|One of the mistakes researchers and dieters make time and again, using the scale as their only guide|
- Going "Hypo" time and again will make you fat (McNay. 2012) -- Usually you think of hyogylcemia as a sign of a lack of energy, yet despite the fact that this may well be the case this very lack in energy has recently been shown to exert obesogenic effects in a rodent model.
The weekly injections Ewan C McNay and his colleagues administered to their rodents and the subsequent episodes of hypoglycemia lead to profound weight gain in the absence of diabetes, hyperphagia, changes in hypothalamic NPY or POMC mRNA expression and the other usual suspects that could explain this phenomenon. The one thing that's left is therefore what the researchers call a "multi-faceted deficit in metabolic regulation" (McNay. 2012) - interestingly enough the 69.5% higher body weight at 12 months went hand in hand with the usual laziness (-25% activity) of people whose brains are starving in abundance (e.g. type II diabetics).
Often a picture says more than 1000 words: Normal (left) and repeatedly hypoglycemic rodents after 8 months of weekly insulin injections (McNay. 2012)
What remains to be seen, though, is whether similar effects would occur in response to "regular" non-insulin induced hypoglycemia. In view of the easy with which crash dieters and people with roller-coaster blood glucose levels gain weight, it is yet not unlikely that it is actually the avoidance of (reactive) hypoglycemia and not so so much the prevention of hyperglycemia that makes low GI diets successful for weight maintenance (for weight loss the picture is more complicated, since this will require a energy deficit and that's a game changer).
- Dietary glycemic index and load are not associated with type II diabetes risk in 12,403 Europeans (Sluijs. 2012) -- Apropos GI, scientists from the University Medical Center in Utrecht did not find statistical significant correlations dietary glycemic index and/or glycemic load and the risk to develop type II diabetes in in a subcohort of the European Prospective Investigation into Cancer and Nutrition Study (n = 12,403 participants).
Even when they compared participants in the highest and lowest quantiles, the increase in risk was only 5% and 7% for GI and GL respectively. Since this is by no means the first study that suggests that the still propagated concept of the beneficial health effects "low GI diets" is faulty, I would suggest you rather watch the actual food items, than their respective glycemic indexes if you intend to ward off obesity and diabetes. Potatoes for example may have a high GI (including sweet potatoes, by the way), but their high potassium and overall mineral content, as well as the mere fact that you can hardly eat the same amount of total carbohydrates you can easily annihilate, when you are eating pasta still makes them one of the best sources of starchy carbs you have (learn more in the Potato Manifesto, Part I & II).
There is use for the GI on a bulk or after a diet, but only if you are concerned about insulin sensitivity (Lagerpusch. 2012) -- While the general value of the GI as a means to distinguish good from bad carbohydrate sources is certainly questionable, the recently published results from a study that was conducted at the Institute of Human Nutrition and Food Science, of the -Albrechts University in Kiel, Germany, does suggest that monitoring the GI of your diet and adding additional fiber to reduce the insulin response to your meals can come quite handy, in phases, where you are particularly prone to store body fat. On a bulk, for example, or even more so when you have been dieting and are trying to return to a normal caloric intake.
Figure 1: There were no statistically significant difference in terms of weight gain or loss, but the 2-week re-feed had a greater impact on blood glucose and insulin levels in the high GI group (Lagerpusch. 2012)
According to the results Lagerpusch et al. present in the November issue of the British Journal of Nutrition even healthy young men who were subjected to a 3-week diet phase (-50% in caloric intake) and subsequent overfeeding (+50% in caloric intake) the subjects in the high GI study arm had a 135% higher increase in fasting insulin levels during the refeed than those in the low GI group. In view of the fact that the glucose clearance (measured in an oral glucose tolerance test) was identical, it is not only no wonder that the weight gain did not differ either (see figure 1), but also unlikely that we would see significant differences as far as the fat gains are concerned (the latter were unfortunately not measured in the study at hand). At the same time, longer hyper-caloric high GI diets are certainly a risk factor for both insulin resistance and obesity, so that you are probably still at lower risk with 65g instead of 27g of fibre per day and a mean GI of 40 vs. 74.
If you are interested in the influence of different diets on weight gain and health during overfeeding, I suggest you check out the following two SuppVersity posts: "194 Bananas in Three Weeks" and "A Tale of Macro- and Micronutrient Modifications".
Further evidence that chronic mild stress is to blame for the obesity pandemic (Takahashi. 2012) -- As researchers from the Tohoku University Graduate School of Medicine in Japan report in the latest issue of the American Journal of Physiology - Endocrinology & Metabolism, the localized re-setting of the clock genes in the liver, yet not the hypothalamic suprachiasmatic nuculeus (SCN), of BALB/c mice in response to chronic mild stress exposure elevated and phase-shifted serum corticosterone levels (see figure 2).
Figure 2: Chronic mild stress leads to an overactivation of the HTPA and subsequen metabolic dysregulations (Takahashi. 2012)
Takahashi et al. argue that the observed changes are indicative of an overactivation of the HPA axis, which induced disturbances in the rhythmic expressions of core clock genes, e.g. Clock, Npas2, Bmal1, Per1 and Cry1 in the liver and subsequently circadian patterns of glucose and lipid metabolism-related genes such as the proliferator activated receptor (PPAR) family which favor the storage and hamper the oxidation of fatty acids.
If you want to learn more about clock genes and how you can modify them, (re-)read the SuppVersity Circadian Rhythm Series!
- Scientists develop improved formula to calculate the resting energy expenditure of diabetics (Ikeda. 2012) -- While I would hope that you don't belong to the group who would have to use the new and improved formula scientists from the Department of Diabetes and Clinical Nutrition at the Kyoto University in Japan have now proposed, you may have clients or relatives who could benefit from its high predictive validity (78% +/- 103kcal vs. 50% for Harris-Benedict; 38% for Oxford, 42% for Liuand 63% for Ganpule):
part III of the Female Athlete Triad series.
Leptin induced weight gain? 13% more body fat in 2 weeks, when it hits the wrong part of the brain (Harris. 2012) -- With the mixed results from intervention trials, the enthusiasm around leptin has abated over the past months, the general consensus is yet still that leptin and leptin resistance loom large in the metabolic dysregulation that's at the heart of the diabesity pandemic. Against that background, the results Ruth B.S: Harris presents in her latest paper in the American Journal of Physiology - Endocrinology & Metabolism are unquestionably surprising.
If you are interested in ways to modulate your leptin levels that may facilitate weight gain, I suggest you take a look at my second "Carbs Past 6PM Won't Make You Fat" post.
When Harris injected twice the amount of leptin (0.6 µg leptin/day) that had previously been shown to decreased 24 food intake, body fat and lean tissue, when it was injected into the third ventricle of the hindbrain, into the fourth ventricle of her lab rats, the rodents gained an almost incredible amount of 13% body fat within only 2 weeks! And that in the absence of statistically significant change in daily food intake, suggests an "increase in efficiency of energy utilization" (Harris. 2012). Fortunately, further experiments showed that the pro-obesogenic effects of leptin in the 4th ventricle was antagonized when both the 3rd and the 4th ventricle were exposed to leptin. In this scenario the leptin exposure of the 4th ventricle did even protect the lean mass of the rodents from the negative effects the exclusive exposure of the 3rd ventricle had. Overall, the study is yet somewhat chaotic and a clearcut message aside from "look people things are even more complex than we already thought", is probably not going to contribute to a solution of the obesity dilemma in the near future.
- the non-existent effects of coffee consumption before bed on the sleep quality of habitual coffee drinkers (read more),
- the problem with inaccurate vitamin D tests and the absence of a reliable and scientifically sound definition of "vitamin D deficiency" (read more), or
- the strength promoting in-vitro effects of sodium bicarbonate, or in other words, a rather alkaline milieu on muscular force production (read more)
- Harris RB. Leptin-induced increase in body fat content of rats. Am J Physiol Endocrinol Metab. 2012 Dec 4.
- Ikeda K, et al. A new equation to estimate basal energy expenditure of patients with diabetes. Clinical Nutrition. 2012 [article in press]
- Lagerpusch M, Enderle J, Later W, Eggeling B, Pape D, Müller MJ, Bosy-Westphal A. Impact of glycaemic index and dietary fibre on insulin sensitivity during the refeeding phase of a weight cycle in young healthy men. Br J Nutr. 2012 Nov 28:1-11.
- McNay EC, Teske JA, Kotz CM, Dunn-Meynell A, Levin BE, McCrimmon RJ, Sherwin RS. Long-term, intermittent, insulin-induced hypoglycemia produces obesity without hyperphagia or insulin resistance: a model for weight gain with insulin therapy. Am J Physiol Endocrinol Metab. 2012 Nov 20.
- Sluijs I, Beulens JW, van der Schouw YT, van der A DL, Buckland G, Kuijsten A, Schulze MB, Amiano P, Ardanaz E, Balkau B, Boeing H, Gavrila D, Grote VA, Key TJ, Li K, Nilsson P, Overvad K, Palli D, Panico S, Quirós JR, Rolandsson O, Roswall N, Sacerdote C, Sánchez MJ, Sieri S, Slimani N, Spijkerman AM, Tjønneland A, Tumino R, Sharp SJ, Langenberg C, Feskens EJ, Forouhi NG, Riboli E, Wareham NJ; on behalf of the InterAct consortium. Dietary Glycemic Index, Glycemic Load, and Digestible Carbohydrate Intake Are Not Associated with Risk of Type 2 Diabetes in Eight European Countries. J Nutr. 2012 Nov 28.
- Takahashi K, Yamada T, Tsukita S, Kaneko K, Shirai Y, Munakata Y, Ishigaki Y, Imai J, Uno K, Hasegawa Y, Sawada S, Oka Y, Katagiri H. Chronic mild stress alters circadian expressions of molecular clock genes in the liver. Am J Physiol Endocrinol Metab. 2012 Dec 4.