13 Weeks: Week 13 — in Which We Speculate
So here it is: week 13 of the 13 Weeks, which officially ends tomorrow. This is also Day One of the next 13 Weeks, which I started today to make everything match with the publishing schedule.
I pretty well explained what I’m doing for the next 13 weeks in my post last week, so I won’t linger on that: same eating plan or similar, but adding a Seinfeld calendar with six days a week of a Tabata protocol workout, plus weightlifting and yoga or Pilates. I have a new spreadsheet which tracks body fat as well as weight and glucose. As of today, this is a new experiment, so I’m starting from an empty spreadsheet. As of today, weight is 272.1, body fat by Withings impedance scale is 33.1 percent, and morning fasting glucose is 109. “After pictures” and a comparison in next week’s column.
So, below the fold, a little change of pace.
See you next week.
“… the history of 20th Century medicine includes several dramatic wrong turns and blind alleys. Many of them were based on ‘Freudian Analysis’, the 19th century pseudoscience that is, nonetheless, the direct ancestor of today’s psychiatric neurology. Under the influence of Freud and his contemporaries, there was a period of about fifty years in which physical illnesses like monoamine synaptic disorder (MSD), mesolimbic development disorder (MLDD), and chronic glucose-sensitive lipodystrophy (CGSL) were called ‘depression’, ‘schizophrenia’, and ‘obesity’ and ascribed to childhood trauma, parental neglect, or in the case of CGSL, simply as a character flaw.”
(From “The 20th Century Detour”, PJ Discovery, published 21130201T0000)
Imagine you are the apocryphal Drug Rep from Arcturus. You’ve heard through the grapevine that the Arcturan Chamber of Commerce plans to initiate First Contact, so you’ve come undercover (you miss your fifth and sixth finger but they’ll grow back) to see what the new market might offer. Through a peculiarity of Arcturan patent law, otherwise out of patent drugs can be re-patented in an emerging market, so new planets are big moneymakers. And you love your job — it’s perfect for a veterinarian who lost his license for rishathra.
Which really was unfair. You just really love animals. You ran into another Arcturan who’s here writing a cookbook, and that’s just wrong.
The key, as always, is to look for diseases that aren’t being effectively treated by the native savages’ own medicine men. And Earth has a doozy: a lipodystrophy that disrupts normal weight regulation, depositing fat in a stereotypical pattern that results in a characteristic fruit on a stick shape.
It’s not just a cosmetic issue, either. Humans with the disease have lots of other consequences — cardiovascular problems, disorders of blood-glucose regulation that lead to neurological problems, just a whole host of issues that cause victims of this degenerative syndrome to sicken and die earlier than their already short-lived contemporaries.
One night — night mail being so much cheaper — you message back to your husbands, wives, pod-mates, children, siblings, and clones.
“… what really crazy is that they do have the beginnings of science here, but they lose their science on the oddest things. This lipodystrophy I’ve been investigating — which would be a lot easier if the Chamber of commerce would just let me perform some experiments — is really widespread and causes immense suffering. But they can’t figure out the cause, so they blame it on a character flaw, something they call the ‘sin of gluttony.’
“So millions of the Earth natives die every year, and the best treatment they seem to offer is to shame the victims and complain that the problems caused by the lack of treatment of this chronic disease are expensive.”
We’ll leave our Arcturan for now — with his love of animals and predilection to rishathra, he has a date for the night anyway, and isn’t she in for a surprise? — and think about the issue he raises. He doesn’t have our human history, so he can look at this with fresh eyes, and he sees something peculiar. There are a couple of rather different populations: one of them regulates their body fat effectively and homeostatically, and the other group can’t.
If we look at it with fresh eyes too, we see this is a pretty significant disease. It kills millions through one mechanism or other related to the symptoms — heart failure, liver failure, diabetes, possibly even Alzheimer’s disease. It’s clearly what we would normally consider a disease, because we know there is a large population who don’t have it: the people who eat what they want and don’t develop the apple-on-a-stick body shape, or slowly lose their ability to regulate blood sugar.
If we forget the notion of shaming obesity and think of this as an actual disease, a syndrome, what would be the result?
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More on Self-Improvement at PJ Lifestyle:
>em>it’s perfect for a veterinarian who lost his license for rishathra.
Been talking to Speaker to (Lab) animals, hmm?
Wow. Just wow. Have you started the novel based on 13 weeks yet? Put me on the pre-order list.
“If we forget the notion of shaming obesity and think of this as an actual disease, a syndrome, what would be the result?”
A perpetual series of moderately effective but extremely dangerous pharmaceuticals able to treat the chronic condition in perpetuity none of which would be possessed of the power to effect an actual cure. The efficacy of said pharmaceuticals would, naturally, expire approximately concurrent with patent rights in same thereby guaranteeing an eternal income stream as new and allegedly more effective treatments arose. The rather serious negative consequences of the ongoing chemical control of the symptoms of the disorder woul give rise to a repetition of this rather virtuous cycle on several other fronts. Wash, rinse, repeat ad infinitum. Because, you see, the size of the income stream associated with a quick & inexpensive “cure” is almost infinitely smaller than that associated with treatment of widespread symptoms in perpetuity.
I’m not sure that you are being cynical enough…
LPL enzyme (Lipoprotein lipase) from adipose or muscle must be hanging in the blood vessel wall to break circulating triglycerides (lipid “fat”) of chylomicrons &/or VLDL (very low-density lipoproteins) freeing fatty acids for “burning” or re-formating subsequently into a lipid droplet (“body fat”). Oriental, African & Caucasian ethnicities have different frequencies of genetic variants LPL – of course modern populations are quite intermixed.
There are also factors which interfere with the LPL enzyme function. One of the post-prandial lipids is sphignomyelin & it is involved in cell signalling. Cell signalling is largely where modern man’s diet problems get messed up – we can benefit when eating most things .
Basically, if sphingnomyelin is carried by HDL one benefits & if not then sphignomyelin can become a rogue factor. Fish oil supplementation will boost HDL sphignomyelin. Olive oil speeds up liver break down of unbound sphignomyelin & leaves less sphignomyelin loose in the blood plasma.
Too much sphignomyelin loose in plasma bathing our muscle/adipose cells will inhibit LPL enzyme function. And, too much plasma sphignomyelin can interfere with our various lipid carrying lipo-proteins’ normal dynamic with their lipo-protein receptors.
LPL in human abdominal subcutaneous adipose is less inhibited by insulin in diabetics & 1st degree relatives of Type 2 Diabetes (ex: mother diabetic). Insulin normally does shut down LPL’s lipo-lysis in adipose, whether gut or thigh. The genetics in diabetes of poor insulin control over lipo-lysis causes more churning of adipose lipids & other metabolites.
In long skeletal muscles (ex: leg) insulin does not inhibit LPL lipolysis (all tissue do not respond similarly to insulin). 1st degree relatives of Type 2 & diabetics have more lipids in their myo-cytes than “normal” – this messes up their insulin signalling.
Exercise training does not play out the same for “normal” exercisers as it does for 1st degree relatives of Type 2 & diabetics. All do get better volume oxygen (VO2max), mitochondrial capacity & decreases in both insulin & fasting glucose.
But, insulin sensitivity in 1st degree relatives of Type 2 & diabetics does not always improve over time with training.
Also, for “normal” adult exercisers glucose (as opposed to insulin) driven glucose going into skeletal muscles does increase with exercise training. This seems to be largely due to insulin mediating increased peripheral blood flow.
1st degree relatives of Type 2 & diabetics do not get as much base line (basal) insulin driven extremity blood flow as “normal”. And, despite exercise training, their leg skeletal muscles do not improve their basal level glucose uptake as notably much as “normal” exercisers. Which seems to extend to whole body glucose uptake being largely unchanged by exercise training for 1st degree relatives of Type 2 & diabetics, whereas for the “normal” exerciser training notably increases whole body glucose uptake.
As for adipose tissue, the exercise training does increase it’s local insulin sensitivity, for even 1st degree relatives of Type 2 & most diabetics. But there is a notable individual distinction. If exerciser is relatively newly diabetic training will increase Beta cell insulin output. On the contrary, if exerciser has been a long term diabetic then training will decrease Beta cell insulin secretion.
So, tie in the above & leading paragraphs for 1st degree relatives of Type 2 & diabetics….When genetics pre-dispose a person so their insulin level doesn’t inhibit adipose tissue LPL lipo-lysis the loosed lipids/metabolites downstream go on to interfere with insulin signalling (like lipids sphignomyelin/ceramide can mess up). If Beta cells can increase insulin secretion with training in some the higher level of insulin can inhibit adipose LPL lipo-lysis. The end game here is not that insulin keeps “fat” in adipose cells, when insulin limits LPL from letting fat clear out of adipose tissue. The benefit is when that person is not actively going to “burn” some lipid “fat” there are fewer downstream lipids (sphignomyelin/ceramide) messing up cellular signalling. On the other hand, for long term Type 2 diabetics, training seems to spare the Beta cells from exhausting themselves (beta cells) & ameliorates complications due to that. Although these long time diabetic individuals will lose less weight as a result of training, since not enough insulin to block LPL lipo-lysis provoking the gumming up of cell signalling (ex: sphignomyelin/ceramide).
Should we begin to classify every variation in metabolism that can result in disease a disease in and of itself, even if it remains un-triggered because the person holding the gene has simply chosen a lifestyle or diet in which the genetic propensity remains unexpressed? I think this discussion boils down to Aristotle’s categories of being. A potentiality that remains unexpressed is in practice a non-entity. If that potentiality is expressed only under special circumstances, and those special circumstances involve a lack of restraint as regards type of food and the intake thereof, it can hardly be considered a disease in the classic sense. If the behavior is necessary for the gene expression to occur involves said lack of restraint, it is the behavior that is the proximate cause of the disorder, and not the gene. The average person does not think in terms of these categories of ontology, but has an intuitive insight that is sometimes displayed in a crude manner. The fact that such an insight is displayed crudely does not negate the truth behind that insight, and is not an excuse for obscuring that truth by clever (or not) fictions. Sorry, but that’s the way it is. I once had a patient who flew a bunch of generals in to see the concentration camps. He said he didn’t see any overweight people there, so he never believed any of that crap about people being necessarily doomed to obesity. I think that it can be genetically selected for, but the gene expression can only take place when it is allowed to, just like type II diabetes. Life is only partially deterministic.
Doc, the thing is that what you’re describing is very much like Hansen’s Disease (ie, leprosy, for the general audience.) It appears to require both a genetic flaw and an outside insult — Mycobacterium leprae for leprosy, long-term exposure to high-glycemic foods in metabolic syndrome. And remember, we’re not actually clear on what the cause of metabolic syndrome is — there’s a suspicious collection of studies accumulating suggesting is actually being caused by an intestinal bug.
As long as it’s considered simply the result of self-indulgence and moral fault, though, it’s pretty hard to study the underlying cause.
“those special circumstances involve a lack of restraint as regards type of food and the intake thereof”
Those “special circumstances” don’t. Fat people don’t eat noticeably more than thin people per pound of lean body mass. What you seem to be describing – eating more than your body needs for long periods – is an eating disorder, and OCD (of which eating disorders are one type) is generally regarded as a disease needing treatment, not a character flaw.
Now, it is true that someone who has inherited a tendency to develop insulin resistance will do better if they avoid wild blood glucose swings: chronic hyperinsulinemia causes weight gain over time, as well as other bad consequences. Avoiding this requires eating in a completely different way than has been generally advised by doctors, the federal government, the media, and the culture in general for the last several decades. You must be aware that “eat lots of whole grains” and “limit fat” and “don’t eat much meat” have been key phrases of almost all mainstream advice on diet for that long, and that this advice causes insulin resistance – and hence weight gain – in the vulnerable.
And now you want to blame that vulnerable population for the consequences of following this near-universal advice. Tell me, how many fat people have you told to eat whole grains, avoid fatty food, practice dieting behaviors? And how many of them have achieved permanent large-scale weight loss (that is, loss significantly greater than 10% of body weight lasting five years or more)?
“I once had a patient who flew a bunch of generals in to see the concentration camps. He said he didn’t see any overweight people there, so he never believed any of that crap about people being necessarily doomed to obesity.”
What an entirely disgusting thing to say, on several levels. And what an unpleasant thing to repeat here. No, you will not see many fat people in a population that has been deliberately starved for years, most of whom are dead of hunger, the remainder of whom will have physical health problems the rest of their lives as a result of this inhuman treatment. But at least the survivors were thin and attractive!
Based on your info, I started a ‘lower’ carb, higher fiber diet. For three weeks, I lost weight during the week and put it back on during the weekend when I enjoyed normal food. The past two weekend, I had some considerable gas pain, perhaps from the extra fiber, so I didn’t eat as much. Sure enough the weight loss during the week wasn’t regained during the weekend.
I’ll try another few weeks but I really, really miss things like Hershey’s nuggets. Fortunately, I’m ‘only’ about 30 or 40 pounds overweight.
I wish you the best – but you’re plan sounds a little bit like “I’ll only take heroin on the weekends – that’ll help!”
I’m on the same track – cutting the carbs has helped me a lot, but sometimes I feel like eating them as if it were my job.
If anyone has an answer for that it will be a big help to me – even just an encouraging word would be good…
Garth (btw, the name “Yukio” wouldn’t ring a bell would it?) I think it matters very much what your metabolism is like. Taking vacation days hasn’t worked at all well for me, but then I’m pretty clearly type II diabetic — the blood sugar spike is just not really tolerable. On the other hand, a lot of people find one vacation day a week is very helpful. My suspicion is is that there are metabolic differences among different populations.
In any case, I think you’re doing the right thing — you’ve noticed it’s not working well for you, and you’re correcting. The only reason I made this a 13 week experiment was that it seemed long enough to see the results, without making it too long.
1. I’m not yukio – never heard of it. Lord Garth is what a crazy guy told Capt Kirk to call him in one episode.
2. I’ve had no gas pains for a few days and I’m going to try to avoid a major vacation from diet this weekend anyway. We’ll see if I can do it.
Okay — I was trolling for an old f4iend who used the name “Garth” in the Society for Creative Anachronism.
Charlie:
I was fat from age 11-34. At 34 I was 280lbs+ at 5’9″ and wearing extremely tight 42″ pants. At 46, I am 170lbs with a 31″ waist.
My advice for anyone wanting to drop serious weight and keep it off:
1. Find a primal/paleo/or LC diet you can follow.
2. Avoid Chronic Cardio.
3. Workouts should be brief and as intense as safely possible (45 min max).
4. Beware of overdoing the exercise. Too hard too fast frequently leads to injury or burnout (P90x syndrome). Rest and recovery are far more important than is commonly understood. The older you are, the more time you must allow for recovery.
5. Walk whenever possible.
Here is where I’m gonna get pushback:
1. Almost everything accepted as conventional wisdom regarding weight loss and fitness is wrong.
2. Exercise is not nearly as effective for weight loss as everyone believes. Exercise is important for the hormonal, mitrochondrial, strength, and fitness changes it generates — not for the calorie burn.
3. If you can do the Tabata Protocol six days a week, you aren’t doing the Tabata Protocol. Olympic athletes can manage, at best, Tabata 2 times a week and then have to take breaks between Tabata cycles to allow recovery. You are doing intervals, not Tabata.
Be proud of your efforts, losing weight is no easy thing. Best wishes and good luck.
Chipper
I agree with you almost completely; the one point I differ on is this:
3. If you can do the Tabata Protocol six days a week, you aren’t doing the Tabata Protocol. Olympic athletes can manage, at best, Tabata 2 times a week and then have to take breaks between Tabata cycles to allow recovery. You are doing intervals, not Tabata.
You forget that I’m a guy who’s fat and massively deconditioned; I’m not an Olympic athlete. But the original Tabata Protocol simply looks for 20 seconds of effort at greater than aerobic heartrates. It just takes super-conditioned athletes a total effort to get there.
Me, I’m getting there easily right now with something like kettlebell swings with a 10 lb kettlebell, but I’m satisfying the conditions that Tabata defined. Maybe really massive effort followed by vomiting would be better, or more efficient, and maybe I couldn’t do it 6x a week. Certainly if I notice a problem with recovery I’ll dial back somehow. But at least for this 13 week experiment, right now, I’m okay with this.
Insulin receptors can form up as hybrids. In Type 2 diabetics’ (I can not say if also for 1st degree relatives of Type 2 or metabolic syndrome)skeletal muscle & adipose tissue there are more blended receptors; with both Insulin-like Growth Factor receptors & Insulin receptors together (hetero-dimmer).
These hybrid receptors end up readily binding Insulin-like Growth Factor 1 (IGF1) & not binding insulin. This physical aberration complicates insulin sensitivity. For it’s part insulin resistance can feedback into how splicing of insulin receptors plays out.
Type 2 diabetics (& others ?) have lower than “normal” IGF1 receptors – so IGF1 molecules like to use insulin receptors. Then the issue becomes how much free IGF1 is around that is still potentially active (unbound to receptor).
The body senses low plasma free IGF1 fostering secretion of growth hormone under orders from pituitary &/or hypothalamus. Growth hormone signal stimulate IGF output, but at the same time the growth hormone also increases release of free fatty acids.
Indirectly this IGF1 snagging on skeletal/adipose hybrid insulin receptors (& out-binding insulin) leads to growth hormone activity. The incident growth hormone secretion causes more gluco-neo-genesis and in the process also causes less glucose uptake to occur – even beyond the ongoing limited insulin reception driven impaired glucose uptake (due to those hybrid receptors).
Morning fasting glucose is indicative of gluco-neo-genesis activity & quite integral to obesity. Gluco-neo-genesis is carbon molecule storage. Our inherent body survival program is to hijack carbon molecules already in the body toward gluco-neo-genesis (& glycogen) as the body tries to recycle “stores” (rather than “burn”) & weight loss stalls for dieter.
Here is the measuring conundrum of high fasting blood sugar in obesity & Type 2 diabetics (as well as advancing age). The low carb dieter sees quick results in post-prandial (after meal) blood glucose levels, progress with HbA1c & yet fasting glucose often seems to be slower to normalize.
It is more than just what kind of carbon energy substrate (ex: glucose, fat, protein) our body is putting toward our redundant pathways for fueling itself (ex: ATP). The same metabolic cycles (ex: TCA/a.k.a. citric acid, glyoxylate, beta oxidation) that let us produce useable energy in a form to run our body cells are sometimes going to shunt the cycle’s transitional molecules into other internal dynamics instead of going all the way to always yield energy to run on. For aging, obesity, Type 2 diabetes & weight loss diet this is a distinction with a difference.
Adipose (fat) cells do provide lots of fatty acids in circulation, yet the obese aren’t using enough for fuel (ATP). However, this does not mean body is not mobilizing some of those fatty acids into a metabolic cycle.
Obese have fatty acids (some) undergo beta-oxidation, which yields the acetyl-CoA molecule that an enzyme (malate synthase) needs to then make the transitional molecule malate. But in the obese this malate molecule is diverted from producing useable ATP energy.
If like technical details: fatty acid degradation derived malate is shunted (in the obese, Type 2 diabetic & increasingly with age) so that another enzyme (cytosolic malate dehydrogenase) acts on that malate to make the molecule oxaloacetate. This carbon molecule oxaloacetate via enyme (PEPCK) transmutes into phosphoenolpyruvate.
Simply put:
fatty acid derived malate can be hijacked to form a transitional carbon molecule (phospho-enol-pyruvate), that is a molecule itself able to put the carbon molecule in 2 directions. One potential direction is into making pyruvate destined for mitochondrial energy processing to make ATP.
The 2nd direction is more often the fate in obesity for a fatty acid/malate engendered carbon molecule. From this phase (phospho-enol-pyruvate) it is reverse engineered “back” toward making other transitional molecules, that end up again stashing that carbon as glycogen (a glucose storage molecule) &/or as gluco-neo-genesis recylced glucose molecules that go out in circulation.
For pyruvate is to be made into acetylCoA in the mitochondria for downstream creating ATP it is the ratio of NAD to NADH that is a rate limiter. The pyruvate transformer enzyme (pyruvate dehydrogenase) has to use NAD to make acetylCoA.
Obese/Type 2 diabetic/aged usually have lots of glucose from eating yet manifest a low energy level. They can’t use enough of the glucose that actually gets into the cell. This is because when make glucose into pyruvate their NAD is insufficient to take the next step necessary (acetylCoA) for mitochondria to make that carbon into ATP.
By the way, see David Swindle’s piece today talking abut fitness plans for me.
http://pjmedia.com/lifestyle/2013/02/04/charlie-martin-late-blooming-athlete-week-1/
Yes, I am absent minded. I mean David Steinberg.
I still think I’m fat because I eat too much and don’t excercise.