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Ciao bello, ti ho risposto dillà dai Crazy per il dolcificante...
sei un amore
Originariamente Scritto da Gary
lanciamo la manina e nascondiamo il sasso. non zi fa non zi fa, ormai hai spezzato il cuore del piccolo povero campagnolo davide, che non si è più connesso da quando il modello cappelluto ricco e vergato è apparso in foto. non zi fa non zi fa.
WO DAY Colazione Caffè/Tortino con 150gr albumi+Fiocchi d’avena 25gr+Crusca 25gr+Cacao 10gr Durante la mattinata The verde Pranzo Verdura 200-500gr/Petto di Pollo 100gr o Bresaola 70gr o Manzo 150gr o Albumi 120ml+Tuorlo 20gr o Tonno 100gr o Prosciutto 90gr o Salmone 100gr o Sgombro 90gr o Merluzzo 150gr/Pane integrale 75gr/Olio EVO 5gr Post WO Pro Isolate 20 gr/Frutta 200-300gr (ananas, mele, kiwi, fragole, pesche, frutti di bosco, …) o Gallette di Riso 30gr Cena Verdura 200-500gr/Petto di Pollo 100gr o Bresaola 70gr o Manzo 150gr o Albumi 120ml+Tuorlo 20gr o Tonno 100gr o Prosciutto 90gr o Salmone 100gr o Sgombro 90gr o Merluzzo 150gr/Olio EVO 10gr
REST DAY Colazione Caffè/Latte PS AD 200ml/Fette biscottate integrali 30gr/Marmellata SZ Durante la mattinata The verde Pranzo Verdura 200-500gr/Petto di Pollo 100gr o Bresaola 70gr o Manzo 150gr o Albumi 120ml+Tuorlo 20gr o Tonno 100gr o Prosciutto 90gr o Salmone 100gr o Sgombro 90gr o Merluzzo 150gr/Wasa 50gr/Olio EVO 5gr Cena Verdura 200-500gr/Petto di Pollo 100gr o Bresaola 70gr o Manzo 150gr o Albumi 120ml+Tuorlo 20gr o Tonno 100gr o Prosciutto 90gr o Salmone 100gr o Sgombro 90gr o Merluzzo 150gr/ Olio EVO 10gr
FREE 1 Pasto Free a settimana
Sono 100Euro grazie... Ma non darmeli, compraci la valeriana
Devo controllare l'insulina, a parte cibi a basso IG e cannella, sto anche eliminando il caffè e non volendo usare integratori specifici, avete qualche cosa da consigliarmi in proposito, su come, cosa, quanto etc???
Devo controllare l'insulina, a parte cibi a basso IG e cannella, sto anche eliminando il caffè e non volendo usare integratori specifici, avete qualche cosa da consigliarmi in proposito, su come, cosa, quanto etc???
ciao simo!!!
ma la cannella ke ruolo ha nel controllo dell' insulina?? io la prendo spesso a colazza xkè mi hanno detto ke la stimolava... ma credevo fosse una caxata
le cose più belle della vita, o sono illegali, o sono immorali..o fanno ingrassare! "George Bernard Shaw"
ciao simo!!!
ma la cannella ke ruolo ha nel controllo dell' insulina?? io la prendo spesso a colazza xkè mi hanno detto ke la stimolava... ma credevo fosse una caxata
Anche io la uso, ma non mi basta. nel senso che non posso vivere di cannella, ok che mi piace, però, condirci anche l'insalata è troppo
facciamo i seri (anche se non è una scemenza quella degli shortini di aceto...ma è una pratica un po' )
aumenta i grassi mono e poliinsaturi (specie questi ultimi...da olio di pesce/omega3 ecc) a scapito dei saturi;
non demonizzare caffè e caffeina (hanno diversi effetti, tra l'altro (leggi gli studi, non ho avuto tempo di leggerli tutti, ma qualcosa di interessante c'è))
Greenberg JA et. al. Coffee, diabetes, and weight control. Am J Clin Nutr. 2006 Oct;84(4):682-93. Links
Several prospective epidemiologic studies over the past 4 y concluded that ingestion of caffeinated and decaffeinated coffee can reduce the risk of diabetes. This finding is at odds with the results of trials in humans showing that glucose tolerance is reduced shortly after ingestion of caffeine or caffeinated coffee and suggesting that coffee consumption could increase the risk of diabetes. This review discusses epidemiologic and laboratory studies of the effects of coffee and its constituents, with a focus on diabetes risk. Weight loss may be an explanatory factor, because one prospective epidemiologic study found that consumption of coffee was followed by lower diabetes risk but only in participants who had lost weight. A second such study found that both caffeine and coffee intakes were modestly and inversely associated with weight gain. It is possible that caffeine and other constituents of coffee, such as chlorogenic acid and quinides, are involved in causing weight loss. Caffeine and caffeinated coffee have been shown to acutely increase blood pressure and thereby to pose a health threat to persons with cardiovascular disease risk. One short-term study found that ground decaffeinated coffee did not increase blood pressure. Decaffeinated coffee, therefore, may be the type of coffee that can safely help persons decrease diabetes risk. However, the ability of decaffeinated coffee to achieve these effects is based on a limited number of studies, and the underlying biological mechanisms have yet to be elucidated. Lyle McDonald's comments: This was a full scale review looking at the effects of coffee and caffeine (and please note that there may be differences) on both diabetes and bodyweight.
I bring this up because a lot of people have a fairly negative opinion about caffeine. It's been claimed that caffeine raises insulin, causes insulin resistance and deteriorates blood glucose control.
And there is some truth to this, at least if you're looking at high doses of caffeine right before a meal. Typically doses of 5 mg/kg are given which is 500 mg of caffeine for a 100kg (220 lb) person. Contrast this to a typical soda or cup of coffee which might have 60-100 mg of caffeine. Of coure, if you drink the whole pot, to the tune of 8 cups of coffee, then you might be getting close to the doses used in the studies.
At the same time, as this paper mentions above, epidemiological studies suggest that regular caffeine/coffee intake may actually be beneficial in terms of limiting the incidence of diabetes and may play a role in weight loss.
So clearly it's a bit more complicated than it looks and this paper set out to uncomplicate things.
The first data set the review looked at was epidemiological data. Now, I'm no fan of epidemiology in general, there can be a lot of confounding factors when you're trying to determine what causes what. At best, that kind of data gives a starting point and some possible correlational data to do direct work; at worst it's useless.
In any event, looking at 20 studies on the topic, they found that 17 of the 20 showed a beneficial effect of habitual coffee/caffeine intake on diabetes and glucose metabolism, 3 found no effect and none showed a negative effect. Four of the studies suggested that non-caffeine components of coffee were involved (that is, pure caffeine and coffee per se may have different effects) and four studies found an effect of decaf coffee (suggesting that non-caffeine components are playing a role here). One study suggested that the impact of coffee was due to an effect on bodyweight (weight loss) which was the next topic of the paper.
Looking first at rat data, the paper examines data showing that caffeine can reduce bodyweight, fat pad weight and even fat cell number. However, humans aren't rats and human data on this topic is mixed at best. One human study found no impact of caffeine on weight loss but it may be that coffee and other non-caffeine components explains the epidemiological data.
Next up, the paper looked at the impact of caffeine on thermogenesis (calorie burning) and lipolysis (fat mobilization). It comments that a habitual caffeine of 600 mg/day (~6 strong cups of coffee) could lead to an extra caloric expenditure of 100 cal/day (equivalent to walking about 1 mile for a 150 lb person). This effect also occurs with ground and instant coffee, but not decaf so the effect is probably mediated via the caffeine itself. Do note that the body can develop tolerance to these effects so any effect might not be very long lasting.
Related to this, caffeine has also been shown to increase lipolysis (fat mobilization) and fat oxidation and both caffeine and coffee have this effect; decaf does not. Again, the effect is most likely related to the caffeine content per se. Interestingly, both the impact on lipolysis and fat oxidation is more pronounced in non-obese than obese individuals; leaner individuals, probably due to a greater sensitivity to lipolytic stimuli, get a larger effect.
The paper also mentions that caffeine may increase energy expenditure. Doses of 3-30 mg/kg in rats increase spontaneous activity and this type of activity (called NEAT or non-exercise activity thermogenesis in humans) can amount to a fairly considerable energy expenditure. Basically, caffeine may help with weight loss by making you move around more. Again, decaf does not have this effect.
Additionally, a very well known effect of caffeine is improved exercise performance. Caffeine pre workout decreases fatigue, causes more fat to be used (sparing glycogen) and has a host of other effects. By allowing exercisers to work harder, caloric expenditure can be increased.
The next topic discussed has to do with the direct impact of caffeine/coffee on insulin and blood glucose tolerance with a majority of short-term studies showing a negative impact of coffee/caffeine on glucose tolerance when given right before a carbohydrate containing meal. Note that caffeine was not found to raise insulin or blood glucose when not given with a carbohydrate meal; the fear of caffeine on low-carb diets (it's often claimed that caffeine will raise insulin and should be avoided) appears to be unfounded. However, this data is at odds with the epidemiological data suggesting that chronic caffeine/coffee intake decreases diabetes risk.
Data comparing the effects of decaf to caffeinated coffee suggests a possible explanation; decaf coffee tends to lower blood glucose, suggesting the presence of non-caffeine compounds in coffee that may beneficially impact on blood glucose levels.
Note also that animal research suggests a tolerance to any impact of caffeine on blood glucose levels although this has not been studied in humans. However, humans are known to develop a tolerance to the stimulant, thermogenic and other effects of caffeine, it may be that chronic intake of caffeine has a very different effect on blood glucose levels that studies looking at single dose intakes.
Mechanistically, caffeine probably impacts on blood glucose tolerance by raising blood fatty acids and catecholamine levels, both of which impair skeletal muscle insulin sensitivity.
Additionally, the potential impact of coffee/caffeine on fullness was noted but this has not been well researched in humans, some studies indicate higher satiety in folks using coffee/caffeine habitually.
Next the paper delved into other potential health effects. Acutely, caffeine/coffee can raise blood pressure a bit but the body develops partial tolerance rapidly. High caffeine intakes have been found, in animal studies, to cause problems with pregnancy; as well, it may potentiate the negative effects of alcohol and tobacco in this regards. Intakes of >3 cups/day of coffee can decrease fetal birth weight.
Additionally, caffeine withdrawal can cause headaches, irritability, anxiety, depression, drowsiness and fatigue. Folks wanting to reduce their caffeine/coffee intake (for whatever reason) should do so gradually to avoid problems.
High doses of caffeine can also contribute to the risk of kidney stones in elderly individuals and could cause problems with osteoporosis; this is mainly seen with daily calcium intake is low to begin with.
Early research suggested a link between coffee and an elevation of blood lipids but this turns out to only hold for boiled coffee, not brewed.
Finally, the paper discussed the issue of non-caffeine compounds in coffee that might have additional effects on the body. One (I'll spare you the name) has been shown to decrease glucose uptake from the intestine, this might offset negative potential effects of caffeine on blood glucose levels (caffeine alone accelerates glucose uptake from the gut).
Another compound (called a quinide) was shown to enhance glucose uptake and insulin sensitivity in rats, and both the high antioxidant content of coffee along with the magnesium intake may improve insulin sensitivity in the long-term; this might explain the discrepancy in the short-term and epidemiological data.
More research into the non-caffeine components of coffee still needs to be done.
Whew, ok, that was a long one and I was wordy even for me. What's the take home in this? Caffeine/coffee intake appears to have different effects when looked at in the short and long term. In the short-term, caffeine can impact positively on a number of factors (such as delaying fatigue during exercise, increasing lipolysis, and increasing fat oxidation and caloric expenditure) but negatively on others (decreased glucose tolerance/increased insulin response, slight increase in blood pressure). However, longer term studies suggest that habitual caffeine/coffee intake is, overall, beneficial: it decreases the risk of diabetes and may contribute to preventing weight gain Tangentially, of course, any benefit of coffee/caffeine itself is going to be more than outweighed if you fill it up with sugar, cream and other high calorie goodies.
Whether this is due to the body developing tolerance to the short-term effects (wrt: caffeine) or to the presence of non-caffeine compounds in coffee that have additional benefits still awaits further research.
Coffee acutely modifies gastrointestinal hormone secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and caffeine1,2,3
Kelly L Johnston, Michael N Clifford and Linda M Morgan
The objective of this study was to assess whether the consumption of dietary amounts of CGA in coffee had any effects on plasma concentrations of glucose, insulin, GIP, and GLP-1 in humans. Welsch et al (9) postulated that 5-CQA–mediated dissipation of the Na+ electrochemical gradient was responsible for the observed decrease in glucose uptake in rat BBM vesicles; therefore, we suggest that coffee consumption in humans would have similar effects on intestinal glucose transport. This study showed that both caffeinated and decaffeinated coffee drinks significantly attenuated postprandial GIP secretion compared with the control beverage. Postprandial secretion of GIP occurs in the proximal region of the small intestine and is stimulated by the absorption of nutrients from the gut rather than by their presence in the intestinal lumen (12). The rate of absorption of glucose determines the magnitude of the GIP response (15); therefore, these data strongly suggest that coffee decreases the rate of intestinal absorption of glucose. Glucose homeostasis is known to be achieved by a coordinated physiologic response to the ingestion of food, the 2 main effectors of which are 1) limitations on the delivery of glucose into the pool, ie, the maximum rate of glucose absorption, and 2) the rate of disposal of glucose into the tissues, which is itself mainly a consequence of increased insulin action (16). Up until 30 min, the increase in plasma glucose concentrations can be attributed solely to increased delivery into the circulation as a result of increased intestinal absorption in response to the load. Once this has peaked, peripheral metabolism of glucose (ie, delivery into muscle and fat tissue in addition to hepatic glucose metabolism) will have a significant effect on overall plasma concentrations and, thus, any differences seen cannot be solely attributed to effects on absorption (17). Glucose, insulin, and GIP profiles were therefore analyzed over the initial postprandial time period. Differences in GLP-1 were additionally assessed during the latter parts of the study, because this hormone is secreted from the distal region of the small intestine (18).
Plasma glucose concentrations were significantly higher after consumption of caffeinated coffee than after consumption of the control beverage or decaffeinated coffee when a comparison of the means and of the TAUCs was made. The nature of the interaction between coffee consumption and glucose tolerance remains controversial. However, most of the physiologic effects of coffee can be attributed to the presence of caffeine (19). The physiologic effects of coffee began to receive attention when caffeine was first shown to inhibit the action of phosphodiesterase, an enzyme involved in the catabolism of cyclic adenosine monophosphate (cAMP) (20). Increased concentrations of cAMP have been shown to increase glycogenolysis, which may be partially responsible for the significantly impaired glucose tolerance seen after consumption of the caffeinated coffee compared with both the control and the decaffeinated coffee beverages. Caffeine is also an adenosine receptor antagonist (21) and therefore can inhibit muscle glucose uptake, even in the presence of insulin (22). Moreover, Sharp and Debnam (23) have shown that acute luminal exposure of enterocytes to cAMP in vivo has stimulatory effects on sugar transport across the BBM and the basolateral membrane, and Debnam et al (24) provided evidence for a similar effect of cAMP in the regulation of sodium-dependent glucose transporter–mediated glucose transport across isolated rat renal BBM. Taking into consideration the known actions of caffeine, we propose that the differences in plasma glucose profiles further confirm the potent pharmacologic actions of caffeine but also imply that CGA has an antagonistic effect on glucose transport, because integrated glucose concentrations were lowest after consumption of the decaffeinated coffee beverage.
Pizziol et al (25) previously suggested that caffeine causes impaired glucose tolerance by inducing a rise in blood glucose concentrations that is independent of insulin. However, these authors use the terms caffeine and coffee interchangeably and do not consider the action of other biologically active components present in coffee, namely CGA. In our study, plasma insulin concentrations showed small differences in the early part of the postprandial period, which were consistent with the mildly impaired glucose tolerance seen after consumption of the caffeinated beverage compared with the decaffeinated beverage. However, the small differences in plasma insulin observed in this study lack the statistical power to refute the claims by Pizziol et al with any confidence.
Although glucose is the major regulator of insulin secretion, incretin gut factors have been estimated to be responsible for as much as 50% of the insulin secretion observed after an oral glucose load and the term "enteroinsular axis" was introduced to encompass the gut factors responsible for this (26–28). The secretion of the incretin hormones GIP and GLP-1 were significantly altered in response to the test beverages compared with the control. GIP secretion was attenuated after consumption of both the caffeinated and decaffeinated coffees compared with that after consumption of the control beverage. GLP-1, in contrast with GIP, is secreted from the distal portion of the small intestine and responds to the presence of nutrients in the gut lumen rather than to their absorption (29). Its secretion can be increased when the absorption of carbohydrate is delayed (30). Circulating GLP-1 concentrations were significantly enhanced after consumption of decaffeinated coffee, later in the postprandial time period. These opposing effects of incretin hormones would have minimized any effects of coffee on insulin secretion. However, the gastrointestinal hormone data are consistent with delayed glucose uptake in the small intestine, ie, uptake occurring further down the small intestine.
We suggest that at the level of the BBM, coffee exerts it physiologic effects via CGA-mediated Na+ electrochemical gradient dissipation—the driving force for active glucose assimilation. This is reflected in and supported by the gastrointestinal hormone profiles but not in those for plasma insulin and glucose. However, the potent biological effects of caffeine on both hepatic glucose output and muscular uptake suggest that plasma glucose and insulin concentrations are a poor biomarker when interpreting the gastrointestinal effects of coffee on glucose transport in the small intestine.
Our previous work showed that consumption of the same volume of commercial apple juice containing significant amounts of CGA ( 500 µmol/L) as well as other bioactive dietary phenols, such as phloridzin ( 60 µmol/L), significantly delays glucose uptake and shifts absorption to a more distal region of the gastrointestinal tract, as indicated by a similar change over time in plasma GIP and GLP-1 concentrations (31). Compared with the present study, in which the test beverages contained 2.5 mmol total CQA/L (the dietary equivalent of 2 small strong cups of coffee), the effects after apple juice consumption were less pronounced but not as much as would be expected if CGA were the only agent responsible given the large difference in CQA concentrations between the 2. It is therefore likely that most of the effects seen after apple juice consumption were mediated by phloridzin, a potent competitive inhibitor of sodium-dependent glucose transporter 1 and one that is commonly used in physiologic studies to abolish glucose transport (32).
Recent evidence to support the clinical effects of dietary polyphenols is provided by van Dam and Feskens (33), who showed in a prospective cohort study that the risk of developing clinical type 2 diabetes was 0.5 times as likely in individual persons who drank 7 cups (1659 mL) coffee/d than in those who drank <=" BORDER="0"> 2 cups (474 mL) coffee/d. The results of their study strongly suggest that coffee consumption can have clinical benefits; the results of our study suggest a possible mechanism whereby these benefits might be mediated.
ciao simo!!!
ma la cannella ke ruolo ha nel controllo dell' insulina?? io la prendo spesso a colazza xkè mi hanno detto ke la stimolava... ma credevo fosse una caxata
oggi sono in vena di studi:
Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects1,2,3
Joanna Hlebowicz, Gassan Darwiche, Ola Björgell and Lars-Olof Almér
1 From the Departments of Medicine (JH, GD, and L-OA) and Radiology (OB), Malmö University Hospital, University of Lund, Lund, Sweden
Background: Previous studies of patients with type 2 diabetes showed that cinnamon lowers fasting serum glucose, triacylglycerol, and LDL- and total cholesterol concentrations. Objective: We aimed to study the effect of cinnamon on the rate of gastric emptying, the postprandial blood glucose response, and satiety in healthy subjects. Design: The gastric emptying rate (GER) was measured by using standardized real-time ultrasonography. Fourteen healthy subjects were assessed by using a crossover trial. The subjects were examined after an 8-h fast if they had normal fasting blood glucose concentrations. GER was calculated as the percentage change in the antral cross-sectional area 15–90 min after ingestion of 300 g rice pudding (GER1) or 300 g rice pudding and 6 g cinnamon (GER2). Results: The median value of GER1 was 37%, and that of GER2 was 34.5%. The addition of cinnamon to the rice pudding significantly delayed gastric emptying and lowered the postprandial glucose response (P < 0.05 for both). The reduction in the postprandial blood glucose concentration was much more noticeable and pronounced than was the lowering of the GER. The effect of cinnamon on satiety was not significant. Conclusions: The intake of 6 g cinnamon with rice pudding reduces postprandial blood glucose and delays gastric emptying without affecting satiety. Inclusion of cinnamon in the diet lowers the postprandial glucose response, a change that is at least partially explained by a delayed GER.
Esco a prendermi subito il caffè allora
Poi quando passi a Roma, una stecca di cannella per'uno, una passeggiata per depletare e poi pizza e gelato :supelol:
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