Amazoniac
Member
I'm often impressed by how people that eat intuitively develop some sort of sustainable system for them. Calcium products are readily available everywhere, if there's a trend that people are shying away from them and decreasing calcium consumption, there must be a good reason for it and it's not just a matter of forcing more calcium back in the diet.
Low-calcium diet prevents fructose-induced hyperinsulinemia and ameliorates the response to glucose load in rats
There is no doubt these guys were after the headlines since they could've used starch and sucrose (instead of a combination of both and fructose alone) with much more subtle effects, yet perhaps still present. But the main point is that calcium restriction helped their insulin function when under stress:
If you have clients that are avoiding calcium out of intuition, don't encourage more consumption right away before addressing what led them to decrease their intake. A generalized vit D deficiency should definitely be considered.
All is full of love, you have to trust it.
Low-calcium diet prevents fructose-induced hyperinsulinemia and ameliorates the response to glucose load in rats
"The progressive increase in intake of high-fructose corn syrup is related to the rise in the consumption of soft drinks, for which it is the main sweetener (e.g., [11]). One other major consequence of the increased intake of sweetened soft drinks is the displacement of milk from the diet [12]. Milk is an important source of calcium, so its disappearance from the diet has exacerbated suboptimal calcium intakes [12, 13]. Calcium deficiency leads to impaired insulin release in experimental animals, and there are indications that the same is true for humans [14, 15, 16]; decreases in circulating levels of both calcium and vitamin D are associated with changes in glucose homeostasis [17, 18, 19]. Thus, calcium and sugar intake, and their homeostasis are intertwined; however, little is known about how calcium status influences the regulation of metabolism under conditions of sugar overconsumption.
We investigated whether the combination of a high-fructose diet along with marginally inadequate calcium might have combined detrimental influences on glucose metabolism. To this end, we compared the metabolic profiles of rats fed diets with the carbohydrate provided either as a standard mixture of cornstarch and sucrose or as fructose, and with the calcium provided either at replete or marginally deficient levels. We found that relative to calcium-replete controls, rats fed low-calcium diet had improved insulin sensitivity and did not develop hyperinsulinemia when fed the high-fructose diet."
We investigated whether the combination of a high-fructose diet along with marginally inadequate calcium might have combined detrimental influences on glucose metabolism. To this end, we compared the metabolic profiles of rats fed diets with the carbohydrate provided either as a standard mixture of cornstarch and sucrose or as fructose, and with the calcium provided either at replete or marginally deficient levels. We found that relative to calcium-replete controls, rats fed low-calcium diet had improved insulin sensitivity and did not develop hyperinsulinemia when fed the high-fructose diet."
There is no doubt these guys were after the headlines since they could've used starch and sucrose (instead of a combination of both and fructose alone) with much more subtle effects, yet perhaps still present. But the main point is that calcium restriction helped their insulin function when under stress:
"The results demonstrate that fructose-induced hyperinsulinemia and impaired glucose tolerance depend on calcium status: In line with earlier work, plasma insulin concentrations and blood glucose levels in response to a glucose load were markedly elevated in calcium-replete rats fed fructose relative to those fed a standard starch-and-sucrose mixture [10]. These effects of fructose feeding were strongly attenuated in rats that received a low-calcium diet. However, fasting glucose levels in fructose-fed rats were not improved by low-calcium feeding. Thus, eating a low-calcium diet significantly alleviated but did not abolish the effects of fructose feeding on glucose handling.
Relative to the calcium-replete fructose-fed rats, the calcium-deficient fructose-fed rats had lower glycemia in response to a glucose load despite a smaller rise in insulin levels. This implies that the response to insulin is less affected by fructose overfeeding under conditions of calcium deficiency. The drop in blood glucose levels in response to insulin injection was larger in rats that received the low-calcium version than calcium-replete version of the AIN-93G diet. This points towards increased insulin sensitivity of the peripheral tissues under conditions of calcium deficiency.
There are at least two plausible mechanisms by which calcium deficiency could influence insulin sensitivity. One involves the activation of insulin receptor expression by high levels of circulating 1,25-hydroxyvitamin D3 [27, 28, 29]. An increase in levels of 1,25-hydroxyvitamin D3 is a classic effect of calcium deficiency, and it has been observed with the low-calcium diet used here (i.e., AIN25 diet; [30, 31]). Activation of insulin receptor expression through 1,25-hydroxyvitamin D3 action would counteract the suppression of insulin receptor responsiveness that is exerted by fructose feeding [32]. The other plausible mechanism involves activation of the osteoblast-specific factor, osteocalcin. Levels of circulating osteocalcin, including the active uncarboxylated form, increase when rats are fed low-calcium diets [33, 34]. This improves insulin sensitivity in adipose tissue and liver [35]. Consistent with this, injections of osteocalcin improve insulin sensitivity in mice fed high-fat diet, which is a metabolic challenge comparable in some of its effects to fructose feeding [36].
Enhanced insulin sensitivity mediated through the action 1,25-hydroxyvitamin D3 and/or osteocalcin may have emerged as an adaptation to conditions when dietary sources of calcium are scarce in order to overcome the secretory deficiency of pancreatic beta-cells induced by low calcium levels.
Reduced fasting insulin levels in rats fed low-calcium diets, and hampered glucose-induced hyperinsulinemia in fructose-fed rats receiving low-calcium diets, is consistent with the effect of dietary calcium deficiency to interfere with insulin release [14, 15]. Glucose-induced hyperinsulinemia in fructose feeding may have also been ameliorated by what appears to be improved insulin sensitivity in calcium deficiency: Exaggerated insulin release in fructose feeding is thought to be a compensatory response to the development of insulin resistance in the periphery and thus could potentially be prevented if insulin sensitivity is maintained [6]."
No doubt this is a short-term measure with costly long-term consequences, but I doubt it's just an accident or solely because of anti-dairy campaigns.Relative to the calcium-replete fructose-fed rats, the calcium-deficient fructose-fed rats had lower glycemia in response to a glucose load despite a smaller rise in insulin levels. This implies that the response to insulin is less affected by fructose overfeeding under conditions of calcium deficiency. The drop in blood glucose levels in response to insulin injection was larger in rats that received the low-calcium version than calcium-replete version of the AIN-93G diet. This points towards increased insulin sensitivity of the peripheral tissues under conditions of calcium deficiency.
There are at least two plausible mechanisms by which calcium deficiency could influence insulin sensitivity. One involves the activation of insulin receptor expression by high levels of circulating 1,25-hydroxyvitamin D3 [27, 28, 29]. An increase in levels of 1,25-hydroxyvitamin D3 is a classic effect of calcium deficiency, and it has been observed with the low-calcium diet used here (i.e., AIN25 diet; [30, 31]). Activation of insulin receptor expression through 1,25-hydroxyvitamin D3 action would counteract the suppression of insulin receptor responsiveness that is exerted by fructose feeding [32]. The other plausible mechanism involves activation of the osteoblast-specific factor, osteocalcin. Levels of circulating osteocalcin, including the active uncarboxylated form, increase when rats are fed low-calcium diets [33, 34]. This improves insulin sensitivity in adipose tissue and liver [35]. Consistent with this, injections of osteocalcin improve insulin sensitivity in mice fed high-fat diet, which is a metabolic challenge comparable in some of its effects to fructose feeding [36].
Enhanced insulin sensitivity mediated through the action 1,25-hydroxyvitamin D3 and/or osteocalcin may have emerged as an adaptation to conditions when dietary sources of calcium are scarce in order to overcome the secretory deficiency of pancreatic beta-cells induced by low calcium levels.
Reduced fasting insulin levels in rats fed low-calcium diets, and hampered glucose-induced hyperinsulinemia in fructose-fed rats receiving low-calcium diets, is consistent with the effect of dietary calcium deficiency to interfere with insulin release [14, 15]. Glucose-induced hyperinsulinemia in fructose feeding may have also been ameliorated by what appears to be improved insulin sensitivity in calcium deficiency: Exaggerated insulin release in fructose feeding is thought to be a compensatory response to the development of insulin resistance in the periphery and thus could potentially be prevented if insulin sensitivity is maintained [6]."
If you have clients that are avoiding calcium out of intuition, don't encourage more consumption right away before addressing what led them to decrease their intake. A generalized vit D deficiency should definitely be considered.
All is full of love, you have to trust it.