Russ's Grab-Bag Of Assorted PT Forum Goodness

[Kintanon]

3.50 a dozen? Holy crap... I get all the eggs I can hork down for essentially free. I guess it technically costs like 15$/month for the feed.... But we get like 150 eggs a month, easy. And there are only like a dozen chickens. Ahhh, the joys of living in the country. We also have rabbits, which are delicious as well. And tiny pigs, and goats. All of which are way tastier than store bought meat and way healthier.

[Jack Rusher]

3.50 a dozen? Holy crap... I get all the eggs I can hork down for essentially free.

Don't get me started. Real food is hard work in the big city — using farmer's markets for fruit & vegetables and keeping an ongoing relationship with some Pennsylvania Mennonites to source properly pastured meats, milk & butter.

[Kintanon]

That's one thing we don't have going, we don't make butter or cheese.... I wish we did...

[TheRuss]

Make sure to categorize the carbs by glycemic index and fructose content.

*looks up some old posts*
Explain Glucose/Sugar Levels, Insulin, and effects on Muscle Gain... - Page 3 - No BS Martial Arts

Carbonated drinks - Page 4 - No BS Martial Arts


In other words, glycemic/insulin indices are a real mess. I've pondered buying myself a glucometer, but I hate getting stuck with needles. Instead, I'm scheduled to get a second round of bloodwork done a month or two in, so I'll be able to compare my fasting blood glucose level to what it was before I started on the diet.

I haven't gotten to any of the carb-load phases yet... I might keep an eye on my carbohydrate sources, or I might not. Depends on whether I'm planning on being useful over the weekend.

Fructose isn't really an issue in places that aren't wrapped up in corn subsidies*.

I also eat farm eggs, but they cost me US$3.5/dozen (~seven times the lowest price I could get on factory ones).

You can get a dozen eggs for $0.50? How?



* EDIT: Okay, that was a bit snippy. The literature on fructose is... I won't say contradictory, but it's confusing, particularly given that fructose bypasses most of the insulin-glucose machinery in the liver. Once they've figured out how to resolve that, I'll start paying attention.

[TheRuss]

So I'm sure at least a few of you have seen stuff like this:

... When a food is ingested, digested, and absorbed, each component of that food will present itself to the kidneys as either an acid-forming compound or a base-forming one. And when the sum total of all the acid producing and the base producing micro and macronutrients is tabulated (at the end of a meal or at the end of a day), we're left with a calculated acid-base load. If the diet provides more acidic components, it will obviously manifest as a net-acid load on the body. And if it provides more basic components, it will obviously manifest as a net-base load on the body....

-John Berardi, "Covering Nutritional Bases"

Or like this...

... The average American diet, which is high in protein and low in fruits and vegetables, generates a large amount of acid, mainly as sulfates and phosphates. The kidneys respond to this dietary acid challenge with net acid excretion, as well as ammonium and titratable acid excretion. Concurrently, the skeleton supplies buffer by active resorption of bone. Indeed, calciuria is directly related to net acid excretion. Different food proteins differ greatly in their potential acid load, and therefore in their acidogenic effect. A diet high in acid-ash proteins causes excessive calcium loss because of its acidogenic content. The addition of exogenous buffers, as chemical salts or as fruits and vegetables, to a high protein diet results in a less acid urine, a reduction in net acid excretion, reduced ammonium and titratable acid excretion, and decreased calciuria. Bone resorption may be halted, and bone accretion may actually occur. Alkali buffers, whether chemical salts or dietary fruits and vegetables high in potassium, reverse acid-induced obligatory urinary calcium loss. We conclude that excessive dietary protein from foods with high potential renal acid load adversely affects bone, unless buffered by the consumption of alkali-rich foods or supplements....

-Barzel and Massey, "Excess Dietary Protein Can Adversely Affect Bone"

Makes sense, right?

Except I was reading my biochemistry textbook today, and I stumbled across this:

In animals with lungs, the bicarbonate buffer system is an effective physiological buffer near pH 7.4, because the H2CO3 of blood plasma is in equilibrium with a large reserve capacity of CO2(g) in the air space of the lungs....

-Lehninger Principles Of Biochemistry, Fourth Edition (chapter 2.4, p. 69)

Sounds like the former authors were missing a crucial piece of the puzzle.

[Jack Rusher]

In other words, glycemic/insulin indices are a real mess. I've pondered buying myself a glucometer, but I hate getting stuck with needles.

Maybe I wasn't clear, so I'll try again in more detail.

If you plan to fix your diet, you probably want to measure your glucose metabolism to track your progress in reversing the slide toward metabolic syndrome X. I didn't think I had to spell out that glycemic response is person-local, and that the only way you can really know your reaction to various foods is to take multiple timed measurements of your blood glucose after eating those foods in isolation. It'll be unfortunate if you let squeamishness about jabbing yourself act as a barrier to that data collection.

Fructose isn't really an issue in places that aren't wrapped up in corn subsidies*.

HFCS comes in several grades, depending on the ratio of fructose to glucose in the syrup. The most common grade used in American soft drinks is HFCS-60 (60% fructose). The sucrose in table sugar is a disaccharide of α-glucose and fructose that's metabolized via acidic hydrolysis into its component sugars -- a 1:1 ratio, thus 50% fructose.

particularly given that fructose bypasses most of the insulin-glucose machinery in the liver.

The metabolic oddities of fructose were my reason for bringing it up in the first place. MOAR:

http://www.sciencedaily.com/releases...1016074701.htm
(for those who can't get the fulltext of the articles below)

http://www.ncbi.nlm.nih.gov/pubmed/18703413

... specific to sucrose:

http://www.ncbi.nlm.nih.gov/pubmed/8969287
http://www.ebmonline.org/cgi/content/full/229/6/486

I suspect many high-GI bugbears -- especially starchy tubers -- are harmless to anyone with a healthy glucose metabolism, but dangerous to those whose endocrine system (leptin, insulin, &c) has been trashed by a diet containing historically unprecedented levels of fructose, high-linoleic vegetable oils, &c.

You can get a dozen eggs for $0.50? How?

There's a covered market in my neighborhood containing vendors who aim at different points along the price/quality continuum. The one that caters primarily to welfare recipients has the lowest prices, including eggs at $0.99/two dozen. These eggs are a bottom quality factory product at the edge of expiration.

[TheRuss]

If you plan to fix your diet, you probably want to measure your glucose metabolism to track your progress in reversing the slide toward metabolic syndrome X.

I suppose this is my fault for not being clearer about my approach, so let me clarify.

THE GOAL

Right now, my training goal is to reach a low level of subcutaneous fat while preserving as much muscle mass as possible.
-The precondition to any action I take is that it should not negatively impact my recovery from head trauma. As such, any sort of training is currently ruled out (symptoms flare up on exertion).
-There are other preconditions to do with finances and legality that rule out surgical and drastic chemical interventions (see MK-677, an Orally Active Growth Hormone Secretagogue, Reverses Diet-Induced Catabolism for something I wish was on the market)
-I'm aware that "low level" is not quantitative. Once I've got a better handle on taking skin fold measurements with calipers, I'll probably be able to quantify it better.
-Beyond the aforementioned head injury, my only health-related goals are to avoid incurring permanent or incapacitating health problems. That is, I'll accept a trade of increased risk of disease down the road for improved results if necessary.

THE APPROACH

I am currently on day 6 of what I believe to be a faithful interpretation of Mauro Di Pasquale's Anabolic Diet (thread here, one of the eBooks is posted here).

Important to note is that during the "strict" phase and on weekdays, carbohydrate intake (presumably excluding fiber) should not exceed 30g/day. As such, I have eaten a total of roughly 112g of non-fiber carbohydrates over the past six days (for a more specific breakdown, see this spreadsheet).

As such, my position on more fine-grained tracking of carbohydrate intake is as follows:
-There will be no measurable difference as pertains to insulin resistance between any two non-fiber carbohydrates at a level of <30g/day.
-The premise of the diet (which I am currently testing) is that once I have completed the strict phase, I should be able to induce spikes in my insulin levels without attendant insulin resistance by carb-loading for short periods of time (weekends).

Actually, as pertains to the second point, the diet makes claims regarding:
-testosterone
-growth hormone, and
-insulin levels
-in addition to insulin sensitivity.

I didn't think I had to spell out that glycemic response is person-local, and that the only way you can really know your reaction to various foods is to take multiple timed measurements of your blood glucose after eating those foods in isolation. It'll be unfortunate if you let squeamishness about jabbing yourself act as a barrier to that data collection.

Look, I hear what you're saying, and I do dearly love me some data collection. That said, I don't have any institutional support from the university or other formal researchers, and I don't have a pressing medical need that relates to my diet. As such, I'm not at all sure that I even have the option of getting my testosterone + growth hormone + insulin + insulin sensitivity tests done on a regular basis (pre- and post-carb load = 2x/week), given the hoops I had to jump through to get testosterone tested once.

As far as blood glucose levels go, if I had well-defined blood glucose targets to go with the various phases of the diet, I'd force myself through the unmitigated torture that is needle sticks. As of yet, though, the diet's claims re: blood sugar (as opposed to insulin) don't seem to extend beyond "stable", and I'm not sure what I'd even compare the blood glucose (as opposed to insulin) numbers from the weekend carb-load to. Again, if there was a blood sugar target that would tell me when to discontinue the carb load, I'd be more inclined to test blood sugar.

One aspect that might make a glucometer worthwhile will be when I do resume training - tracking blood sugar as the week goes on and training depletes liver glycogen. Even for that, though, I'd need two things for it to be worth doing:
-thresholds to compare blood glucose to (in terms of assessing stored glycogen, or otherwise)
-actions to take based on readings

I have the latter (midweek carb-loads, post-workout carbs, etc.) but not the former.

Fundamentally, either the diet as written will result in an acceptable ratio of fat (particularly subcutaneous fat) to muscle loss when I shift into calorie deficit... or it won't. It'd be cool to be able to monitor its intermediate steps rather than just input (diet) and outcome (body composition), but actually doing so is currently a combination of infeasible, unaffordable, unpleasant, and ineffectual.

HFCS comes in several grades, depending on the ratio of fructose to glucose in the syrup. The most common grade used in American soft drinks is HFCS-60 (60% fructose). The sucrose in table sugar is a disaccharide of α-glucose and fructose that's metabolized via acidic hydrolysis into its component sugars -- a 1:1 ratio, thus 50% fructose.

Point taken.

The metabolic oddities of fructose were my reason for bringing it up in the first place. MOAR:

http://www.sciencedaily.com/releases...1016074701.htm
(for those who can't get the fulltext of the articles below)

http://www.ncbi.nlm.nih.gov/pubmed/18703413

... specific to sucrose:

http://www.ncbi.nlm.nih.gov/pubmed/8969287
http://www.ebmonline.org/cgi/content/full/229/6/486

I suspect many high-GI bugbears -- especially starchy tubers -- are harmless to anyone with a healthy glucose metabolism, but dangerous to those whose endocrine system (leptin, insulin, &c) has been trashed by a diet containing historically unprecedented levels of fructose, high-linoleic vegetable oils, &c.

These studies are not doing me any favours.

Everything I've read so far indicates that leptin influences body composition by way of hunger. As I am not a rat, the composition, quantity and timing of my dietary intake is determined by my goals, not by my hunger or tastes. As such, the (sincere, not rhetorical) question is this:

1) Does leptin influence body composition via a hunger-independent mechanism - that is, when all aspects of diet (quantity, composition, timing) are held equal?

Similarly, in terms of the differential effect of x grams of fructose vs. glucose vs. galactose: different relative sweetness probably evokes different taste-insulin responses, and it's been established that fructose does not directly stimulate insulin release, and must be metabolized by the liver before use by the rest of the body. This has intuitive consequences re: insulin sensitivity, but these studies are making claims that run counter to intuition.

2) Do equal (in terms of mass and/or energy) doses of the aforementioned carbohydrates have different effects on insulin sensitivity when all other aspects of diet are held equal and taste-insulin responses are taken into account?

(Replace "insulin sensitivity" with "glycogen restoration" or any other relevant metric as desired)

Anyways, I have to stress that these questions are not rhetorical, but studies that don't control strictly for diet aren't relevant to my current methods.

[TheRuss]

Random:

The Canadian Nutrient File is available for download - I suppose this means that if some enterprising soul wanted to exploit it for automatic summation of all the nutrient information it contains, they could do so fairly easily.

A co-worker recommended me to a craniosacral therapist today. Quackwatch does not like that idea at all. I'll probably give said therapist a call and apply the smell test. (No, the other smell test... okay, maybe both if I play my cards right)

Still waiting to get in with the ophthalmologist, and I'm not sure if my doctor's gotten me in line for a visit with an orthopedic surgeon and/or MRI yet. On the upside, I heard from a friend that the wait for an actual knee 'scope is on the order of weeks, which is quite reasonable if true.

Pretty stoked for biochemistry class, although the textbook's a lot denser and slow-going than I'd initially thought. Maybe I can get a syllabus off the prof in advance so I know which sections to focus on. Also, anyone want to be my study buddy?

[TheRuss]

More randomness:

-Day 7 of Anabolic Diet strict phase. Been aiming for 4000+ kcal over this period, so it's not really much of a surprise that my body composition hasn't been changing much (aside from glycogen depletion).

-Speaking of body composition, I'm not confident in my metrics. The BIA scales are... well, hopefully they'll be useful on a time-averaged basis. Diameters of left upper arm, left quad and beltline are decent, but the measurements aren't especially accurate, and there are legitimate issues with consistency. The calipers probably have the best potential in terms of tracking subcutaneous fat loss, but I've got a sneaking suspicion that I'm "doing it wrong" my grip position and/or measurement position are off. The AccuMeasure guys say that I should be measuring just above the hip pointer, but I'm thinking of moving closer to the belly button (larger measurement = less relative measurement error, and it's a bit more directly related to my goals).

-Flash photography for body comp shots - yea or nay? The ones I've taken so far seem a bit noisy (camera quality), and on top of that, I think the lighting may be a bit less consistent than I'd thought it'd be.

-I just discovered a powerlifting gym here in town, complete with big dumbbells, reverse hyper, and safety squat bar. If I can ever lift again, I think I know where I'll be doing it.

-My understanding of polysaccharide digestion (see this) is that they can't make it through the intestine until they're broken down into monosaccharides. Anyone know if that's correct?

-And on the subject of leptin, there may be evidence to suggest a non-hunger-mediated pathway for action, but it's not unequivocal (see this).

Edit #2: There's also this...

Analyzing data from many such experiments with the mice, the scientists were able to group the expressed genes into clusters that appeared to behave similarly— increasing or decreasing in expression in tandem— as the mice were subjected to different regimes of leptin treatment or food restriction.

"We were able to find at least half a dozen distinct clusters of genes that were specifically regulated by leptin and that were not regulated in the same way by food restriction," said Friedman. "So, leptin is doing a lot more than just leading to food intake restriction."

The discovery of these leptin-regulated genes offers a glimpse of the complex metabolic machinery controlled by leptin.

"We would infer that for each of the clusters of genes that behave similarly in response to leptin and that there is some unifying regulatory element," said Friedman.

In fact, he said, his group has uncovered evidence of just such a regulatory element— finding that one cluster of genes is regulated by a protein called SREBP-1, which regulates many of the genes that control the synthesis of fatty acids.

[Jack Rusher]

Been aiming for 4000+ kcal over this period, so it's not really much of a surprise that my body composition hasn't been changing much (aside from glycogen depletion).

Meh. Calorie restriction leads to weight loss (via lipolysis + catabolisis), but it's neither necessary nor optimal for your purposes (pure lipolysis). Anecdotally, I've seen big fellas drop fat on 5000 kcal/day, so long as the intake was exclusively fats and proteins.

My understanding of polysaccharide digestion is that they can't make it through the intestine until they're broken down into monosaccharides. Anyone know if that's correct?

Simple question, complicated answer. There are, for example, classes of glucose-terminated fructose chains (fructooligosaccharides) that aren't reduced by starch-targeting enzymes like ptyalin and amylase. These make it all the way to the colon, where they're metabolized by gut flora (to sometimes flatulent effect).

And on the subject of leptin, there may be evidence to suggest a non-hunger-mediated pathway for action, but it's not unequivocal

Leptin is poorly understood (discovered in '94), but as per your link:

The mechanisms by which leptin exerts its effects on metabolism are largely unknown and are likely quite complex. In contrast to dieting, which results in loss of both fat and lean mass, treatment with leptin promotes lipolysis in adipose tissue, but has no apparent effect on lean tissue.

... whatever's going on there, it has much to do with your goals. There's also preliminary evidence for a coorelation between leptin resistence and insulin resistence, the former preceding the latter:

http://www.ncbi.nlm.nih.gov/pubmed/18703413
http://www.ncbi.nlm.nih.gov/pubmed/16129731

... these messengers, and the genes they manipulate, are part of the complex system that maintains homeostasis in vertebrates. Sadly, we've managed to engineer foodstuffs that defeat this mechanism in hominids.