Sunday, August 12, 2007

Calcium Needs After WLS

Calcium is one of the main supplements all bariatric centers require for their post-ops. But just how important is it? If you haven't already read the previous post I did on Vitamins, Medications, and Malabsorption After WLS, take the time to read it now.

Calcium plays a very important role in the human body. Being a woman, I pay particular attention to my calcium intake. Being a WLSer I really pay attention.

The partitioning of the stomach during bariatric surgery results in a dramatic decrease in the production of hydrochloric acid, affecting the absorption of calcium and iron. However, absorption can be increased by using different salt forms or manipulating gastric pH. Calcium carbonate depends on acid for its absorption; calcium citrate does not. One study comparing the bioavailability of both products in achlorhydric patients found the bioavailability of calcium carbonate and calcium citrate to be 4% and 45%, respectively. While calcium citrate is more expensive than calcium carbonate, it is logical to specifically recommend calcium supplementation with the citrate salt in this patient population. Decreased calcium absorption can increase the risk of osteoporosis. While specific guidelines to monitor bone density do not exist for these patients, early bone densiometry testing would be prudent.(I highly recommend this test)
Calcium citrate is the recommended form. Most of the calcium supplements found in stores are the calcium carbonate form. It doesn't work so don't waste your money. That includes those candy type chews many WLSers love. Viactive for example,which happens to be loaded with trans fats and high fructose corn syrup. Who wants that in your body anyway. Also do not waste your money on the ones that have vitamin D in them. Besides being the WRONG type of vitamin D---check out the earlier series. It is also not in an oil based form so it won't be absorbed, PERIOD. You need to read the labels on vitamins just as closely as all the food labels out there.

Since we are at a risk of calcium deficiency---this can lead to osteoporosis. Which I already have a problem with, but I'm working to correct it. Anyhoo, since osteoporosis is a problem many PCPs automatically want to put you on some of the meds to combat it. This is not a good idea.
The oral bisphosphonates (drugs for osteoporosis) are another class of medications that could present problems due to a reduced pouch size, which may increase the risk of gastrointestinal ulceration. Since these patients can be at risk for osteoporosis because of decreased calcium absorption, other treatment options (e.g., calcitonin salmon nasal spray, synthetic parathyroid hormone [teriparatide], raloxifene [for women]) should be considered.
These drugs are caustic to our pouch just like NSAIDS. We've all heard the horror stories about bleeding ulcers, ER trips, etc after taking NSAIDS. So the best thing to do is prevent the deficiency of calcium in the first place. The research is out there to prove it. Here are a few examples:
Metabolic bone disease after gastric bypass surgery for obesity.

BACKGROUND: The popularity of gastric bypass surgery for treatment of morbid obesity has been increasing in recent years. Osteomalacia and osteoporosis are commonly observed in patients who have had partial gastric resections for treatment of peptic ulcer disease. Recently, we encountered four patients with previous gastric bypass surgery who had metabolic bone disease similar to that reported in the older literature in patients who had partial gastrectomies.
METHODS: Review of clinical data of four patients who developed osteomalacia and osteoporosis 9 to 12 years after gastric bypass surgery for morbid obesity.
RESULTS: All subjects were women, 43 to 58 years old. Three had Roux-en-Y gastric bypass, and the other had a biliopancreatic diversion 9 to 12 years prior to presentation. Weight loss averaged 41.8 kg. Patients reported fatigue, myalgias, and arthralgias. They had symptoms for many months or years before the correct diagnosis was established. All were osteopenic or osteoporotic with hypocalcemia, very low or undetectable 25-hydroxyvitamin D levels, secondary hyperparathyroidism, increased 1,25-dihydroxyvitamin D levels, and increased serum alkaline phosphatase.
CONCLUSIONS: Relatively little has been published in the general medical literature about this postoperative complication of bariatric surgery. Yet, nearly all patients after bariatric surgery will receive their long-term follow-up from a primary care physician. Physicians and patients need to be aware of this complication and take measures to identify and prevent it.
Bone and gastric bypass surgery: effects of dietary calcium and vitamin D.

OBJECTIVE: To examine bone mass and metabolism in women who had previously undergone Roux-en-Y gastric bypass (RYGB) and determine the effect of supplementation with calcium (Ca) and vitamin D.
RESEARCH METHODS AND PROCEDURES: Bone mineral density and bone mineral content (BMC) were examined in 44 RYGB women (> or = 3 years post-surgery; 31% weight loss; BMI, 34 kg/m(2)) and compared with age- and weight-matched control (CNT) women (n = 65). In a separate analysis, RYGB women who presented with low bone mass (n = 13) were supplemented to a total 1.2 g Ca/d and 8 microg vitamin D/d over 6 months and compared with an unsupplemented CNT group (n = 13). Bone mass and turnover and serum parathyroid hormone (PTH) and 25-hydroxyvitamin D were measured.
RESULTS: Bone mass did not differ between premenopausal RYGB and CNT women (42 +/- 5 years), whereas postmenopausal RYGB women (55 +/- 7 years) had higher bone mineral density and BMC at the lumbar spine and lower BMC at the femoral neck. Before and after dietary supplementation, bone mass was similar, and serum PTH and markers of bone resorption were higher (p <>
DISCUSSION: Postmenopausal RYGB women show evidence of secondary hyperparathyroidism, elevated bone resorption, and patterns of bone loss (reduced femoral neck and higher lumbar spine) similar to other subjects with hyperparathyroidism. Although a modest increase in Ca or vitamin D does not suppress PTH or bone resorption, it is possible that greater dietary supplementation may be beneficial.
Now that we know what a problem it can be after WLS. Let's get a little background on calcium. I'll reference one of my favorite sites for vitamins and minerals--Linus Pauling Institute.
Calcium is the most common mineral in the human body. About 99% of the calcium in the body is found in bones and teeth, while the other 1% is found in the blood and soft tissue. Calcium levels in the blood and fluid surrounding the cells (extracellular fluid) must be maintained within a very narrow concentration range for normal physiological functioning. The physiological functions of calcium are so vital to survival that the body will demineralize bone to maintain normal blood calcium levels when calcium intake is inadequate. Thus, adequate dietary calcium is a critical factor in maintaining a healthy skeleton.
Calcium is a major structural element in bones and teeth. Bone is a dynamic tissue that is remodeled throughout life. Bone cells called osteoclasts begin the process of remodeling by dissolving or resorbing bone. Bone-forming cells called osteoblasts then synthesize new bone to replace the bone that was resorbed. During normal growth, bone formation exceeds bone resorption. Osteoporosis may result when bone resorption exceeds formation.
Calcium plays a major role in bone formation, this everyone knows. But calcium is so much more than that. The human body is a complex being. There are many checks and balances on the cellular level. One little thing gets out of whack, the whole system is messed up. Here are some functions of calcium:
Calcium plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones like insulin. Excitable cells, such as skeletal muscle and nerve cells, contain voltage-dependent calcium channels in their cell membranes that allow for rapid changes in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions into the muscle cell. These calcium ions bind to activator proteins within the cell, which release a flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein, troponin-c, initiates a series of steps that lead to muscle contraction. The binding of calcium to the protein, calmodulin, activates enzymes that breakdown muscle glycogen to provide energy for muscle contraction.
So it controls cell membranes, muscles, enzymes and hormones too. But it also plays a role in blood clotting.
Calcium is necessary to stabilize a number of proteins and enzymes, optimizing their activities. The binding of calcium ions is required for the activation of the seven "vitamin K-dependent" clotting factors in the coagulation cascade (see vitamin K). The term, "coagulation cascade," refers to a series of events, each dependent on the other that stops bleeding through clot formation.
Regulation of calcium in the body is tightly controlled, through a vast series of checks and balances.
Calcium concentrations in the blood and fluid that surrounds cells are tightly controlled in order to preserve normal physiological function. When blood calcium decreases (e.g., in the case of inadequate calcium intake), calcium-sensing proteins in the parathyroid glands send signals that result in the secretion of parathyroid hormone (PTH). PTH stimulates the conversion of vitamin D to its active form, calcitriol, in the kidneys. Calcitriol increases the absorption of calcium from the small intestine. Together with PTH, calcitriol stimulates the release of calcium from bone by activating osteoclasts (bone resorbing cells) and decreases the urinary excretion of calcium by increasing its reabsorption in the kidneys. When blood calcium rises to normal levels, the parathyroid glands stop secreting PTH and the kidneys begin to excrete any excess calcium in the urine. Although this complex system allows for rapid and tight control of blood calcium levels, it does so at the expense of the skeleton.
The parathyroid glands sense the serum calcium level, and secrete parathyroid hormone (PTH) if it becomes too low, for example, when dietary calcium intake is inadequate. PTH stimulates the activity of the 1-hydroxylase enzyme in the kidney, resulting in increased production of calcitriol, the biologically active form of vitamin D3. Increased calcitriol production restores normal serum calcium levels in three different ways: 1) by activating the vitamin D-dependent transport system in the small intestine, increasing the absorption of dietary calcium, 2) by increasing the mobilization of calcium from bone into the circulation, and 3) increasing the reabsorption of calcium by the kidneys. PTH is also required to increase bone calcium mobilization and calcium reabsorption by the kidneys. However, PTH is not required for the effect of calcitriol on the intestinal absorption of calcium.
Now we see that calcium is strictly regulated. As WLSers, we become deficient simple because we don't absorb enough. Or is something else the cause???
A low blood calcium level usually implies abnormal parathyroid function and is rarely due to low dietary calcium intake since the skeleton provides a large reserve of calcium for maintaining normal blood levels. Other causes of abnormally low blood calcium levels include chronic kidney failure, vitamin D deficiency, and low blood magnesium levels that occur mainly in cases of severe alcoholism. Magnesium deficiency results in a decrease in the responsiveness of osteoclasts to PTH. A chronically low calcium intake in growing individuals may prevent the attainment of optimal peak bone mass. Once peak bone mass is achieved, inadequate calcium intake may contribute to accelerated bone loss and ultimately to the development of osteoporosis.
So once again things fall back on vitamin D deficiency. Now you see why I devoted 4 blog posts to vitamin D alone. It is THAT important. Also, I'm sorry to say, one that is frequently overlooked. Magnesium plays a role here too, so make sure to add that to your arsenal of supplements.

Several things can also play a part in the utilization of calcium by the body, sodium, protein, phosphorus, and caffeine.
High sodium intake results in increased loss of calcium in the urine, possibly due to competition between sodium and calcium for reabsorption in the kidney or by an effect of sodium on parathyroid hormone (PTH) secretion. Each 2.3-gram increment of sodium (6 grams of salt; NaCl salt) excreted by the kidney has been found to draw about 24-40 milligrams (mg) of calcium into the urine. Because urinary losses account for about half of the difference in calcium retention among individuals, dietary sodium has a large potential to influence bone loss. In adult women, each extra gram of sodium consumed per day is projected to produce an additional rate of bone loss of 1% per year if all of the calcium loss comes from the skeleton. Although animal studies have shown bone loss to be greater with high salt intakes, no controlled clinical trials have been conducted to confirm the relationship between salt intake and bone loss in humans. However, a 2-year study of postmenopausal women found increased urinary sodium excretion (an indicator of increased sodium intake) to be associated with decreased bone mineral density (BMD) at the hip. Additionally, a longitudinal study in 40 postmenopausal women found that adherence to a low sodium diet (2 grams/day) for six months was associated with significant reductions in sodium excretion, calcium excretion, and aminoterminal propeptide of type I collagen, a biomarker of bone resorption. However, these associations were only observed in women with baseline urinary sodium excretions equal to or greater than 3.4 grams/day (i.e., the mean sodium intake for the U.S. adult population).

As dietary protein intake increases, the urinary excretion of calcium also increases. Recommended calcium intakes for the U.S. population are higher than those for populations of less industrialized nations because protein intake in the U.S. is generally higher. The RDA for protein is 46 grams/day for adult women and 56 grams/day for adult men; however, the average intake of protein in the U.S. tends to be higher (65-70 grams/day in adult women and 90-110 grams per day in adult men). Weaver and colleagues have calculated that each additional gram of protein results in an additional loss of 1.75 mg of calcium/day. Because only 30% of dietary calcium is generally absorbed, each one-gram increase in protein intake/day would require an additional 5.8 mg of calcium/day to offset the calcium loss. At the other end of the spectrum of protein intake, the effect of dietary protein insufficiency on bone health has received much less attention. Inadequate protein intakes have been associated with poor recovery from osteoporotic fractures and serum albumin values (an indicator of protein nutritional status) have been found to be inversely related to hip fracture risk.

Phosphorus, which is typically found in protein-rich foods, tends to decrease the excretion of calcium in the urine. However, phosphorus-rich foods also tend to increase the calcium content of digestive secretions, resulting in increased calcium loss in the feces. Thus, phosphorus does not offset the net loss of calcium associated with increased protein intake. Increasing intakes of phosphates from soft drinks and food additives have caused concern among some researchers regarding the implications for bone health. Diets high in phosphorus and low in calcium have been found to increase parathyroid hormone (PTH) secretion, as have diets low in calcium. While the effect of high phosphorus intakes on calcium balance and bone health is presently unclear, the substitution of large quantities of soft drinks for milk or other sources of dietary calcium is cause for concern with respect to bone health in adolescents and adults.

Caffeine in large amounts increases urinary calcium content for a short time. However, caffeine intakes of 400 mg/day did not significantly change urinary calcium excretion over 24 hours in premenopausal women when compared to a placebo. Although one observational study found accelerated bone loss in postmenopausal women who consumed less than 744 mg of calcium/day and reported that they drank 2-3 cups of coffee/day, a more recent study that measured caffeine intake found no association between caffeine intake and bone loss in postmenopausal women. On average, one 8-ounce cup of coffee decreases calcium retention by only 2-3 mg.
Sodium is not a problem for me. I don't use very many processed foods. I even make my own ketchup and tomato based products, as well as my own soups. Canned veggies, soups, and prepackaged meals are loaded with sodium. So are deli meats. These are things everyone needs to avoid.

Protein, now that is problem being on a low carb eating plan. Also most WLSers are told to get in at least 70gm of protein a day. So what really is my proper protein requirement? The easiest way to calculate protein intake is use the formula a fellow low carber posted. You don't have to be doing low carb to utilize this formula---although I recommend it---low carb is really the only way to eat after WLS. Especially if you want to be successful.

How to Calculate How Much Protein You Need

Phosphorus, I think it's funny that the main sources people use for there daily calcium intake also contain phosphorus which inhibits calcium. I'm talking about dairy products, milk, yogurt, and cheese. Now ain't that a kicker. I want to emphasize the bit about the sodas. Every bariatric center tells their clients--NO MORE SODAS--but very few listen. Most are addicted to them. If you havent't given yours up, maybe this will convince you to do it. Me included. I don't drink them but maybe one or two a month. But that stopped when I began doing this series.

Caffeine, here is my achilles heel, I'm a coffee hound. I don't drink just one or two cups. It's more like one or two pots. I also live on tea---hey this is the south. So this is an area I sorely need to work on. But I dread the headache I'm sure to have. But I will be better off without it.

Alrighty now y'all, that's it for this post. Remember to take your own health into your own hands. Make sure your doc is doing the proper labs. Get a print out of it to make sure. As for the calcium, most all of us take it post-op. But we don't take the vitamin D and that is the crucial part. So keep a running list of the labs you need to have done as we continue on with this series.

Also this research just came in---Skeleton Is An Endocrine Organ, Crucial To Regulating Energy Metabolism.

Bones are typically thought of as calcified, inert structures, but researchers at Columbia University Medical Center have now identified a surprising and critically important novel function of the skeleton. They've shown for the first time that the skeleton is an endocrine organ that helps control our sugar metabolism and weight and, as such, is a major determinant of the development of type 2 diabetes.
So there you have it---if we take proper care of our skeleton, we can effect our weight too. Need any more reason to make sure your take your vitamins???