An American Justice System for Food ~ Part I Intro and Carbs in General
The cornerstone of the American justice system: Innocent until proven guilty. According to Wikipedia: sometimes referred to by the Latin expression Ei incumbit probatio qui dicit, non qui negat (the burden of proof lies with who declares, not who denies). I like the first part of that Latin expression and suggest that what is truly needed in nutritional circles is to put the burden of proof on those making claims. My point here is not a political one, it is not to argue the merits of my country's justice system or its implementation, or anything of the sort. It is to put forth a suggestion -- that ALL who demonize foods be tasked with proving their charges. I suggest this because it is darned near impossible to do the opposite especially in the face of baseless charges.
It is a bit of a stretch, but keep in mind that many of the compounds, such as water, can be toxic at some level of ingestion. Furthermore, some of the chemical and/or physical properties of many innocuous compounds found in foods can seem quite daunting when taken out of context. This is an obvious spoof, but hopefully it makes a point.
Now, the vegans and vegetarians and raw and fruitarian crowds are all just as guilty of this, but since I've never been even remotely a part of any of those communities, I'll leave it to someone else to call out their hyperbole, scaremongering and outright disinformation. I'm also not talking about new non-foods such as artificial sweeteners, chemically modified foods (e.g. hydrogenated fats), non-food chemicals such as preservatives and I'll even throw in GM in with substances that should be considered unsafe until proven otherwise.
This is the Carb-Sane Asylum so I will focus on some carbohydrate the knocks against carbohydrates in general and some carb-rich foods that are falsely accused. In many cases these foods are convicted despite even the circumstantial evidence (e.g. observational studies and just observations) being exculpatory. First, some definitions:
These are terms bantied about far too flippantly in this community. Things like arsenic, hemlock, mercury and cyanide are toxins and have toxic effects. In other words, they will kill you, and if they don't they will cause severe harm. There was a common meme circulating around the LC web when I found it -- that carbs were like rat poison. Seriously? All molecules not characterized as a protein or fat are the equivalent of rat poison? Yeah, yeah ... I get it. It's a bit of poetic license and all of that. But it is irresponsible fear-mongering nonetheless.
So for this Part I, let's address the topic of the supposed toxicity of carbohydrates in general. One of the biggest fear mongers around in this arena is Dr. Ron Rosedale who has repeatedly asserted that glucose IS toxic at any level. The general idea, embraced by what I would call the "teaspoon crowd", is that we have around one teaspoon of glucose in circulation at any given time which amounts to about 5 g glucose. Thus eating carbs effectively injects a ton of glucose into our blood and because this is toxic, the body must remove it as quickly as possible. This metabolic response to glucose ingestion -- to remove it from circulation and maintain relatively constant circulating levels -- is touted as evidence of glucose's toxic nature. The mechanism by which glucose exacts its toxic effects is purportedly glycation -- the process whereby glucose reacts with proteins (e.g. cellular components, enzymes, etc.) and alters their function. I'll discuss glycation at some future point, but for now let's look at the logic of the "if the body needs to clear it, it must be toxic" rationale. It seems misguided at best.
Thanks to a generous donation, I have been gifted the 2010 Kindle version of Keith Frayn's Metabolic Regulation. I have had the first (1996) edition in paperback since mid 2010, but it has periodically gone missing. An interesting find in my new ebook is a chart that is on p. 114 of the original which is Box 7.1 at Kindle Location 4454 in the 3rd Ed. This confirms the calculations I made in Let's Play Concentration! My calculations are at right. Frayn's analysis uses 500 mmol NEFA and 90 mg/dL glucose fasting. Assuming 5L blood and using his molecular masses, Frayn's analysis is based on 4.5 g glucose and 0.7 g NEFA -- not a whole lot of difference. Also included in Frayn's analysis is lipid as triglycerides, TAG at 1 mmol/L. He estimates the energy in circulation as follows (in kJ/L): glucose = 14, NEFA = 5 , TAG = 34. From the "Box":
Even this is still not a fair comparison, however, because the bulk of triacylglycerol turns over relatively slowly in plasma, whereas plasma non-esterified fatty acids turn over very rapidly. Because triacylglycerol is so heterogeneous in plasma, we shall just compare glucose and non-esterified fatty acids in terms of “energy turnover,” or transport of energy to tissues, in the postabsorptive state. (Kindle Locations 4460-4463)
In doing so, "energy delivery" (Joules or calories) in the postabsorptive (aka fasted state) is roughly 1/3 glucose and 2/3rds NEFA (Westerners are fat burners!) For a 65 kg person, Frayn estimates the turnover rates of glucose = 130 and NEFA = 112 mg/min. This would mean that 0.13/4.5 = 0.029 or roughly 3% of glucose is turning over per minute, while 0.112/0.7 = 0.16 or 16% of NEFA is turning over per minute! Looking at that another way, NEFA is turning over more than 5 times as fast as the glucose.
If toxicity were not an issue with NEFA, why not have higher circulating levels rather than having to regulate such a rapid turnover? The reason is simple -- oil and water don't mix, which is why the bulk of lipid in circulation at any time is triglyceride packaged up in protein "capsules" otherwise known as lipoproteins. But in order to deliver this triglyceride load to the cells the TAG must be hydrolyzed to NEFA. Probably the most crucial time that this occurs is during uptake of dietary fats from chylomicrons, primarily by adipose tissue. The chylo, that are responsible for making your blood cloudy, are cleared relatively rapidly in the healthy person, and the fatty acids liberated are efficiently taken up by the fat cells. This is very carefully regulated and in the postprandial state with a mixed meal, NEFA are supposed to be suppressed. So to summarize NEFA:
- The body works very hard to keep circulating NEFA levels to within a very narrow range amounting to less than 3/4 of a gram.
- Cellular need for NEFA for energy is high in the fasted state so turnover is very rapid.
- NEFA in circulation is much less than dietary influx so that fatty acids must be transported in lipoprotein "vehicles" and efficiently cleared from circulation once liberated from those lipoproteins.
Therefore, the "supporting evidence" for glucose toxicity that is based on the fact that our bodies work to rapidly remove it from circulation would make an even stronger case for NEFA toxicity. The earliest signs of metabolic dysregulation are (1) reduced triglyceride clearance and/or (2) failure to suppress NEFA release in the obese, and hyperglycemia is an end run manifestation of dysregulation. If we are going to look at dietary agents contributing to any possible toxic effects, fat must be viewed at least as skeptically as dietary carb.
Further, on the flip-side, our bodies do go to extraordinary efforts to maintain a minimum glucose level by synthesizing glucose -- gluconeogenesis. The only thing we synthesize in the fasted state vis a vis fat metabolism is glycerol-3-P -- glyceroneogenesis -- the purpose of which is to "fix" the fat in the fat cells and limit NEFA release.
When aboriginal cultures become "contaminated" by so-called Western foods, it is with higher and different fat content in the diet moreso than carbs. Yes, generally carbohydrate quality tends to shift from whole food types to refined flours and such, but often we are talking tripling the fat content of the diet. Such is certainly the case in Gary Taubes' favorite poster population for obesity - the Pima of Arizona.
What of ultimate toxicity? Well, according to the Guiness Book of World Records:
Highest blood sugar level Twelve-year-old Michael Dougherty (USA) had a blood sugar level 19 times above average at 2,350 while still conscious on November 21, 1995.
|source: Guyton & Hall |
Textbook of Medical Physiology 11th Ed.
I've personally known T1's who have had BG's over 500 that "feel" normal and had no adverse immediately life threatening reaction. What kills diabetics? Ketoacidosis. Yeah, yeah, not to be confused with ketosis, nutritional or otherwise. But again let's look at what happens when you depancreatize a dog. The control on fatty acids disappears almost immediately and the levels rise. The high NEFA levels cause ketone production to increase. Note that while hyperglycemia develops, it is leveling off, while ketone levels (acetoacetic acid) are increasing exponentially. Per the text: "in severe diabetes the acetoacetic acid and the b-hydroxybutyric acid can cause severe acidosis and coma, which often leads to death."
Luckily most of us have sufficient basal insulin production so that ketoacidosis is not an issue. But, acetone is one of the ketones produced, and yes, acetone is toxic for human beings to ingest.
- All foods -- both types and constituents -- should be considered innocent until proven guilty to cause harm. This is not carte blanche to eat a boatload of every type of food you can get a hand on, but it is important to not attach the label "toxic" where it is inappropriate.
- Applying the criteria above, carbohydrates cannot be considered toxic, with the possible exception of untreated T1's. (To be discussed in more detail at some future time)
- The characterization of glucose as toxic based on the premise of how hard our bodies work to remove it from circulation would make fats more toxic by the same logic.
The Charge: Carbohydrates are Toxic
Verdict: Not Guilty ( I will address the toxicity of hyperglycemia in diabetes at some future point)
I think that next up I'll take on this notion that sugar is inherently toxic. We'll see ...