|Tip: Restore your muscle and liver glycogen after workouts and before long fasts to ensure a smooth transition from glucose to fat utilization.|
Their reasoning, however, is sound: An increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect.
Chronically low levels of glucose, as well as the glucose excursions we see in the few (still) healthy people after shoveling down packages of twinkies and dingdongs, would thus precipitate overeating and eventually obesity and diabetes.
Compared to the way the hypothesis was originally formulated by Jean Mayer in the 1950s, the theory Chaput & Tremblay present in a 2009 review of the literature is significantly more complex (Mayer. 1953 & 1955. Chaput. 2009) and more of a glucose homeastasis hypothesis of obesity.
In contrast to the mainstream version of the "bad blood sugar spikes", Mayer and later Chaput and Tremblay focus on the role of the blood sugar troughs, we rarely think about. It all goes back to the classic glucostatic theory of food intake which postulates that
"that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating." (Chaput. 2009)In a state of decreased glucose utilization aka "metabolic hypoglycemia" (Mayer. 1955), there is a point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering ‘metabolizing cells’ - this, according to Mayer, is the the signal for meal
Does this mean that fasting is counter-indicated? For most of you probably not. If your liver gylcogen levels are well-stocked at the onset of the fast and assuming that you have a decent degree of metabolic flexibility, the transition into the fast will not put you at risk of metabolic (temporary glucose shortage at the cellular level) and / or full-blown hypoglycemia (really low blood glucose levels). So, fasting is ok, if you don't turn it into "starving" by extending the fast indefinitely and/or not restocking your glycogen levels in the feeding windows.Interestingly, Mayer argued in his previously cited 1955 paper, already that the glucostatic theory would explain the short-term control of hunger and food intake, whereas a lipostatic mechanism would control the long-term regulation of body weight and energy balance.
There is nothing static about the glucostatic theory
Today, the role of glucose in the control of food intake is thought to be dynamic: it is a satiety factor and an initiation signal that has been associated with body fat by Chaput and Tremblay in two studies, which examined the effects of low glucose concentrations on long-term energy balance and weight gain in (Boulé. 2008)
|Figure 1: Surprisingly linear increase in weight and body fat regain in prospective study and experimantal trial with lower blood glucose levels after OGGT (Boulé. 2008)|
- 259 participants between 20 and 67 years of age involved in the Quebec Family Study - A study which revealed a closeassociation between glucose concentrations at the end of anoral glucose challenge and changes in body mass over the course of a 6-year follow up (Boulé . 2008).
- 44 obese participants on a 15-week weight-loss programme in either a drug therapy group or a placebo group coupled with energy intake restriction - A study which showed a higher propensity for weight regain over a follow up period of 83 weeks in those who had glucose levels below fasting values at the end of the oral glucose tolerance test during the weight loss intervention (Boulé. 2008)
The GI does matter - but only before and after you try to lose weight
Of these findings (2) is particularly interesting as it would support the notion that low glycemia can do both: It supports weight loss, when the energy intake is restricted and it increases the risk and extend of weight (re-)gain, when there is no energy restriction.
|Figure 2: When the dietary energy intake is tightly controlled, there is hardly a difference in weight loss and body fat loss with high GI, low GI and high fat dieting in obese men & women (Raatz. 2005)|
It is thus no wonder that Chaput & Tremblay write in their latest review that their results are relevant only in phases without deliberate (significant) energy restriction. In these phases, the present research clearly suggests that weight-reduced obese individuals are at particular risk of weigh (re-)gain; an observation of which the scientists say that it is brought about by a destabilization of the "body homeostasis" that occurs, whenever the weight loss exceeds 10% of the initial body weight. And indeed: Tremblay et al. have observed in 1999, already that the mean glycemia of participants who had reached the point where their weight loss stagnated had reached an all-time low of 3.3 mmol/ l, of which studies by LeBlanc show that that it is significant enough to evoke a significant counter-regulatory hormonal response (LeBlanc. 1982; Tremblay. 1999).
Hypoglycemia and depression? The reduced glycemia could also be the underlying cause of diet induced increases in symptoms of depression as they were observed by Chaput et al. in a previous trial (2005), in the course of which their male volunteers became increasingly depressed, when they had surpassed the 10% weight loss margin (Chaput. 2007a). A direct association between low glycemia and depression in weight loss was confirmed in a follow up that used a low calorie diet (700kcal/day) + aerobic exercise. (Chaput. 2007b). Intriguingly, depression peaked, when the subjects finally hit a weight loss plateau in both studies.These "significant counter-regulatory hormonal responses", which manifest in form of blunted growth hormone and epinephrine responses and appear to be controllable by regular exercise, are of particularly interest for those of you whose weight loss efforts have plateaued. A better glucose control with a focus on avoiding low glucose levels and regular physical activity could thus help you solve this problem... switching to a ketogenic diet which guarantees 100% glucose stability since the glucose is no longer used as a substrate, would be a another option.
Exercise to the rescue!
Another and eventually probably the most promising way of increasing glucose stability, facilitating further weight loss and forestalling future weight (re-)gain would be regular workouts.
"Physical exercise can be described as a stimulus contributing to optimal body functioning. This is discretely expressed at many levels of regulatory processes, be it by stimulating the effect of key enzymes, by increasing the sensitivity to hormones, by facilitating substrate transport through the membranes, by influencing cell receptors in a tissue-specific manner and probably many others. The participation in regular physical activity has also been shown to prevent both hyperglycemia and hypoglycemia, which is concordant with the idea that exercise enhances the accuracy of substrate balance regulation." (Chaput. 2008)It's thus not best to sit around all day to avoid your blood glucose levels from plummeting. On the contrary, individuals who are physically engaged in their daily schedule may expect a better control of both high and low glucose levels and better overall glucose homeostasis. And in fact, previous research also suggests that physically fit individuals are less likely to experience feelings of hunger associated with declines in blood glucose (Chaput. 2008).
Chaput and Tremblay do yet add another factor to the discussion: Mental exercise! The glucose demands of our brain during cognitive activity are a commonly overlooked factor, when it comes to both glucose and energy control and that in spite of the fact that we all know that (with the exception of full ketosis) carbohydrate represents a critical energy substrate for the brain. Against that background,...
"the low capacity of the body to store carbohydrate might be perceived as a paradox of nature, particularly when cognitive activities are dominant in the daily activity schedule. This limitation is exacerbated by the inability of the body to synthesize glucose from free fatty acids." (Chaput. 2009)It is thus not surprising that Cognitively and thus energetically demanding tasks will influence the ad-libitum meal intake, even if the measured energy expenditure during sitting at the desk doing nothing and performing a reading–writing task for 45 min is practically the same (13kj difference in Chaput. 2007c).
The brain may be your hungriest muscle
|Figure 3: In contrast to both high (HIE) and low intensity exercise (LIE) 45 minutes of knowledge-based work will increase energy intake at a subsequent buffet (McCann. 1990)|
In conjunction with the increase in the variability of glycemia, Chaput et al. observed in a 2008 follow up (Chaput. 2008), this may well explain the increased food intake the researchers observed in response to "cognitive work" in the broadest sense in all three studies.
Unquestionably, Chaput & Tremblay are right, when they warn that these observations raise the question as to whether other sedentary leisure activities (for example, video game playing, television viewing, chatting on internet) are also hyperphagic stimuli. In other words, whether they will make you overeat similar toknowledge-based work; and whether associations with glucose instability, as they were observed by Chaput et al. in 2008 exist for "texting", as well. And even if that wasn't the case, the mere fact that knowledgebased work represents the main working modality in the current way of living, alone, would warrant further research in this direction.
Apropos "modern lifestyle", sleep or rather a lack thereof figures, as well
If you take a look at the data in Figure 4, you will realize that another feature of the modern way of living, i.e. a lack of sleep quantity and quality is associated with glucose excursions into hypoglycemia as well.
|Figure 4: Mean glucose area below fasting glucose concentrations (GABF | higher values increase more severe / longer episodes of hypoglycemia) in men and women according to their habitual sleep duration (Chaput. 2007d)|
In that, it is interesting to see that the differences in mean glucose area below fasting glucose concentrations reflect the contemporary evidence of associations between sleep duration, obesity and type II diabetes - both sleeping too short (Xi. 2013) and too long is associated with increased risk of metabolic syndrome and/or type II diabetes (Ohkuma. 2014).
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