Why Ray Recommends Eating Lots Of Calcium

[Travis]

The pineapple actually does have trichosomes:

'The trichomes occur evenly over the entire upper leaf surface (Plate 1 A). There are only half as many trichomes as occur on the lower leaf surface (Krauss, 1949). However, the distribution of trichomes over the leaf surface appears similar to that reported for other Bromelioideae (Benzing, Seemann and Renfrow, 1978).' ―Sakai (1980)

'This combined with the presence of the polysaccharide material in the vacuole provide good indirect evidence for the function of these trichomes in uptake of dissolved nutrients.' ―Sakai (1980)

'More recently Benzing et al. (1976) have shown uptake of labelled amino acids into stalk cells of several species of Bromelioideae and Tillandsioideae. In Hawaii much of the nutrients supplied to pineapples (Bromelioideae) is through foliar sprays.' ―Sakai (1980)​

Also relevant is that the pineapple also has leaf chinitase enzymes capable of breaking-down the exoskeleton of insects. The pineapple now has everything it needs to digest insects—(1) leaf trichosomes, (2) leaf enzymes, (3) waxy exfoliating leaf powder, (4) emits attractive scent—and could then perhaps be considered a protocarnivorous plant. Perhaps nobody realizes this because they're always planted in open fields, not under a natural canopy where this could be observed. Do wild pineapples digest insects that cannot escape from its leaf rosette?

[1] Sakai, W. S. "Ultrastructure of the water-absorbing trichomes of pineapple (Ananas comosus, Bromeliaceae)." Annals of Botany (1980)
[2] Taira, Toki. "Purification, characterization, and antifungal activity of chitinases from pineapple (Ananas comosus) leaf." Bioscience, biotechnology, and biochemistry (2005)​

 

[Runenight201]

So I’ve been interested to see if insects could be a potential quality source of nutrition, primarily calcium and protein.

A report by the Food and Agricultural Organization lists several different insects and their mineral/vitamin/amino acid/fatty acid profiles. http://www.fao.org/docrep/018/i3253e/i3253e06.pdf

I don’t think insects are a good form of calcium, as the mopane caterpillar has about a 1:5 calcium/phosphate ratio, although it’s total calcium content is high at 174mg per 100g, different insects might yield different results, so looking at the original nutritional studies could be enlightening.

What’s cool is the palm weevil larvae actually contain a relatively high amount of vitamin E, 35mg and 9mg per 100g of a-tocopherol and b-tocopherol respectively. However, this is accompanied by a relatively high PUFA load in the insect, which mirrors nuts. It seems that vitamin e and PUFA go hand in hand in nature.

There are insects that have a low fat profile, such as the variegated grasshopper, which is comprised of 9% fat, of which only 35% is PUFA, so definitely some interesting candidates there....

I think the icing on the cake though is the relatively poor glycine/proline amino acid profile, with the mg/kg of dry matter being no more impressive than beef. I guess in a worst case scenario insects could replace beef, but gelatin + calcium would still need to be obtained through green leaves and dairy.

These were all selective examples, perhaps there are insects that have much more attractive nutritional properities....

 

[Amazoniac]

Gershom Zajicek - Researching the Gates
↳ Calcium Supplements Interact Significantly with Long-Term Diet while Suppressing Rectal Epithelial Proliferation of Adenoma Patients

"The intake of dietary calcium varies among individuals and among populations of westernized countries, and, overall, it has been noted that the western-style diet is relatively calcium-deficient. Based on this epidemiologic evidence and the high-risk for colorectal cancer in western populations, it was postulated that calcium supplementation may play a role in colorectal cancer prevention.[1–5]"

"However, results of a number of international ecological and analytic epidemiologic studies did not support the hypothesis that calcium-deficient diet is a risk for colorectal cancer and did not find a cancer preventive value for calcium supplementation in humans. [11,13,14,16,22,26,31,32] These findings were in contrast to the findings of experimental studies in animals, where a calcium deficient or supplemented diet had a marked protective effect on large bowel epithelial proliferation and also on the process of carcinogenisis. [6,23,28–30,33]"

"Suppression of large bowel epithelial proliferation by calcium has been explained by intraluminal binding of bile and fatty acids to calcium that thereby reduces the damaging effects of bile and fatty acids on colonic epithelial cells and/or by the strengthening their intercellular bonds by calcium and/or by systemic strengthening through calcium and vitamin D metabolism.[1,7,9,25,33–36] The extent of the dietary calcium protective action may depend on the dietary intake of calcium and/or relative amounts of other nutrients such as fat, fiber, phosphate, and total mean daily caloric intake.[1,37] In contrast to animal experiments, it was noted that the intake of these dietary constituents was poorly controlled in human clinical intervention trials, and this possibly led to discrepancies in analyses of their results.[37,38] This was done in some of the more recent human intervention studies, where dietary intakes of fat and fiber specifically were taken into account.[15,19]"

"Patients who consented to treatment were given 5 chewable calcium carbonate tablets daily, with meals, for 12 months. These were Tums-Ex tablets (Norcliff Thayer, USA) each containing 750 mg of calcium carbonate, equivalent to supplementation of 1.5 g calcium ion/day."

"This small, but carefully evaluated, long-term trial of calcium supplementation demonstrated a significant suppression of REP [rectal epithelial proliferation] levels in the intervened group. We already had demonstrated this effect of calcium in adenoma-free, first-degree relatives of colorectal cancer patients and again now in adenoma patients without such a family history.[8] Moreover, we also demonstrated the existence of significant interactions between the degree of LI [labeling index, to grasp abnormal cell behavior] response to calcium with levels of intake of specific major dietary components, such as fat and carbohydrates, and a trend with other nutrients such as fiber and fluids as well as tobacco use."

"The usefulness of colonic epithelial cell proliferation as an intermediate biomarker of response to calcium intervention has been reviewed by Bostik,[17] who concluded that the main effect of the calcium was to normalize the distribution of proliferating cells within the colonic crypt.[17] In the current study, we obtained a significant effect on the total crypt-labeling index [grasping cycle], which is a more powerful and biologically important effect than one that is localized just to the crypt compartments."

"The small number of suitable volunteer participants who entered the trial limited the study. In addition, a large proportion of participants did not complete the 1 year of calcium intervention and/or comply with the 1-year rectal biopsy; even so, the results were significant."

"These initial findings suggest that a high dietary fat intake can interfere with supplemented calcium and prevent its beneficial local or systemic effects on suppressing proliferation. This was not anticipated from the response to calcium supplements in experimental animals that were fed diets mimicking the western-style diet in composition, or from human adenoma- recurrence studies, where the greatest benefit was found among high-fat consumers.[19,28] However, the current study results are consistent with two experimental studies: one in rats that found that calcium supplements to a low-fat diet significantly reduced LI, and a clinical study giving low-fat dairy foods to adenoma patients who were consuming a low fat basal diet and, again, found a significant reduction in the LI.[6,27] All together, these are possibly consistent with a direct beneficial effect of calcium, even in the absence of a high-fat diet, in preventing colorectal neoplasia."

"In conclusion, calcium supplementation will suppress REP in persons at risk for colorectal neoplasia. Within the intestinal milieu, calcium by itself probably has only a minor modulating effect in preventing colorectal cancer.[5,17,20,24,31] So, for calcium supplements to play a role in the prevention of colorectal neoplasia, it would seem reasonable to give them with additional relevant dietary and lifestyle counseling."

 

[Dolomite]

@Amazoniac , Thanks, I have a family member who had colon cancer and I would like avoid it. I read a post by Dr J where he described good motility and regularity by consuming enough calcium and magnesium. I quit drinking as much milk recently and upped the eggshell powder and I noticed improvements in my gut.

 

[Amazoniac]

Could the beneficial effects of dietary calcium on obesity and diabetes control be mediated by changes in intestinal microbiota and integrity?

 

[Birdie]

This is good, but his words seem a bit quaint. Ignoring his lack of the terminal "e" in ornithine, there is a more serious dilemma. Arginine is thought to become ornithine and urea, not guinidine, by the action of arginase. Perhaps we can assume that guinidine was synonymous with urea back then.

View attachment 7019 click to embiggen

But regardless of whether or not urea or guinidine is formed by the action of arginase, this would be impossible in the presence of high methylglyoxal concentrations. Here is why:

It is well-known that methylglyoxal forms an imidizole ring on contact with methylglyoxal. This has been proven. Below is a brief representation of the event:

View attachment 7020

More detailed ones can be drawn. A similar image can be seen here, but it's given an improper name that doesn't account for the methyl group.

• Chumsae, Chris, et al. "Arginine modifications by methylglyoxal: discovery in a recombinant monoclonal antibody and contribution to acidic species." Analytical chemistry 85.23 (2013).

It's probably best called 5-methyl-4-imidazolon-2-yl ornithine, or 5-methyl-4-imidazolone when talking about the ring itself. It's called MG-H1 for short. These are the names that Thornally uses, and he has been publishing articles on methylglyoxal since the early 80s. He has designed a powerful glyoxylase I inhibitor and has published extensive reviews on the glyoxylase system. I don't think anyone knows more about methyglyoxal than Paul Thornally.

• Westwood, M. E., et al. "Methylglyoxal-modified arginine residues—a signal for receptor-mediated endocytosis and degradation of proteins by monocytic THP-1 cells." Biochimica et Biophysica Acta (BBA)-Molecular Cell Research 1356.1 (1997): 84-94.

So obviously, urea (or guanidine) cannot form from arginine in the presence of high methylglyoxal concentrations. The chemical species has transformed. Methylglyoxal can, of course, also react with free urea. This was shown as far back as 1927 by Seekles.

• Seekles, L. "The action of methylglyoxal on urea." Recueil des Travaux Chimiques des Pays-Bas 46.2 (1927): 77-84.

The action of methylglyoxal on urea might be expected to form 5-Methyl-2,4-imidazolidinedione, or 5-methylhydantoin. There is little data on this compound although the similar allantoin is a normal component of urine.

Here is an image of a few arginine–glyoxal products. Methylglyoxal mops-up nitrogen groups and many things can be formed. Two methylglyoxal's can form a pyrimidine ring. Interesting things may come of this:*

Methylglyoxal is a product of carbohydrate metabolism. It's concentrations are kept in-check throught the two enzymes glyoxylase I and glyoxylase II. First, methylglyoxal reacts with glutathione at the sulfhydryl. This is then slightly-modified by glyoxylase I and glyoxylase II does the rest: regenerating glutathione and forming lactic acid.

If Umeda suggests that uric acid can be formed from urea lactic acid, then he probably wouldn't mind the suggestion that it could be made by methylglyoxal—having the same amount of carbons yet more reactive. I don't think that lactic acid is a good candidate for uric acid formation. Armand Quick reports that the ingestion of lactic acid depresses uric acid excretion (Table I) while the ingestion of glucose raises it.†

You would certainly expect a fair amount of interplay between arginine, urea, and methylglyoxal. It's easy to see how methylglyoxal can turn-off cancer by transforming the some molecular growth factors, such as nitric oxide and polyamines, into more inert molecules such as substituted allantoins and pyrimidines. Or is it the other way around? . . . where these nitrogen compounds lower methylglyoxal and it's this that causes growth? I suspect the former. The glyoxylase system could be an endogenous recycling mechanism for amines, an another way in which the cell regulates growth.

Thornally has published a massive article on the glyoxylase system.‡ He has even shown that the methylglyoxal–arginine controls a nuclear transcription factor in the manner of a post-translational mechanism.§ An arginine side-chain in the sensitive DNA-binding domain is methylgloxylated, causing a shift in gene transcription.


*Rose, William C. "The influence of food ingestion upon endogenous purine metabolism. I." Journal of Biological Chemistry 48.2 (1921): 563-573.
†Quick, Armand J. "The relationship between chemical structure and physiological response III. Factors influencing the excretion of uric acid." Journal of Biological Chemistry 98.1 (1932): 157-169.
‡Thornalley, Paul J. "The glyoxalase system in health and disease." Molecular aspects of medicine 14.4 (1993): 287-371.
§Yao, Dachun, et al. "High glucose increases angiopoietin-2 transcription in microvascular endothelial cells through methylglyoxal modification of mSin3A." Journal of Biological Chemistry 282.42 (2007): 31038-31045.

Regarding Koch’s lack of the final e in ornithine, this would be the German spelling.

Ornithin
Chemische Verbindung, Aminosäure im Harnstoffzyklus
Ornithin (von griech. ornis, Vogel) ist eine basische, nichtproteinogene α-Aminosäure. Sie tritt in der L-Form hauptsächlich im Harnstoffzyklus als Trägersubstanz auf.

 

[TeaRex14]

I've found that if I eat too much calcium in relation to phosphate I get insomnia. This only usually occurs if I'm above a 2:1 ratio though. A 1:1 or 2:1 ratio of calcium/phosphate seems to be ideal, for me.

 

[Birdie]

Could the beneficial effects of dietary calcium on obesity and diabetes control be mediated by changes in intestinal microbiota and integrity?

Interesting. Thanks.

A bit from the abstract:

Published studies from 1993 to 2015 about this topic were searched and selected from Medline/PubMed, Scielo and Lilacs databases. High-Ca diets seem to favour the growth of lactobacilli, maintain II (especially in the colon), reduce translocation of LPS and regulate tight-junction gene expression.

We conclude that dietary Ca might interfere with gut microbiota and II modulations and it can partly explain the effect of Ca on obesity and T2DM control. However, further research is required to define the supplementation period, the dose and the type of Ca supplement (milk or salt) required for more effective results...


(PDF) Could the beneficial effects of dietary calcium on obesity and diabetes control be mediated by changes in intestinal microbiota and integrity?. Available from: https://www.researchgate.net/public...hanges_in_intestinal_microbiota_and_integrity[accessed Dec 31 2018].

 

[Mateo Wiechers]

This is certainly only one reason, but given how important for metabolism it is I thought it is worth mentioning. Calcium activates the enzyme pyruvate dehydrogenase (PDH), which takes the pyruvate produced by glycolysis, converts it to Acetyl-Co-A and thus starts the Krebs cycle. Calcium also seems to activate the other enzymes participating in the Krebs cycle.
Without properly functioning Krebs, cells will be stuck in glycolysis with excess pyruvate production. The excess pyruvate will get converted into lactate by the enzyme LDH, thus exhibiting the Warburg effect.
Finally, the proper functioning of the Krebs cycle and synthesis of its intermediate metabolites fumarate and succinate seems to restrain the enzyme HIF, which is so important in human pathology and especially cancer.
Citric acid cycle - Wikipedia

"...Calcium is used as a regulator. Mitochondrial matrix calcium levels can reach the tens of micromolar levels during cellular activation.[27] It activates pyruvate dehydrogenase phosphatase which in turn activates the pyruvate dehydrogenase complex. Calcium also activates isocitrate dehydrogenase and α-ketoglutarate dehydrogenase.[28] This increases the reaction rate of many of the steps in the cycle, and therefore increases flux throughout the pathway."

"...Recent work has demonstrated an important link between intermediates of the citric acid cycle and the regulation of hypoxia-inducible factors (HIF). HIF plays a role in the regulation of oxygen homeostasis, and is a transcription factor that targets angiogenesis, vascular remodeling, glucose utilization, iron transport and apoptosis. HIF is synthesized consititutively, and hydroxylation of at least one of two critical proline residues mediates their interaction with the von Hippel Lindau E3 ubiquitin ligase complex, which targets them for rapid degradation. This reaction is catalysed by prolyl 4-hydroxylases. Fumarate and succinate have been identified as potent inhibitors of prolyl hydroxylases, thus leading to the stabilisation of HIF."

Hi,
If i take some calcium carbonate, would it be better to take it with meals or it doesn't matter?

Also i have noticed that the high calcium intake has helped with my depression, i assume it is lowering serotonin along other stress mediators.

 

[Amazoniac]

Vitamin D (978-0-12-381978-9) - David Feldman*
*(do not confuse with Foster, whose book is on Aspirin)
[Chapter 34] Vitamin D: Role in the Calcium and Phosphorus Economies​

"Into and out of [the] ECF compartment passes all the calcium entering and leaving the body from the outside, as well as entering and leaving bone. These fluxes are summarized schematically in Figure 34.1. Together they involve daily quantities amounting to 35-50% of the size of the entire compartment in healthy adults, and to several times that compartment size in infants. Without tight regulation, ECF [Ca2+] would oscillate between possibly fatal extremes of hypo- and hypercalcemia as the organism goes from fasting to feeding."

Multiply values in mmol by 40 to get them in mg.

"Obligatory loss consists of a combination of cutaneous loss and the fixed components of urinary and endogenous fecal calcium excretion. Cutaneous losses consist not just of sweat calcium but of the calcium contained in shed skin, hair, and nails. As has been noted above, all cells contain substantial amounts of calcium, and their loss from body surfaces inexorably takes calcium with them. Cutaneous losses have been hard to quantify but are estimated to be at least 0.4 mmol/day and more likely closer to 1.5 mmol/day [5,6]. Much higher losses have been reported with vigorous physical activity [7]."

"The fixed component of endogenous fecal and urinary calcium losses is somewhat more complicated [8]. On average, 3.5-4.0 mmol calcium enters the gut each day from endogenous sources, principally as a component of digestive secretions, but also as the calcium contained in shed mucosal cells (which turn over once every 4-5 days). The precise quantity varies directly with body size and with the amount of food consumed. For reasons not understood, the amount of calcium entering the gut in the digestive secretions varies directly also with phosphorus intake [8]. In any event, this endogenous calcium mixes with food calcium and much of it is subject to absorption, just as is the calcium of food. However, as noted earlier, calcium absorption is always incomplete. Gross absorption [without considering exchanges] averages about 25-30% in healthy adults, and net absorption about 10-11%. Hence much of the secreted calcium is lost in the feces. Moreover, some of the endogenous calcium secretion enters the intestinal stream at a point so low in the gut as to be essentially unreclaimable (e.g., the calcium in colon mucus and in shed colon cells). On a normal diet this distal component has been estimated to be about 0.6 mmol [8]. Typical endogenous fecal calcium values average in the range of 3 mmol/day. Since absorption efficiency in adults is essentially never above 60%, even on a very-low-calcium diet (see later discussion), there is an irreducible minimum loss of endogenous calcium through the gut averaging close to 2 mmol/day. If gross absorption is not greater than this figure, the gut becomes a net excretory organ for calcium."

"The third obligatory loss is through the kidney. It is generally held that renal calcium excretion is controllable, but this is only partly true. PTH certainly regulates tubular calcium reabsorption. However! There is a fixed limit to what that mechanism can accomplish. This limit is itself a function of other variables that are outside the regulatory loop. Best studied of these factors is the renal excretion of sodium, dietary intakes of protein and potassium, net endogenous acid production (NEAP), and absorbed dietary phosphorus. Sodium [9-11], protein [12,13], and NEAP [14] increase urinary calcium loss; phosphorus and potassium decrease it [15,16]. Their aggregate effect on renal calcium excretion constitutes obligatory (rather than regulated) loss because their input to the body is itself unregulated."

"Because sodium and calcium compete for the same reabsorption mechanism in the proximal tubule, the two ions influence one another’s excretion [17]. On average, urine calcium increases from 0.5 to 1.5 mmol for every 100 mmol (multiply by 23 for mg) of sodium excreted [9,10]. Similarly, urine calcium rises by about 0.25 mmol for every 10 g of protein ingested [12]. The result, for an adult woman ingesting the RDA for protein and the median sodium intake for North Americans, is a level of obligatory urinary loss amounting to about 2 mmol/day. Reducing sodium intake would certainly reduce this obligatory loss. Nevertheless such voluntary dietary change is clearly not a part of any physiological regulatory loop. And thus, to the extent that sodium intake influences obligatory calcium loss, it constitutes a demand to which the calcium homeostatic system must respond. Given typical adult diets in Europe and North America, the sum of these obligatory losses through skin, gut, and kidney is about 5 ± 1 mmol/day, or about one-fifth of the total calcium in the ECF [brew the first image]. To offset these losses (plus the demands of bone mineralization), the organism regulates countervailing inputs into the ECF from food and bone. It is in these transfers that vitamin D plays its role. The input from the first source is dependent both upon the presence of food in the upper GI tract and the presence of sufficient calcium in that food. Because neither condition can be guaranteed, the second source, bone, is the more reliable and constitutes, in fact, the first line of defense against hypocalcemia.[2]"

"[..]under conditions of wealth, it is the renal calcium threshold that is the primary determinant of ECF [Ca2+]. The threshold is, conceptually, the level of ECF [Ca2+] below which renal tubular reabsorption of filtered calcium is essentially quantitative, i.e., urine calcium is very low and ECF [Ca2+] coming out of the kidney is about the same as that going in. The principal determinant of the threshold is PTH (which is why serum calcium rises in patients with hyperparathyroidism and falls in those with hypoparathyroidism."

"Briefly, a fall in ECF [Ca2+] evokes a prompt rise in parathyroid hormone [PTH] release. PTH acts in a classical negative feedback loop to raise the ECF [Ca2+], thereby closing the loop and reducing PTH release. The mechanisms by which PTH raises ECF [Ca2+] illustrate well the complexities of the calcium economy. These mechanisms include:
(1) increasing renal phosphate clearance, thereby lowering ECF phosphate levels;
(2) increasing renal tubular reabsorption of calcium, thereby allowing system inputs to elevate ECF [Ca2+];
(3) augmenting osteoclast work at existing resorption loci;
(4) activating new bone resorption loci; and
(5) increasing the activity of the renal 1-a-hydroxylase, thereby increasing serum levels of 1,25(OH)2D and augmenting absorption efficiency for ingested food calcium."

"These five effects reinforce one another in important ways. The earliest effects, occurring within minutes, are a decrease in renal tubular phosphate reabsorption and the resulting fall in serum phosphate. The latter immediately augments existing osteoclastic bone resorption [20] and increases activity of the renal 1-ahydroxylase [21]. The elevated production of 1,25 (OH)2D leads to increased intestinal absorption, elevating ECF [Ca2+] and thereby closing the feedback loop. (1,25(OH)2D also suppresses parathyroid hormone release in its own right.) Finally, 1,25(OH)2D is necessary for efficient osteoclast work. In this last role, it is not known whether variations of 1,25(OH)2D in the physiologic range produce corresponding alterations in bone resorption, and it is a difficult question to study because of the tight regulation of the various components of the system. Nevertheless, it is well established that resorptive work is severely impaired in vitamin D deficiency states (see Fig. 34.2 and later discussion), and that 1,25 (OH)2D in supraphysiologic doses is capable of causing substantial increases in bone resorption. Finally, all of the components of the intestinal calcium transport system, including vitamin D receptors and calbindins, are also found in the distal tubule of the nephron [22]. In this way, 1,25(OH)2D may enhance recovery of filtered calcium and contribute to the PTH effect of elevating the renal calcium threshold."

"The diets of hominids were high in calcium [25], just as are the diets of contemporary deer and other higher mammals. Foods available to contemporary hunter-gatherers exhibit an annual mean calcium nutrient density of 1.75-2 mmol (70-80 mg)/100 kcal. For individuals of contemporary body size, doing the work of a hunter-gatherer, that value translates to calcium intakes in the range of 50-75 mmol (2000-3000 mg)/day. But, as noted, the environment could not be relied upon to supply calcium-rich food continuously. Periods of fasting, famine, or drought would undoubtedly have threatened hypocalcemia. This fact underscores the importance both of bone as a calcium reserve and of the vitamin D-parathyroid hormone control system, with its ability to release calcium rapidly from bone.[3]"

"As noted elsewhere in this volume (Chapters 7 and 19), there is a gradient of concentrations of vitamin D receptors and of calbindin in mucosa along the gut, with highest levels in the duodenum and lowest in the colon mucosa. Accordingly, the avidity (or rate) of active absorption is highest in the duodenum. It is sometimes said that absorption itself is highest there, but this is not correct. That conclusion is based on studies of isolated loops or gut sacs, where movement of the chyme along the intestine cannot occur. Absorbed quantity is the product of absorption rate and residence time; and residence time of the chyme in the duodenum is very brief. Only at very low calcium intakes (or test loads), and with maximal 1,25(OH)2D-stimulated active transport, will it be true that most of the calcium absorbed will be from the duodenum. At more usual intakes, the much longer residence time in the jejunum and ileum means that most of the quantity absorbed occurs from the lower small intestine. The importance of length of exposure to the absorptive surface is reflected in the finding that absorptive efficiency varies directly with mouth-to-cecum transit time [36]."

"Absorption does not occur from the healthy stomach, and thus the beginning of absorption is delayed until gastric emptying begins. This, in turn, is dependent upon the character of the ingested meal or other calcium source. Emptying tends to be most rapid with small fluid ingestates and is slower with solid food and with fat. In healthy individuals ingesting light meals (such as would commonly be employed to test absorption efficiency), calcium absorption is nearly complete by 5 hours after ingestion [37]. Figure 34.3 presents data on the time course of absorption, using the ratio of the time-dependent apparent absorption fraction to its ultimate value in the individual being tested. As the figure shows, absorption has reached better than 80% of its ultimate value by 3 h after ingestion, and 96% by 7 h. There is then only a very gradual approach to completion over the next 20 h. This last component probably reflects a small amount of colonic absorption (or, alternatively, cecaleileal reflux, with delayed ileal absorption). It should be stressed that the percentage values in Figure 34.3 refer to the quantity absorbed, not the quantity ingested. Thus, with typically only 25-30% of a load absorbed (see later discussion), the 4-5% colonic component represents absorption of only about 1% of the ingested load."

"It has long been recognized that absorption efficiency varies inversely with intake. Figure 34.4 illustrates this relationship with data obtained from healthy, middle-aged women in whom unidirectional (i.e., gross) absorption fraction was measured under controlled metabolic ward conditions and plotted as a function of their ingested intakes [38]. The best fit regression line through the data shows the expected rise in gross absorption fraction at low calcium intakes. (Note, however, that even at the lowest intakes, predicted mean gross absorption efficiency is only ~45%.)"

"The higher efficiency at low intakes is traditionally attributed to adaptation, specifically to higher production of 1,25(OH)2D, with a corresponding increase in active calcium absorption. While that explanation is undoubtedly correct, it is also substantially incomplete. This is shown by the data in Figure 34.5, which plots non-adaptive absorption fraction as a function of a broad range of calcium load sizes. These studies were performed in women, assigned randomly on any given morning to intake loads spanning a 30-fold range, from 0.4 to 12.5 mmol [39]. Clearly, an inverse relationship is present, just as in the data of Figure 34.4. Equally clearly, it cannot be due to adaptation, since the test load was the first exposure these women had to the intake level concerned."

"Figure 34.6 plots these two sets of data together and shows that, while both exhibit an inverse relationship between absorption and intake, there is in fact a difference between them, with the adapted women absorbing more at low intakes than the non-adapted (as would be predicted). The zone between the two lines is a semiquantitative expression of the PTH-vitamin D-mediated adaptation to the lower intake.[5]"

"The most likely explanation for the inverse relationship observed under both sets of conditions is that calcium transfer, whether active or passive, is a slow, inefficient process, with only a limited number of carrier molecules or pores available at any given instant. In the brief interval between exit of a bolus of food from the stomach and the time it reaches the colon, only so many calcium ions can use the available transport. If the number of ions reaching the absorptive site is small, then by numerical necessity the fraction absorbed will be larger than when the number of ions is large."

"Absorption fraction (or efficiency) is thus a potentially misleading measure (at least if we stop there). It is, however, a necessary starting point because it is the primary datum available from most studies of absorptive physiology. Figure 34.7 presents the regression line from Figure 34.4 and adds a second line representing the actual quantity of calcium absorbed in these same women (i.e., the product of absorption fraction and intake). This variable is obviously the nutritionally relevant one since, in offsetting obligatory losses (or special demands such as antler building or fetal skeletal development), it is a quantity of calcium (not a fraction) that is needed to balance the drains created by calcium leaving the ECF."

"Figure 34.7 also illustrates another important aspect of this input to the calcium economy. At low intakes, absorption is quantitatively low, despite being relatively more efficient. A moment’s reflection suffices to show that a large fraction of a small number is, of necessity, a smaller number still. Thus, absorbing even a large fraction of a small intake cannot produce much calcium. The result is that, in the range of intakes commonly encountered among contemporary, industrialized humans, absorptive adaptation (via vitamin D) mitigates the problem created by a low intake, but it does not fully counterbalance it. A concrete example, employing realistic numbers, will help illustrate this point, and will show additionally how optimal operation of the vitamin D hormonal system is dependent upon -- and in fact presumes -- the kinds of high calcium intakes found among hunter-gatherer humans and high primates (in whom the system evolved)."

"Contrast how two individuals are able to respond to the increased obligatory loss occasioned by regular daily ingestion of an additional 100 mmol sodium (approximately the sodium contained in a single fast-food chicken dinner). Assume that one individual is ingesting 5 mmol Ca (200 mg)/day (corresponding to the lower quintile of calcium intakes in US women [40]), and the other, 40 mmol (1600 mg) (approximately the NIH Consensus Conference recommendation [41] for estrogen-deprived, postmenopausal women). Using data from the curve in Figure 34.4, the individual with the lower intake absorbs at an efficiency of 44.5% prior to the extra sodium load, and the individual with the higher intake, at 17.8%. (The first, therefore, has a gross absorbed quantity from the diet of 2.2 mmol/day, and the second, 7.1 mmol/day.) The increase in obligatory urinary loss occasioned by the increase in sodium intake will be about 1 mmol/day (see earlier discussion). To offset this loss, the first individual, with the low intake, would have to increase the absorbed quantity to 3.2 mmol/day, which means increasing the already high absorption efficiency by a factor of nearly 1.5 (from 44.5 to 64.5%). By contrast, the individual with the high intake needs to increase only from 17.8 to 20.3%. (These calculations are summarized in Figure 34.8.) The adjustment for the individual with a low calcium intake is substantially more than most adults can accomplish, while the second is easily accommodated. The first individual is forced, therefore, to get the needed additional calcium from bone, while the second easily gets it from her food."

The monovalent cations of sodium antagonize this protective action of calcium. Hence, the diet should take this fact into consideration by feeding less sodium while giving more calcium.

"Thus, while vitamin D plays a critical role in increasing absorptive efficiency in response either to increased losses from the body or to decreased intake, it must be stressed that there is little room in which the PTH-vitamin D endocrine system can operate when calcium intakes are already low. That does not mean that ECF [Ca2+] regulation suffers. The bony calcium reserves are vast e effectively limitless. So long as vitamin D status is above rachitic levels, those reserves will readily be drawn upon to support ECF [Ca2+], using the well-studied mechanisms already described. Naturally, if this drain continues, bone mass will inevitably decline. At high calcium intakes, such as prevailed during hominid evolution, the vitamin D hormonal system not only helps maintain ECF [Ca2+], but total body calcium as well; at low intakes, only the ECF is protected."


"Because of the relative scarcity of phosphorus in the biosphere, most organisms get the phosphorus they need by consuming the tissues of other organisms (plant and animal), and they absorb that ingested phosphorus with high efficiency. In adult humans, for example, net phosphorus absorption typically ranges from 55 to 80% of ingested intake, and in infants, from 65 to 90%. The most active site is the jejunum."

"Because phosphorus is intimately involved in virtually all of the functions and structures of living organisms, phosphorus content of most animal tissues varies little, ranging from 0.25 to 0.65 mmol [multiply by 31 for mg] per gram protein. The resulting ubiquitous distribution of phosphorus in all natural foods makes it all but impossible to construct, for patients on renal dialysis, a diet that is both nutritionally adequate and low in phosphorus."

"Most protoplasmic phosphorus in ingested foods is quickly hydrolyzed by intestinal phosphatases, and hence most absorbed phosphorus is in the form of inorganic phosphate [Pi]. The principal exception is the phosphorus in phytic acid (inositol hexaphosphate), which is the storage form of phosphate in seed foods (e.g., wheat, soy, etc.). The human intestine cannot hydrolyze phytic acid; hence absorption of phytate phosphorus is low. However colonic bacteria possess phytase and some phytate phosphorus is thus absorbed from the distal bowel. With this exception, intrinsic bioavailability of most food phosphorus sources is high."

"Absorption of phosphorus, as for calcium, is considered to be by a combination of active transport and passive diffusion, with the former being the regulated component. It is widely held that active phosphorus absorption is influenced by vitamin D status. Indeed, it is almost an article of faith that the canonical function of vitamin D is to promote absorption of calcium and phosphorus. However! Much of the evidence for this conclusion comes from animal experiments involving isolated gut loops or everted gut sacs, methods which, unfortunately, do not reproduce normal intestinal functioning. However, Ferrari et al. [35] showed in 29 normal humans that induced extreme changes in phosphorus intake induced not only the predicted changes in serum FGF-23 and urine phosphorus, but corresponding changes in serum 1,25(OH)2D. Briefly a large increase in phosphorus intake led to a decrease in serum 1,25 (OH)2D level, a change which, if associated with a reduction in phosphorus absorption, would suggest endocrine feedback regulation of phosphorus absorption. Ramirez et al. [45], using an intestinal wash-out method, showed an appreciable effect of large daily doses of calcitriol on meal phosphorus absorption in five patients on chronic hemodialysis, producing essentially normal phosphorus absorption efficiency, and suggesting that the loss of renal synthesis of calcitriol reduced phosphorus absorption in patients with end-stage renal disease. Nevertheless, as is well recognized clinically, dietary phosphorus absorption in ESRD patients is higher than the body can handle -- which is the rationale for use of intestinal phosphate binders. It is also true that the molecular apparatus for vitamin-D-stimulated active absorption of phosphorus exists in the intestine (see Chapter 19). That being said, it is unclear whether vitamin D exerts any strong regulatory control over phosphorus absorption under normal circumstances. And, instead, such vitamin D effects on phosphorus absorption as can be found in intact humans may be more indirect than direct."

"Heaney and Nordin [46] showed that, over a wide range of ingested calcium:phosphorus ratios, the principal determinant of fecal phosphorus (and therefore inversely of absorbed phosphorus) was fecal calcium, with phosphorus intake itself exerting a significant but weaker effect. Together, and altogether apart from vitamin D status, these two factors explain nearly three-fourths of the observed variance of phosphorus absorption in a large series of adult women. In their studies each 10 mmol of ingested calcium, by complexing phosphate in the intestinal lumen, blocked the absorption of ~4 mmol of diet phosphorus. (This phenomenon is, of course, the basis for the use of calcium salts as phosphate binders in patients with ESRD.) As calcium absorption rises in response to vitamin D, less calcium is left behind in the intestinal lumen to bind still unabsorbed phosphorus, and hence phosphorus absorption would predictably rise under conditions of high vitamin D status. But that would not necessarily mean that vitamin D directly stimulated phosphorus absorption."

 

[Vinero]

Hi,
If i take some calcium carbonate, would it be better to take it with meals or it doesn't matter?

Also i have noticed that the high calcium intake has helped with my depression, i assume it is lowering serotonin along other stress mediators.

I also notice calcium helps with with depression. Calcium carbonate is the one I use, I feel it raises dopamine considerably. Unfortunately I always seem to get irritated intestines. I wish there was a way to take calcium carbonate on a regular basis without getting the intestines irritated.

 

[Amazoniac]

I also notice calcium helps with with depression. Calcium carbonate is the one I use, I feel it raises dopamine considerably. Unfortunately I always seem to get irritated intestines. I wish there was a way to take calcium carbonate on a regular basis without getting the intestines irritated.

There's calcium acetate, malate, pyruvate, succinate, blossomate, georgiate, gilsonate, inautate, janellate, makroskate, mitate, tarmandate, travisate, vinerate, wagnerate, and many others. They all sound familiar.

 

[Vinero]

There's calcium acetate, malate, pyruvate, succinate, blossomate, georgiate, gilsonate, inautate, janellate, makroskate, mitate, tarmandate, travisate, vinerate, wagnerate, and many others. They all sound familiar.

Are any of those recommended by Peat?

 

[Amazoniac]

Are any of those recommended by Peat?

I don't know, but calcium carbonate contacts these acids during digestion, so I can't imagine a problem with them if not for contaminants or due to unreasonable amounts being used. Just to be clear, I'm not encouraging catabolism between members.

 

[RisingSun]

Is raw milk cheese an acceptable daily source of calcium?

 

[Spartan300]

Is serum calcium level much of an indicator?

The reason I ask is that blood test for me showed - Serum calcium level 2.46 mmol/L [2.2 - 2.6] but I feel my mood improves when I take supplemental calcium carbonate

 

[Wagner83]

I doubt the calcium/phosphorus ratio in white potatoes is to blame for immediate effects, but a ratio of 1:6 is concerning over time (2 kg gives you about 200 mg of calcium and 1200 mg of phosphorus) if not balanced with enough leafy greens, orange juice and other sources of calcium.

But sweet potatoes are much better, their ratio is 1:[1.5-2.5]. There are other tubers with a good profile as well.

Spoiler: Nutritive values of tropical root crops

Roots, tubers, plantains and bananas in human nutrition - Nutritive value

Effect of Soil Characteristics on Potato Tuber Minerals Composition of Selected Kenyan Varieties

This one may be a decent source of references : Phosphorus balance in potato tubers - [PDF Document]

I don't know about the reliability of this quote:
Cooking Methods May Help Dialysis Patients Control Phosphorus

"Frying potatoes in oil lowered phosphorus content by 37%, whereas steaming them reduced phosphorus content by 27%. Roasting frozen hake in oil led to a 49% decrease in phosphorus content. Soaking pork in water and then roasting it in oil led to a nearly 12% decrease in phosphorus content. Eliminating the soaking step eliminated this decrease, the investigators noted.

Boiling increased the calcium content in all foods because of calcium absorption from the hard water.."
​

One could use a high calcium water to steam them, but anytime I used the carbonated one for rice I had problems, although that may have had to do with an anti-acid effect (?). I wonder if steaming would allow for the calcium content to increase without any interference with digestion.

Tyw mentioned that Asians had less of a need for calcium intake, could the lowish phosphorus content of white rice be a reason?

 

[baccheion]

Calcium increases serotonin.

 

[Vinero]

Calcium increases serotonin.

Source?

 

[InChristAlone]

There's calcium acetate, malate, pyruvate, succinate, blossomate, georgiate, gilsonate, inautate, janellate, makroskate, mitate, tarmandate, travisate, vinerate, wagnerate, and many others. They all sound familiar.

Don't forget calcium amazoniate