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Calcium and Vitamin D Supplements in the Management of Postsurgical Hypoparathyroidism


My usual tx for hypoparaT is around 2000 mg calcium (Ca++) per day in 2 or 3 divided doses with meals (Ca++ carbonate or Ca++ citrate are fine). That should be enough Ca++ for most people. Any further adjusting of the Ca++ level is done with calcitriol, which is an activated form of vitamin D. We have to use that instead of Vitamin D2 or D3 (the typical Vit D supplement products) because parathyroid hormone (PTH) is needed for the activation step in the body. If you’re hypoparathyroid, we have to give a form of Vit D that skips that step.

I'll just go through your email and address your questions as they come:

--in hypoparaT Ca++ blood levels should be low normal or even a bit low, as long as symptoms are controlled (little or no tingling or cramping or spasms)--this helps avoid exposing the kidneys to too much Ca++, which can cause kidney failure over years.

--you mention albumin in the urine--that's likely unrelated to the Ca++ issues but if present above certain levels indicates kidney disease, such as the type caused by diabetes. The only way the Ca++ issue would relate to albumin in the urine would be that if you had low renal function due to some other problem, or likely future deterioration in function due to some other problem, you'd want to be as careful as you can that the Ca++ doesn't add to the kidney trouble.

--That said, it is critically important to keep adequate Ca++ levels in the blood, and it sounds like you're where you need to be, so I wouldn't worry about the urine Ca++ level. This is never going to be an ideal situation--hypoparaT puts the patient between a rock and a hard place--renal damage from the Ca++ tx is a real risk if things aren't done very carefully. It's not an easy disease for the doctor to manage.

--I especially wouldn't worry about the urine Ca++ if you don't have recurring kidneys stones or known renal insufficiency

--you are correct--active Vit D mainly helps gut absorption of dietary Ca++ and Ca++ tablets. It also tells the kidneys to reabsorb Ca++ into the blood and reduce loses via the urine. PTH does the same thing to Ca++ in the kidney but if you're missing that then the Vit D is more important. Eventually though, once the blood levels of Ca++ get high enough the Vit D effect is overwhelmed and Ca++ "spills" in the urine--and you want that--if it didn't happen you could get a dangerous high Ca++ in the blood. That's why I say, for the most part, let the kidneys do their thing and ignore the urine Ca++. The kidneys, if they're working right, are smarter than we are--we shouldn't be trying to outguess them.

--I think I've answered your question about Ca++ intake already--whatever combination of around 1800-2000mg Ca++/day plus calcitriol that results in the goal Ca++ level (right around the low end of normal) and good symptom control. If those criteria are met then I wouldn't adjust anything to "fix" the urine Ca++. If there are stones or other significant renal disease going on besides the hypoparaT then that is a complicated situation your doctor (preferably an endocrinologist or nephrologist in that case) has to figure out.

--I don't have a clue what good potassium bicarbonate would do--manipulating urine pH is something nephrologists do and if you need that you should be seeing one--I doubt you need it though, and my knee-jerk answer is don't take it, especially on your own, without the advise of the doctor managing this problem.

--You said "Vit K2"--Vitamin K affects blood clotting and has nothing to do with this--I assume you mean Vit D2, and I've already addressed that--D2 and D3 build up the storage form of Vit D but they can't be converted to the active form in HypoparaT (or for that matter, if there is significant kidney damage from any cause, because the activation step is done by the kidney). So, no, Vit D2 or D3--the stuff you can get over the counter--would be of no use in the situation as you described it to me. Calcitriol is your only Vit D (there are other similar prescription products but I just use calcitriol).

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Kuhnian Philosophy and the Glycemic Index


I have concerns about how the academic elite of medicine develop clinical practice guidelines intended to direct the care given by other physicians, as well as to inform insurers what ought and ought not be covered. There is a special need for scrutiny in this era where legitimate cost-containment, coupled with the increasing influence of third party payers, like federal and state governments, and the massive private insurance industry—which prioritize costs often over the wants and needs of patients and doctors—are driving “evidence-based medicine” and risk denying patients care and treatments not anointed by the “evidence.”

By this I mean a certain treatment or test, unless called for by a few top docs, at major medical schools, in their published guidelines, or supported by excellently conducted research reported in a scientific journal, might not be available to real-world patients. Perhaps worse, I think physicians today come out of training cowed by these top experts, devaluing their own thoughts and practice styles, subjugating them to evidence-based (“cookbook”) medicine. Keep in mind that every licensed medical doctor has an undergraduate degree, a four-year medical degree, and usually three-to-five-or-more years of post-graduate training. Such professionals are well trained enough to formulate their own preferred ways of managing patients, if encouraged and allowed (that is, paid) to do so, which they are often not.

Now, don’t misunderstand. Well-conducted research and peer-reviewed papers and clinical practice guidelines are necessary to good medicine. But once that information is out there, it should be the independent physician figuring out how to apply that data to each unique patient. No matter how good the research and conclusions, they can never anticipate all the variables confounding a real-world situation. And even if evidence-based medicine’s answers could be accepted as 100 percent valid, there will never be adequate evidence to answer every question faced by every physician in the course of one routine week.

Our original question from the text was:
Why did it take until less than ten years ago for low-glycemic-index dieting to get taken scientifically seriously? Smart people were talking about it. Why didn’t opposing theories get a fair shot at the height of the gung-ho all-fat-is-bad days? Isn’t the job of science to consider all possibilities, test for them, throw out ideas proved wrong, and refine ideas proved right, until gradually, inexorably we approach some great universal truth?

I used to think so.

Yet my experience has not always shown science to work that way.

There are several questions—low-fat versus low-carb being one, but there are others—in just my subspecialized area of medicine, where it seems to me experts wear bizarre blinders about even contemplating dogma-threatening new ideas. And I stumbled upon an explanation—or at least, objective confirmation of what I’ve observed—a mere few weeks prior to this writing.

Harvard-trained physicist, turned historian and philosopher of science, Thomas S. Kuhn (1922–1996) published a landmark book in 1962 titled, The Structure of Scientific Revolutions. In it, he threw out the notion that I had, and most of us have: That romantic view of science as, in the words of North Carolina State University philosopher, Jeffery L. Kasser, “straightforwardly cumulative, progressive, or truth-tracking.”

This traditional, romanticized image of science includes an “openness to criticism,” an almost obsession with disproving itself, that Kuhn felt did not exist in real-world science.

Normal science, according to Kuhn is governed instead by paradigms. A paradigm is an object of consensus, not open to criticism. The paradigm is assumed to be correct. It is dogma. It determines the puzzles to be solved, which involve fitting nature into the paradigm, and defines the expected results and the standards for evaluating those results. Science doesn’t seek truth, it seeks to prove the paradigm. “Dietary fat is unhealthy and the main promoter of obesity” was the paradigm in our discussion, and few mainstream researchers were allowed to, funded to, do research other than to prove that proposition. Read More 
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New Guidelines Call for Wider Use of Weight Loss Drugs


As Interim Medical Director of NexSlim at MMC, I wanted to take this opportunity to update you on the just-published AACE (Amer. Assn. of Clinical Endocrinologists) Comprehensive Diabetes Algorithm, which includes sections on prediabetes management, glycemic control in T2DM, and dyslipidemia—each of which begins, no surprise, with lifestyle modification. But, in each case that recommendation expressly includes “medically assisted weight loss.” Further, a separate algorithm for overweight and obesity calls for “medical therapy” if BMI is greater than 27 with cardiometabolic or biomechanical complications of either low, medium, or high severity, if lifestyle modification fails to achieve goals. They specify this medical therapy can include phentermine, orlistat, lorcaserin, or phentermine/topiramate ER—the latter two being Belviq and Qsymia, both approved by the FDA in 2012.

I find these recommendations groundbreaking, and no doubt will be controversial. Use of anorectic drugs has a historically poor reputation, and has been fraught with toxicity issues—in fact, every drug introduced prior to 2012 for long-term use for weight loss has had to be withdrawn from the market for that purpose, starting with thyroid extracts 120 years ago. My own experience with anorectics is admittedly limited, nor have I been impressed with their efficacy to the extent that I have used them. To be sure, there are genuine concerns about a lack of long-term maintenance of any weight loss that is achieved, but lifestyle interventions have the same failing.

All that said, we need to sit up and take notice that a major mainstream medical organization is strongly calling for the use of these drugs as part of a comprehensive, multifaceted effort. This is a recognition, and a call to action, that mainstream clinicians need to be managing overweight/obesity seriously, and specifically, and with every tool in the box, not just with vague advice, if we are to curb the epidemic of obesity and obesity-related diseases.

In light of the new AACE guidelines, I ask you to give consideration to the use of medically supervised weight loss, to include anorectic drugs when appropriate. Perhaps if we all used these drugs more, and smartly, as part of a comprehensive effort, we might see better results from them. Too often patients use them in a vacuum and street-corner weight-loss clinics dispense them that way, such that their failure is inevitable—perhaps we can do better.

Additionally, the prediabetes portion of the AACE algorithm called for metformin or acarbose use in mild prediabetes not resolving with lifestyle change, and consideration of adding pioglitazone and/or a GLP-1 receptor agonist, like exenatide, if needed, in more severe cases (high fasting and post-meal glucoses, for example).

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