire in the mail and did one health check in 11 years! That’s really close observation of these people, isn’t it. But even more importantly:

At the baseline medical examination, participants were instructed by trained interviewers on how to complete the 7-day food diary. Completed diaries were returned by post to the coordinating center at the University of Cambridge.

Now this single 7-day diary is the ONLY data collected from these people about their F&V consumption. So it’s an 11-year study with data, at least about food consumption, from only one week. AND, the diary was returned in the mail so no one actually interviewed these people (just to see if they did the diary correctly) and certainly no one actually observed what they ate. Now self-reported nutritional data is known to be very very poor data. People are lazy and don’t do a good job on the diary, people make mistakes, and most of all people lie (trying to look good since someone is watching them). So out of 572 weeks of the study duration we have 1 week of dubious data. And from this all the rest of the conclusions flow.

Now here’s a place where they’re being careful (more detail I didn’t quote):

Participants who gave a self-report of history of diabetes that could not be confirmed against any other sources of ascertainment were not considered as a confirmed case of T2D.

So we can be relatively sure of the T2D incidence data, it’s the dietary data that is dubious. There is a lot of tedious (but important) detail explaining how the diaries were analyzed, but this bit is interesting:

Variety of fruit, vegetables, and combined F&V intake was derived by calculating the total number of different items consumed at least once in a 1-week period, irrespective of quantity of intake.

So if these participants ate one grape or one green bean, wow, that’s “variety”. As to the total consumption, well, that hasn’t been explained by this point in the article. Notice also they’re ignoring whatever else they ate, so for instance, if the non-consumers of F&V also ate greasy fast food burgers, well, we’ll never know that, or if the consumers of F&V ate little else, we’ll never know that. IOW, F&V as a fraction of the total consumption is NOT being considering in the analysis of the results. What about fat, sugar, booze, carbs? What about exercise level? What about total calories? From other studies, it’s fairly well known that high consumers of F&V tend to be “health conscious” and generally have “good” calorie intake and exercise levels, so perhaps it is those factors that matter more than F&V consumption. Oh my, certainly one reason any conclusions, at most, are just an association.

The statistical analysis section is well explained (although frankly somewhat overkill for the poor data), but as an exercise for the reader, note this tidbit:

all P values >0.32

So now what about conclusions and the commentary:

After accounting for potential confounding factors and the effects of quantity of intake, each different additional two item per week increase in variety of F&V intake was associated with an 8% reduction in the incidence of T2D.

Sounds impressive, but does it make any sense. Remember only 1 out of 27 people showed T2D, IOW, around 100 people. And so a mere two items has the 8% improvement! Think about it a minute, exactly how was this conclusion reached? Is it credible? Is it statistically significant?

These folks are scientists, so they’re honest and note what they report:

Previous epidemiological studies have reported inconsistent findings for an association between quantity of F&V intake and risk of T2D. Two separate meta-analyses have reported no overall association between fruit, vegetables, and combined F&V intake and diabetes risk,

IOW, they’re willing to pass on the information that other studies have different (and null) results. See how many politicians will do that! Or religious types? But is this just a ploy to gain credibility for this study? If so, why is this study reaching conclusions when the others aren’t? Sample sizes, perhaps? Quality of data, perhaps?

And here’s their answer:

in the EPIC-Norfolk study,mean consumption of F&V was much higher when assessed by FFQ (6.5 portions per day) than by a food diary (3.8 portions per day) (11). For this reason, FFQs are not ideal for examining adherence to, or for informing, public health guidelines

FFQ, btw, is

food frequency questionnaire (FFQ) to assess F&V intake, which is suitable for ranking individuals according to their relative but not absolute intake

yet, in terms of one of their conclusions in this study they ignore quantity when assessing the benefit of variety – let’s be consistent, fellows.

The authors carefully go through an argument why they think their study is better than others and it sounds convincing enough, so we’ll just grant that, but so what? Does this study actually show anything?

But let’s dig in a little more in science (biochemistry, not vague food diaries). They say:

The biological mechanisms for the inverse associations of F&V intake and diabetes risk are not clear.

Good, again I’ll compliment these authors are openness and honesty (unlike the quick and overly-broad summaries in popular press). But let’s look at what they hypothesize (meaning guess about the biochemistry, since in fact, it is actually unknown, since opening up peoples’ small intestines to see what is going on isn’t likely to get IRB approval).

A plausible biological mechanism to explain the beneficial effect of quantity of F&V intake on T2D is via the low energy and high fiber content of F&V, and as such their ability to reduce the overall energy content of the diet. It has previously been demonstrated that those who consume the highest quantity of F&V, in comparison with low consumers, have a lower risk of weight gain (24,25), a major risk factor for diabetes (26). A decreased risk of T2D with increasing quantities of vegetable intake in particular may be explained by the fact that vegetables are generally consumed with other foods as part of a meal and therefore may displace or buffer the harmful effects of deleterious foods from the diet, such as energy-dense foods or foods that increase the risk of T2D

Note the use of the word plausible, meaning certainly possible and logical, but completely unproven (otherwise they could say proven). But what are they saying here? This is exactly the same argument in favor of whole grain bread over pure white flour bread – FILLER! If you eat F&V (or cotton balls or anything that would fill you up and clog your intestines) then you don’t get the bad stuff. Fine, F&V do the exact SAME THING as eating less would. I’ve made this argument about bread – eating 15% less white bread has exactly the same effect as eating whole grain bread, no magic, just less calories. Plus, they’re as much as saying it’s the weight gain from excess calories that drive the T2D, not any magical secret spiritual ingredient in F&V. So eat anything that isn’t the bad stuff and you’d get exactly the same benefit. So if F&V fill you up and keep you from getting hungry and eating too much, terrific, they’ve done their job. But that IS what F&V do – cut your calories.

And then they go on to say:

Alternatively, higher consumption of specific vegetables, particularly green leafy vegetables, might reduce the risk of T2D due to the presence of relatively high concentrations of potentially beneficial bioactive compounds

Ah, the magic of kale! But note what they DO NOT say – they do not claim they made any measurements of this “plausible” explanation. In their methodology they’d didn’t split out leafy green vegetables. They didn’t measure anything about this. And, being honest, they don’t claim anything – they just hint at it. IOW, they repeat the “conventional wisdom” about the wonders of green leafy vegetables with NOT A SHRED of PROOF. So the old saying, repeat some claim often enough and people will believe it. A lot of people say they’ve seen UFOs, so they must exist. A lot of people read astrology, so stars must rule our destiny. Sorry, popularity of an idea is NOT PROOF.

And finally they say:

These findings support current public health recommendations encouraging consumption
of F&V as part of a balanced diet and place particular emphasis on the important and independent role that both quantity and variety in F&V intake may play in helping to prevent the development of T2D.

Big surprise – they go along with the crowd. Now proof of crowd view would be interesting and contradiction would be even more interesting, but really their statement about all this is very timid, certainly not deserving the headlines HuffPo gave this study, a done deal, all wrapped-up, scientifically-proven solid answers.

And then there is this:

This study was supported by grants from the Medical Research Council, the Food Standards Agency, Cancer Research UK, and the British Heart Foundation.

In general this is good. At least, unlike the Mediterranean Diet study, that was paid from by an olive oil company and the California Nut Association (guess what that study found was wonderful) they don’t have any corporate sponsorship. But they don’t say what portion of their funding came from the underlined agency, which, of course, has a vested interest in this conclusion. I’d be a lot more impressed if their funding came from Beef Growers or McDonalds or beet sugar association, where the study would be biting the hand that feeds it, that being funding by the nutrition “establishment”.

 

What determines life’s outcomes?

This is an interesting study I just stumbled on. The short of it is that genetically identical mice with more-or-less identical environment developed significantly different activity profiles. And these differences showed in actual brain development (determined after the poor mice surrendered their brains for science).

I once saw an experiment (no reference) that interested me and that I’d love to duplicate (perhaps only as a simulation). Someone built an apparatus with a large box filled very smoothly with very uniform fine dirt. The box was then placed at various angles. A very few water mister was suspended far above the box so that a fine (random) spray would fall on it. Over time you got what you’d expect, an eroded landscape. But of course each landscape was different and predicting what would happen was impossible. Yet there is some notion if we could do enough precision in such an experiment we could model this and predict it, but that never seems to work.

It’s the same with the simple experiments in chaos of a simple device to drop grains of sand, one-at-a-time, and watch the cones develop and then sustain a sudden collapse (mini-landslide). Despite attempting to get totally uniform particles and perform the experiment isolating all possible external randomness, nonetheless the nature of the pile of sand was unpredictable.

So to it appears to the be the case in biology, at least based on this study. Somehow despite controlling for as many differences as possible in the starting conditions of the experiment the mice developed differently. The idea, as expressed in the paper, is that some small and seemingly random difference appears early in the mouse’s life and this is then reinforced over time. The activity level of each mouse thus seems to be unpredictable independent of starting conditions.

So does this apply to humans? Who knows, certainly a controlled experiment like this is not possible. Even identical twins rarely have exactly the same environment, so the control exercised in this study is not possible with humans. So without evidence we can only speculate.

But it does appear that chance plays a bigger role in who we are that perhaps we’d like to admit.

I know in my own there have been “chance” events (at least those that I had no control over or say in) that had major effects. But at the same time, the notion of “attractors” in chaos theory might suggest these events don’t matter, that while the path through life might vary, the overall outcome probably does not. Again, without evidence, nothing but speculation.

But I think these hints violate two cherished concepts much of humanity holds:

1. we are masters of our own fate. Certainly the Repugs want to believe this because they want to denounce any attempts at social engineering to correct for bad luck. (Come on, guys, imagine you’d been born poor and a different race or a different gender and tell me that your life would have worked out the same for you just due to your drive and determination).
2. to the extent something meddles in our life it is a personal god. Yes, some people want to believe they have someone watching over them and helping them through life. A random path, only somewhat influences by accident of birth, is just too scary. Even if you don’t believe you’re 100% master of your own fate, then you want to believe your piety does the rest.

Nope, I’ll go with chance playing a far bigger role. All the determination in the world can’t overcome an excess of unlucky obstacles. All the great advantages, genes and environment, can’t guarantee success (whatever that even means). And rest assured, despite your desire to believe, there is no one “upstairs” looking out for you – you’re on your own in that regard (prove it otherwise if you can!).

So I guess we just have to plod on our random path. Not only is our genetic heritage completely unique, but all those life events are unique as well, so life just plays out as it will, like those sandpiles or eroding boxes of soil. Enjoy what you can.

Applied Nate Silver – major milestone

At last! I finally broke through my plateau zone of the 190s, 189.6 today! Hurrah - me! I’ve been stuck in the 190s now for 10 weeks which is more than 2x as long as it took me to break through the previous decades. The vacation cost 4 weeks (up, back down) and my loss rate since vacation has been much lower, but that’s partly according to my Phase 2 plan (real bike riding, less duration but more intense exercise, focus on protein intake and strength training rather than just weight loss).

I’m still shooting to hit 180 but that will be a “fake” weight. During the time I’m doing extreme calorie restriction my weight is artificially low (compared to steady-state maintenance calorie intake and exercise levels). So actually achieving 180lbs, while in severe diet mode, means I’ll probably do 190lbs as a target maintenance weight, hopefully counting a bit more muscle mass, not just restoring fluid. But I won’t achieve this goal soon (at least two more months) since I have some other planned disruptions of my strict regimen where I’ll bounce up (temporarily).

So here’s the two “money graph” with enough of the Phase 2 data to slightly show a trend:

The blue markers are pre-vacation data showing a 2.4lbs/week drop over 24 weeks, definitely a good showing. The two red markers are the anomaly from vacation (missing week 25, no way to get data since away from scale). And now finally the green markers show the new Phase 2 beginnings of a trend, with the much lower weekly loss of 1.7lbs/week (still too little results to get a solid value for the trend).

But today’s weigh-in is definitely not quite real. This week has not been a good week for loss. During the week I started my strength training workouts, reduced my duration of “easy” workouts and started emphasis on short and intense workouts, plus spent time on real bike (since I finally have some decent weather). So it was looking touch-and-go whether I’d have any loss, as the seven-day moving graph shows:

In fact, until today’s weigh-in the trendline for the week was actually up, as you can see from several of the higher points. So how did I pull it out today – dehydration. You see this is my girls-away-and-I-will-play week. My wife and her sister took off from their annual visit to Arizona which normally means yours truly gets to live a rowdy bachelor life for a week. But this year, instead of heading to grocery store and buying vast amounts of junk food and booze, I held back, at least mostly. So knowing I’d get a few more liquid calories (aka booze) yesterday I cut back on the solid stuff, definitely awful nutrition.

Plus last week I started my attempt at 5:2 fasting. On “feast” days I’m emphasizing protein intake. Amazingly I discovered I could make smoothies from blueberries (which I normally don’t like and don’t eat), almonds, non-fat yogurt, and agave and couple those with Muscle Milks, plus generally eating more in the 2000 calories range. I had two “fast” days, one actually achieving the 600 calorie target, the other initially below 600 but then a cheat when I made some very high cal cookies for my wife to take on her trip (fortunately they’re out of the house since each one was probably 200 calories). I actually find the fast part not too hard if I only eat a single meal (dinner) and use a portion controlled (Weight Watchers) meal plus just enough other stuff to reach 600. We’ll see if I can keep that up.

But clearly last week wasn’t working right, with all the variability. My BodyMedia calories burned and consumed app shows I should have had nearly 2.5lbs loss, but I was gaining during the week. So yesterday’s mostly liquid diet really just dehydrated me, as any significant amount of alcohol always does. This produces a 1.48lb drop today which is obviously false. But what I think I’ve found is that whenever I eat more volume this allows an increase in retaining fluid. So, for instance, I also had a one-day gain of 1.76lbs which is also bogus. So the “noise” is really making it hard to see the “signal”, just as Nate explains. The daily variability, solely due to water retention, swamps whatever real change there may be in fat burning. I expect this pattern to continue.

And it will be hard this week to maintain my discipline since there is ample temptation to enjoy my week alone with a little extra consumption (I ignored 11May as “Eat What You Want Day” just so I’d have a good weight today). And today will be a big meal as I’m planning a feast for my mother on Mother’s Day and after spending hours cooking up that meal I certainly am going to have some. And the weather is forecast to be warm so I’ll do more real biking (good for muscles, not so good for calorie burn). So I’m going to predict that I will be lucky to just stay even this week, so my prediction for next Sunday is:

189.9

Now one more bit of data trivia. I think I hit “bottom” on my rapid shedding of vacation weight about three weeks ago, so my daily weigh-ins since then have been more “steady-state” and not affected my anomalous vacation effect. So here’s what that looks like:

The trendline shows a better prediction for my next few months, a weekly loss about half as much as I achieved during the first 24 weeks. But this is the plan. With a bit more calorie intake (emphasizing protein) and less total calorie burn with emphasis on intensity and strength training I’m now focused on achieving a “healthy weight” I’ll use as my baseline for the rest of my life as I move toward maintenance, an achievement I’ve never succeeded at before. I hope to achieve a 10lbs fat loss, 5lb muscle gain and 5lb fluid bounce to set my steady-state for the future. Check back in a few months to see if I succeed in what will actually be a more difficult, but better, goal.

 

My new blog

Since WordPress.com allows multiple blogs in the same account I’m started a new one dedicated to cooking. Cooking is very popular blogging subject so I’ll join the crowd. I’m separating my cooking posts (leaving the bread posts here) so readers can enjoy that subject without all my current events opinion posts.

But I have another goal in mind. I/we have a huge library of cookbooks, overflowing all our bookshelf space. Cookbooks are wonderful items but with so many they’re almost useless since finding anything is a major task. So we constantly swear not to get any more cookbooks (already having thousands of $’s invested), but naturally more sneak into our collection. We’ve thought about various ways to make their information more accessible so we actually try more of the recipes.

But where do we get our recipes from? The Net, naturally. It’s so much easier to search online than to try to remember which book has the great recipes we want to try. I’ve thought about various approaches to somehow making my own collection of cookbooks searchable, even considering writing my own app (still may do, yet another retirement “hobby”). But meanwhile the first step is to get some of the information from the books into digital form, a real chore. I use my Dragon Naturally Speaking to enter the basic information, primarily the index of all the recipes. Speech recognition is handy since handling the cookbooks is awkward and takes my hands away from the keyboard. Thus, despite the mistakes I have to manually correct from the speech recognition the process goes quicker than typing. Nonetheless it will take years (a nice time filler) to enter all the information and probably we’ll acquire more cookbooks faster than I process the backlog so this activity will probably take the rest of my life.

But what to do with all that data? Obviously online search is handy but my blog posts aren’t likely to appear in the first search results. So hopefully I’ll find a way to enter an unlikely term (‘douqbook’ which I’m trying doesn’t seem to work) so I can force my blog posts to come out first in the search results so I can find my own recipes before all the others, often trash, that searches will provide. Over time I’ll have to evolve a tagging strategy to improve the search results from just using titles of recipes. Thus far my first attempts haven’t worked well (I believe the search algorithms don’t like either long and/or multi-topic pages). This will be a continuing exercise to fine-tune how to get optimal results.

Meanwhile I expect to supplement just having indexes of all my cookbooks with separate posts of actual recipes/menus I’m trying. This may make the blog more interesting to readers and maybe generate a few more hits, plus contribute more to the group-sourcing of cooking information on the net, which I’ve consumed, but not contributed to very much. I’ll use the comments feature to include my own reactions to the results of trying each recipe.

My experiments with bread and the posts I’ve made in this personal blog have gotten a steady number of hits. Obviously cooking is a “neutral” subject and thus something readers like more than my opinion posts. So the new blog, dedicated to cooking, may actually be more of a contribution to public knowledge and reader interest.

Obviously there is one challenge with putting information from published works on the Net and that is honoring copyright. Clearly many bloggers don’t pay much attention to this and often recipes I find are almost word-for-word from published sources. I’ll try to avoid that. Putting an index of recipes fits into an already establish public source of information as Google Books and also Amazon are already often publishing these so I’m not putting anything on the net that isn’t already there.

So this new blog is a new way for me to use my “spare” time and thanks to WordPress.com the web resources are readily available.