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Hypothyroidism management options

I will take this from the beginning, assuming that I am seeing a patient not previously on thyroid replacement who has just had a total thyroidectomy. Your subject heading specifies athyreosis; however the principles and my practice are the same for a spontaneously hypothyroid patient with, say, Hashimoto's thyroiditis, except that the starting dose will be higher for the postsurgical patient, since they will obviously require full replacement—all of their thyroid needs met by exogenous replacement. As I say, most of what follows applies to both situations, although you are correct that there can be additional challenges in the athyreotic patient.

I'm going to take this from the beginning because—while your question specifies "not responding to monotherapy" (which I take to mean levothyroxine [LT4] monotherapy)—because I think "currently failing monotherapy" is different from saying "monotherapy is inappropriate." It depends on how effectively and skillfully the LT4-only treatment is being implemented. I am a firm believer based on over 30 years of doing this, that most doctors, including most endocrinologists, don't dose LT4 high enough. LT4-only Tx tends to get a bad rap on patient-oriented websites, not because it doesn't work in many, if not most, cases, but because it gets underdosed.

Why? There are a number of reasons:
—It is a common, but I believe wrong practice to monitor TSH only. I believe it is easy to miss underreplacement if you don't also look at a T4 level, usually a modern FreeT4 assay. FreeT3 is less often truly useful, although it can be very important as we will get to. So, to answer one of your questions, I usually get a TSH + FT4 + FT3, especially early on, until it is clear the additional information provided by the FT3 isn't worth the additional cost. But, I almost always get at least a TSH + FT4, even in people I've been following for years.
—And, regardless of what tests are ordered, I find it all too common that ANY level somewhere within the lab report's published reference range ("normal" range) is accepted as an indicator of adequate thyroid replacement. Often that ends up meaning dosage adjustments are stopped if the levels are JUST BARELY normal. That might be okay and it might not, and the determining factor is the patient's symptoms. If the patient feels good we're done, and if not, we're not. Although too often symptoms are ignored in the face of "normal" lab results. Endocrinologists are particularly guilty of this because we tend to be taught to treat the numbers not the patient, which flies in the face of my earlier internal medicine training to treat the patient not the numbers. The statistical disconnect is this: The lab's reference range represents what is STATISTICALLY normal for the population, NOT what is necessarily PHYSIOLOGICALLY ideal for an individual patient. That individual physiologically ideal range is always narrower than the population statistical range, usually, but not always lying within the population range. Sometimes an individual's ideal level will lie outside of the lab's reference. In fact, by statistical definition 5% of normal people will have an abnormal result on any given lab test (2.5% above, and 2.5% below).
—Relatedly, another reason LT4 gets underdosed is that low TSH's are almost universally interpreted to mean the patient is overreplaced, and same with high FT4's and FT3's. When in fact there is no question that some patient's need to be run with a low TSH or a high FT4 or FT3 (these are people with central hypothyroidism and thyroid hormone resistance, respectively).
—Lastly, it is not generally recognized that if a TSH does become suppressed by true overreplacement, or other reasons, it can be very slow to rise back to normal—leading to obsessive, repeated reductions in LT4 dose to get the TSH up. This is a good reason not to follow TSH's alone.

Okay, so I will start LT4 at some appropriate starting dose (I encourage Synthroid or one of the other branded products, but if cost is an issue, starting with generic LT4 is okay). It takes at least 5 weeks to see the full effect of any given adjustment, so it is almost never appropriate to check labs sooner than that. Generally speaking I will increase the LT4 dose in baby steps—one dosage at a time (125, to 137, to 150, to 175, etc., for example)—until the TSH is <2.0 and the FT4 is mid to high normal and the patient is no longer symptomatically hypothyroid.

If hypothyroid symptoms remain in spite of labs meeting those criteria, then I make further cautious upward adjustments, monitoring FT4, FT3, and TSH, and symptoms. If the TSH becomes low and the patient is not symptomatically HYPERthyroid, I often will not back off because of that—although I warn you most doctors will.
—if the patient is taking generic LT4 I will switch to synthroid or another name brand, and sometimes people feel better just from that.

If the above does not find a dose that resolves the hypothyroid symptoms—which is getting to the meat of your question—especially if the FT4-to-FT3 ratio is high, suggesting inadequate T4 to T3 conversion, then I will add brand-name Cytomel or generic liothyronine (LT3) 5 mcg once daily, taken first thing in the morning on an empty stomach. Depending on a number of factors I might or might not reduce the LT4 dose at the same time. If all that is added or adjusted is LT3, then labs can be checked in 3 weeks, but any adjustment in LT4 demands labs be delayed for 5 weeks or longer. When using combination therapy (LT4 + LT3) the labs I monitor are: TSH + FT4 + FT3 + SHBG, and I calculate a FT4-to-FT3 ratio.

SHBG is sex-hormone binding globulin—which is simply a protein the liver produces more of, the more the thyroid-hormone receptors deep within the nuclei of the liver cells are stimulated. This makes SHBG a sometimes useful biomarker for TISSUE thyroid levels, as opposed to SERUM levels. Remember, what we really care about in the situation you are asking about is not how much thyroid hormone is in the blood—which is what we measure out of necessity—but rather how much the thyroid hormone receptor (THR) is being stimulated deep in the body's tissues. The SHBG reflects PERIPHERAL THR stimulation, and the TSH is a reflection of BRAIN and PITUITARY THR stimulation. One thing almost no doctor considers is that the amount of thyroid hormone that adequately stimulates those BRAIN THRs, thereby suppressing TSH, is less than what it takes to adequately stimulate the PERIPHERAL THRs all over the body outside the brain. This is how you can have a low TSH, suggesting overtreatment, while the patient still feels hypothyroid because the peripheral THRs want more thyroid hormone. (This represents relatively recent research that is not widely disseminated—but was discussed in a meeting I attended in Chicago a couple of years ago, conducted simultaneously and virtually with a meeting of endocrinologists in London).

Before finishing up, let me back up and talk about the general topic of LT4 + LT3 combination therapy. As you may know, T3 is the less abundant but more potent form of thyroid hormone—it is the more active form of the hormone. The thyroid gland directly secrets about 6% of the body's daily need for T3. The rest is produced all over the body (brain, liver, kidney, muscle) via T4 to T3 conversion. For this reason, most hypothyroid patients don't need to be given LT3. Their bodies take the LT4 and convert it to however much T3 is needed by any given organ at any given time. However, some patients do benefit from the combination if they convert less efficiently—sometime the LT4 replacement will suppress conversion—and a clue to that as I've said, can be a high FT4-to-FT3 ratio (although that is not a terribly commonly used parameter by most doctors), or simply the scenario that you present: failure to respond well to monotherapy. The athyreotic patient will of course lack that small percentage of T3 that the thyroid gland directly produces, and so they are at least theoretically more likely to benefit from the combination. Some not-particularly-well-informed pundits on the Internet will argue that "natural" thyroid products that contain both T4 and T3 are always better than LT4 alone, which is simply not true. In fact, LT4 monotherapy, with the body making its own T3, mimics normal human physiology more closely (where the thyroid makes a lot of T4 and very little T3) than giving a lot of LT3 does.

There are two ways to give LT4 + LT3 combo therapy. My preference is, as I presented above, adding once daily LT3, 5 mcg, to LT4. If needed a second or even third daily dose can be added, generally taken no later than 3 p.m. so as not to disrupt sleep. Some people do okay taking the 2 or 3 LT3 pills all together in the morning for convenience and better compliance, but usually spreading the doses out through the first half of the day is more effective. Unlike LT4, LT3 does not have a long enough serum half-life to last all day on just a single dose.

The other option some patients prefer—and this isn't my first choice, but I will not uncommonly switch to this route if the response to LT4 + LT3 is inadequate, or the patient really wants to try it—is a desiccated thyroid extract (DTE) product. There are a number of these out there but the best known—and most reliably available—is Armour Thyroid. These products get their thyroid hormone from pork thyroid glands harvested from slaughter houses (the "Armour" name literally came from the Armour meat packing company). Some argue that DTE products are better because they are "natural." Not true. Whether or not they work better for some individuals, the "natural" part has nothing to do with it. The main active ingredients are chemically identical to synthetic LT4 and LT3. That said, these animal thyroid glands probably contain some minor metabolites of thyroid hormone (T1, T2, sulfated TH, etc.) that would not contaminate the synthetic products, and it is at least theoretically possible some people do detect some benefit from them. It is very unclear however that these things have any significant biologic activity.

One problem with DTE monotherapy that is clear is that it contains more T3 relative to T4 than is appropriate for humans, resulting in a low T4-to-T3 ratio. The practical result of that is that in virtually all cases in my experience, if the FT3 is adjusted to normal, then the FT4 is low, and if the FT4 is adjusted to normal, the FT3 is too high. It may in fact be that a "stimulant" effect from that extra T3 results in the "cult following" DTEs have amongst some so-called experts, but that does not make the situation safe, or physiologic, or even "natural." If a patient really wants to be be on a DTE, or seems to truly benefit from it, what I will often do is add a small dose of LT4 to the DTE, and fine-tune the two drugs to achieve a normal FT4-to-FT3 ratio. The labs I monitor for either DTE monotherapy or combined LT4 + DTE are the same as I gave above for monitoring LT4 + LT3 combo therapy, because all the issues are the same.

I hope that helps. Perhaps more than you wanted to know, but I think one of the problems with run-of-the-mill hypothyroidism management these days is that most doctors, including many endocrinologists, think it is a lot simpler than it really is.

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"Rescue Kits" for an Adrenal Crisis

(Be sure to read the comments below for important updates regarding newer guidelines for using home rescue kits in AI--Dr Rone)


I have been corresponding with the daughter of an elderly physician who passed away at least partly as a result of inadequate management of an "adrenal crisis" in which an illness or injury or surgery can't be tolerated by a patient missing adequate adrenal function, if they don't receive emergency doses of glucocorticoid steroids. In the wake of recent new stories about EpiPens, she asked me about home injection kits for adrenal patients, paralleling products available to severely allergic patients and those with diabetes, who might suffer a low blood sugar. Here was my reply to that interesting question…

I haven't specifically looked but I have never heard of a specific "rescue kit" manufactured for adrenal insufficiency patients, analogous to the EpiPen for anaphylactic shock and GlucaGen for diabetes. Obviously injectable and suppository hydrocortisone products do exist and could be prescribed to patients to have on hand for emergency use, although it is not to my knowledge and common or even recommended practice. I don't believe I have ever done so. And, no, I have no specific manufacturers to recommend.

I have two answers to why this is so. The first might not be very satisfying: adrenal insufficiency is not as common as diabetes or severe allergies to penicillin, bee stings, and peanuts. The second answer is that the "rescue kit" for AI is patient education plus the usual oral glucocorticoid replacement agents, typically hydrocortisone or prednisone. By that I mean, patients should be instructed by their physicians to double their usual doses on certain kinds of sick days (high fever, for instance). When the illness or developing adrenal crisis is so severe as to cause nausea and vomiting, preventing oral intake of glucocorticoids, then the patient must either contact his or her physician urgently, or go to the ER. That of course presupposes that the resource--the ER for example--believes the patient and knows what to do. The wearing of a Medic-Alert bracelet identifying the patient unequivocally as an adrenal insufficiency suffer IS a common recommendation and should cut through any questions in an ER.

Proper treatment then in the ER would be to treat the underlying illness causing the crisis, making sure hydration is maintained with IV fluids if needed, and providing adequate (often "stress dose") glucocorticoid replacement by IV or rectally, until oral dosing can reliably resume. That of course may involve a hospital admission.

So, why should not parenteral (that is, rectal or by intramuscular shot) glucocorticoids be available to patients at home? Simple. A single big dose of hydrocortisone, for instance, would provide short-term support, but once it's cleared from the body in 8 or 12 hours, the patient will be right back in trouble again, and perhaps worse. If for example the crisis were brought on by a severe infection, like pneumonia, the situation might well be worse in 8-12 hours if the infection hasn't gotten treatment. It might be worse due to the normal progression of the infection if unchecked by antibiotics, or the hydrocortisone shot might have made things worse. Steroid replacement might well be life-saving for some of the patient's problems, but since it suppresses the immune system, the pneumonia might easily worsen, the patient become septic possibly, and die for that reason.

In other words, it is much more likely that a single patient-administered dose of epinephrine or glucagon will definitively see a patient through an entire episode of a food allergy or "insulin shock," than a single steroid shot would see an AI patient through a crisis.

I hope that helps.

Dr. Rone

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The Millennial Medical License

I am president of a large multispecialty group, and a “Boomer.” By that I mean, Baby Boomer. Recently the chief executive officer of our group and I and one of our office managers got an email from a young physician who had left us on good terms four months earlier. As far as we are aware, the only motivation behind his departure was his spouse, a surgical specialist, accepting an attractive job offer out of state. In the email, the physician—let’s call him, “Dr. M” for “Millennial”—described receiving a forwarded piece of mail from his old address. It was a bill for $400 from our state tax agency, stating his Professional Privilege Tax was overdue. Dr. M protested that he had expected us to deactivate his license, and requested we pay the tax bill resulting from this “lapse.”

Now, as I’m sure is common in bigger practices, our office managers and other administrative support personnel do routinely handle the physicians’ licensing issues, along with all the other myriad credentialing matters necessary to modern health care. When I arrived fresh from more than a decade in the Air Force 18 years ago, except for providing a few documents and signatures, all the hoop-jumping required to obtain my shiny new state license was indeed accomplished by my new office manager. And ever since, all those annual taxes and every-other-year renewals have been dealt with, virtually without my knowledge, by her, or her successor. Dr. M’s experience was no doubt similar in his 3 years with us. Accordingly, I can understand the nuts and bolts of state licensing—of maintenance as well as divestment—slipping through the cracks of a busy mind, preparing for a big move of both family and career.

I was however struck by the callousness of Dr. M’s thinking about his license once the matter came to the fore. When advised, in so many words, to take the issue up with the state, he replied he had never intended to maintain the license, and again emphasized his expectation that we would have “retired” it upon his departure.

It is Dr. M’s prerogative—no argument—to surrender or inactivate, or whatever, the relevant license assuming he no longer plans to practice medicine here. Be that as it may, it is neither our responsibility, nor within our power, to surrender any physician’s license. This confusion seems stranger still, since Dr. M came to us out of a fellowship program not far away—in other words, already possessing the license in question. Do large academic institutions, with bureaucracies far bigger than ours, apply for and maintain licenses for their trainees? I don’t know. But for whatever reason, it seems Dr. M never took ownership of his state medical license. Perhaps the fault of “helicopter office-managering.”

I took from this exchange, however, deeper concerns, and proposed a hypothetical. What if he loved some picturesque corner of our state and wanted to spend a month there annually doing locum tenens work? Even if the furthest thing from his mind today, what about in a year, or 5 or 10 years in the future? Not a likely scenario, I’ll grant you. My point being, it would be inappropriate for any soon-too-be ex-employer to assume Dr. M did not wish to avail himself of that freedom.

At that point he probably thinks I went a little “survivalistic” on him. What was really nagging me was the disrespect being shown the ethos, the essential nature, of medical licensure. To me, a “license to practice medicine and surgery” framed and mounted on my wall represents my right to ply my skills as a physician unfettered (relatively so) within the stated jurisdiction. It represents, at the basest level, my ability to earn my living in my chosen profession. It is a valuable personal and professional asset. And it is intrinsic to the physician. It represents his or her covenant with the state, with one of the fundamental governing instruments of our social order. It does not belong to an employer, to a hospital, to a clinic: it belongs to the doctor. In my reply to Dr. M I counseled he ought not want any third party having enough power and privilege over him to intervene between him and the agency granting him his right to practice. He believes we erred not unilaterally inactivating his license? Careful what you ask for… I shudder over the ramifications of the opposite error—curtailing a physician’s license without his/her knowledge or consent.

Most assuredly, differing fee schedules from state to state render it more or less practical for licenses to be maintained that are not required in a current practice setting. I don’t know what Dr. M’s financial options were here, and again, keeping or not keeping that license was entirely his affair. Speaking for myself—I have maintained a license in my home state since 1989, even though I haven’t cared for a patient there since medical school. I worked off that license in the military but I haven’t have that need for it in 18 years. To me—the “readiness is all” survivalist in me—it represents insurance. The peace of mind and security of knowing I can move to that other state anytime I need or want to and establish a medical practice without asking anybody’s permission, or waiting for the gears of bureaucracy to slowly mesh before I can start earning a living.

I don’t know if Dr. M’s emailed concern was idiosyncratic or generational or what it was. Perhaps I’m overreacting. Or perhaps this is yet another symptom of our profession devaluing itself—more “cookbooking” and “corporatizing” and “out-sourcing” and “shift-working” of medicine. My clarion call to Dr. M and to all of us: grant the medical license the respect it deserves, consider it a professional asset, a source of personal pride, alongside one’s diplomas and board-certification documents. In other words—more than just a piece of red tape you expect somebody else to cast aside for you. Read More 
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My Health is Not Where I Want it to Be

A lady from another state contacted me by email stating that she was diagnosed with hypothyroidism at age 13, and that she had rising thyroid peroxidase antibody (TPOAb) levels, which concern her. She is frustrated because her physicians haven’t been “interested in looking at that [the antibody levels].” I don’t have details, but she reports having been on the “gamut” standard and alternative therapies for hypothyroidism, yet her health is still not where she would like it to be—her words.

What follows is an edited, and somewhat augmented, version of my reply to her, which I prefaced with the statement that there were positives and negatives in those comments regarding whether I might be able to help her, or at least provide her what she said she was looking for—essentially a partner in holistic therapy of her thyroid condition.

My positive comments, with respect helping were as follows:

If she was diagnosed with hypothyroidism at age 13, the diagnosis was likely fairly definitive, and abnormal TPOAb’s add weight to that. My point being, if there is good hard laboratory evidence of hypothyroidism and/or Hashimoto’s thyroiditis (not the same thing: hypothyroidism is a lack of thyroid hormone, which can be due to a number of causes; Hashimoto’s is an autoimmune disorder that is an important cause of hypothyroidism, though not all Hashimoto’s patients are hypothyroid), then it is much more likely that there is some relatively straightforward therapy that will help. As opposed to: well, it sounds like hypothyroidism, but the numbers don’t clearly show it. I do treat some of those people and sometimes it helps and sometimes it doesn’t. I went on to tell her—the fact she has been on some form of thyroid therapy for over 25 years makes it likely her hypothalamic-pituitary-thyroid axis has been to some degree suppressed by outside thyroid hormone. This might result in lower TSH levels than expected for any given situation, which would lead many physicians, many endocrinologists included, to undertreat.
So there are features to this individual’s story, and I’ve heard similar ones quite often, that make me think I might be able to help her, and I told her that.

Now for the negative—and I really shouldn’t say negative, I just mean, advice, counsel, constructive criticism, disclaimers… First she mentioned as part of her plea that she had been under stress for a long time. I’m unaware that there is any general recognition that a stressful lifestyle causes or worsens Hashimoto’s or hypothyroidism, except perhaps amongst certain authors and internet “experts” who may or may not really know what they’re talking about. In fact, I might argue the opposite—that hypothyroidism, causing fatigue and depression, makes life more stressful, and lessened one’s ability to cope with the ordinary stresses of life. In other words, hypothyroidism causes stress, rather than stress causing hypothyroidism.

Having said that, I will hasten to add two points: (1) a catastrophic emotional event, like the death of a spouse, or beloved pet, is well known to trigger Graves’ disease, an autoimmune thyroid disorder causing hyperthyroidism—high thyroid levels—but that type life event is different from chronic “normal” stress; and (2) one thing I do believe stress can do is elevate cortisol (a type of steroid) release from the adrenal glands, and cortisol suppresses TSH release. If TSH is suppressed, the thyroid gland might not be properly stimulated to make thyroid hormone. This would be a form of so-called “central hypothyroidism,” in which the person is hypothyroid without the expected elevation of TSH that is usually seen. This is one of the big differences in my approach to hypothyroidism from other doctors, including endocrinologists. Nobody doubts central hypothyroidism exists, but it is felt to be rare and is seldom considered. I, on the other hand, think it might be quite common and rampantly missed. And since there is no test to confirm it (the test is the TRH stimulation test, which requires a drug that is no longer available in the United States), the only thing to do if it’s suspected is to start thyroid hormone replacement and see if it helps.

So, I should modify my above statement about stress. I doubt chronic life stress causes primary hypothyroidism due to Hashimoto’s thyroiditis, but it might cause central hypothyroidism, either as a problem by itself, or one that might further worsen existing primary hypothyroidism.

I agree therefore that stress could be part of this lady’s problem; we just need to be clear what it is or isn’t doing. Also, the very stressful, busy lifestyle she described to me, can make one feel lousy for all kinds of reasons—for example, a lack of good quality exercise leading to poor physical and cardiovascular conditioning, or lack of sleep causing fatigue during the day—the lack of sleep being due to time constraints, or inability to relax due to thinking about stressful things. The point being, all the thyroid hormone in the world won’t fix those things.

She said her TPOAb’s have been climbing, and her doctors aren’t interested in looking at that. Her doctors may be right. We don’t track TPOAb’s in the same way we track, say, TSHs in thyroid patients and glucoses in diabetics. The fact that TPOAb’s (a type of thyroid antibody) are elevated tells us a person is at risk of becoming hypothyroid, or in this lady’s case (having already been diagnosed) that the cause of her hypothyroidism is autoimmune. There is no advantage, however, in continuing to check it. In fact, if a person comes to me with new hypothyroidism, I hardly ever check TPOAb’s. They don’t change anything. Unless there is some other obvious cause, like thyroid surgery, most people in the United States who are hypothyroid have Hashimoto’s. I can just assume that and don’t need to do a blood test to prove it, because the treatment is the same regardless of cause. Thyroid hormone replacement.

It would be different if there were a way to stop or reverse the autoimmune destruction of the thyroid, but there isn’t. Nothing proven safe and to work, and certainly nothing anywhere near as safe and reliable and inexpensive as thyroid hormone replacement is for most people, and I’m one of those people. Steroids might shut down TPOAb production but we wouldn’t go that route because it would be a case of the cure being worse than the disease—the steroids would cause diabetes, weight gain, osteoporosis, infections, and so forth. Now, maybe there is something out there that is safe and effective, some supplement, or diet, but we don’t know what it is yet. Until we do, giving thyroid hormone is the most reliable path to feeling better.

I and most endocrinologists do know very well that many people, like this patient, on thyroid hormone for hypothyroidism don’t feel 100 percent. To that I have two comments: (1) few things in life are perfect—that’s not a cop out; it’s wisdom and truth; and (2) I believe some of those people not feeling good on thyroid hormone aren’t on enough medication. My approach to hypothyroidism is pretty standard—that is, thyroid hormone replacement, usually with Synthroid or similar products—but I often use higher doses than most doctors are comfortable with, and I think that’s why I seem to get better symptom control in some patients than they do.

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More on Diabetes Progress

More on Diabetes Progress

This is a follow up to my 4/27/14 posting “Diabetes Progress—a Tale of Two Studies,” in which I mulled the significance of recently published data on improvements on blood-sugar control and complication rates in diabetes over the last quarter century. I largely argued that there was good news and bad news, but that the improvements might be less impressive than is obvious, when you consider the hugely expanded variety and costs of anti-diabetes therapies over the same period.

An online medical publication called MedPage Today, in collaboration with the American Association of Clinical Endocrinologists, on 5/29/14, published an article titled, in part: “Complications of Diabetes Down? Not So Fast.”

In it the main author, David H. Newman, MD (who wrote the book “Hippocrates’ Shadow: Secrets From the House of Medicine”) argues that the improvements in diabetes complication rates, that even I acknowledged looked pretty impressive, were overblown. He correctly points out that not quite halfway through the study period the definition of diabetes was changed from a fasting glucose to 140 or above, to 126 or above. He persuasively posits that, effectively, overnight the number of diabetes patients increased, and that the added patients were all by definition milder cases of the disease. In other words the population of diabetics at most risk of complications was diluted by all those milder diabetics. Thus, there was a false lowering of, for example, the portion of diabetes patients suffering heart attacks, or having limbs amputated.

From this and other equally persuasive points (for example that higher quality trials have often not shown fewer deaths, heart attacks, strokes and so forth with glucose-lowering treatments), Dr. Newman concludes: “We should be proud of our public health accomplishments and particularly proud of any real improvements in outcomes for chronic conditions like diabetes. But if we delude ourselves into believing that failed, high-intensity, high-cost treatments are the reason then we are destined to repeat our failures instead of finding genuine solutions.

My take: drug therapies can often help improve diabetes control and reduce complications, but sometimes don’t or sometimes even may make things worse. Physicians are not maliciously complicitous with the pharmaceutical industry in some great moneygrubbing plot as certain wackos charge. But it is high time physicians and their diabetes and prediabetes and other at-risk patients accept the fact that the only real solution/cure for diabetes in many (not all) cases is massive lifestyle change—not small, but major diet changes, and changes in almost every aspect of life, and even society at large (much of which I discuss in my book “What About My Weight?”). I think these are the genuine solutions to which Dr. Newman alluded.  Read More 
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Clomid Doesn't Work for Every "Low-T" Patient

I was contacted via email by a gentleman providing very little information other than he has a low testosterone level, and that he wanted to try Clomid, and did not want testosterone replacement. Going on, he wrote: “Who can get that done for me…Need a doctor that will make it happen. Can’t find any.” And that was it—a man of few words.

Clomid is a drug usually used as a female fertility treatment. In certain cases it can raise testosterone levels in men by blocking estrogen receptors that inhibit release of LH, the pituitary hormone that drive testosterone production by the gonads. In part here is my reply to my emailer:

(1) I realize physicians tend to be a pretty conservative lot--by that I mean it can be difficult to find one willing to color outside the lines of standard care and evidence-based medicine (what's proven to work and be safe by published mainstream research), even in cases where common sense might make such an unproven therapy seem like a good idea. There are legitimately reasons for that, but it can frustrate patients. In my own case, I have a lot of knowledge and experience with difficult hypothyroidism cases. Based on that, I'm sometimes willing to handle things differently than the average doctor. In areas where my knowledge and experience is average compared to my peers, however, I'm as conservative (read: stubborn?) as the next guy.

(2) Clomid use in men is non-standard. There is increasing interest in it as a male fertility therapy, and I have used it that way a couple of times. Fertility treatment though is always short term—once pregnancy occurs, treatment stops. Use of Clomid as a long-term treatment for permanent hypogonadism (low testosterone, or "Low-T") presents different issues. I doubt anyone knows whether it's safe for men to take it for a long time. In fact, as an estrogen blocker, there is real concern that it weakens bones, causing fractures. Remember, estrogen strengthens women's bones—same with men. With that in mind it may well be that no good physician would agree to what you're asking. I wouldn't, not without there having been quality research proving long-term safety. Now, were there reason to believe this might be short-term therapy, Clomid might be a consideration, but you've given no details to suggest that's the case. The right therapy for anything is highly dependent on details.

(3) Which leads to my last point: Just because you want something does not make that something medically appropriate—always a primary concern of a good physician. And no good physician ought to promise a certain therapy without seeing and evaluating you. The only doctor who would promise to "make it happen" would most likely be a quack.

The simple fact is, there are causes of "low T"—most causes perhaps—where Clomid would not work. These include any serious defect in the testes interfering with testosterone production, and any serious damage to the pituitary gland's ability to make LH, which tells the testes to make testosterone. All Clomid does is block estrogen-caused inhibition of LH production, but after that the pituitary still has to be able to make LH and the testes still have to be able to make T. Sometimes it's obvious from a complete set of labs what the situation is, other times not.

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It was the best of times, it was the worst of times…
—Charles Dickens

By coincidence I was recently honored with an invitation to lecture on a topic of my choosing for my local AARP chapter (it was strongly suggested diabetes be the focus), and in the process of preparing what I titled TYPE 2 DIABETES UPDATE: 2014, I pondered a question I didn’t know the answer to…Since the early 1990s have we really improved outcomes—that is, improved glucose control, and rates of complications, such as eye, kidney, and nerve damage in diabetes sufferers?

The early 1990s were a watershed for diabetes: the DCCT was published in 1991—this was the study that at long last conclusively proved strict blood-glucose control and low hemoglobin A1c’s of <7.0, prevented complications. This had a profound impact on diabetes management in the years and decades to come. A short time later, in 1994, metformin was approved by the FDA in the United States. Metformin had been available in Europe for decades, but at that point became the first drug for diabetes available to the US market other than insulin and sulfonylureas, the latter being pills that stimulate insulin release by the pancreas. In other words, before metformin, all we could offer in the realm of drug treatment for diabetes was more insulin, either in the form of a shot or a pill (as my father would say: “six of one, half-dozen of the other”). Metformin was the first really new thing in diabetes drugs since the 1920s, and eight totally new classes of drugs have been introduced to diabetes management since, the last in 2013.

In other words, in 1990 we had 2 drug classes for diabetes: insulin and sulfonylureas. In 2014, we have those, plus metformin, plus eight others, some shots, some pills. A total of 11 options to mix and match in our diabetes patients, not to mention radically new insulin types.

In practical terms, this means diabetes management today is a lot more complex and costly than it was almost a quarter century ago. What have we gotten in return? The coincidence I referred to above was that I was asked to give that AARP talk, which led me to ponder this question, which I wasn’t sure there was a known answer to. Yet, less than 1 week after my talk, two scientific papers appeared—one in the NEW ENGLAND JOURNAL OF MEDICINE (NEJM), the other in ANNALS OF INTERNAL MEDICINE (AIM)—which directly answered my questions about whether we’re seeing better control and fewer complications.

The complications issue was addressed in the NEJM study and the answer was overwhelmingly positive. Between 1990 and 2010, among Americans with diabetes, there were 68% fewer heart attacks, and 64% fewer deaths due to a high-glucose crisis, such as diabetic ketoacidosis. There were 53% fewer strokes and 51% fewer leg and foot amputations, and a 28% reduction in severe renal failure.

Those data are of course very good; however, in that same period, the number of people with diabetes tripled from almost 7 million to almost 21 million. And if you look at those same diabetes complications and express them as a percentage of all Americans, rather than as a percentage of just Americans with diabetes, it turns out that there were still fewer diabetes-related heart attacks and hyperglycemic crises, but no improvement in amputation, stroke, or kidney-failure rates. Kind of supports the old adage about being able to prove anything with statistics. Yes, we have greatly improved the lot of the individual person with diabetes—reduced for example that person’s risk of having to have a leg amputated—but we haven’t reduced the number of diabetes-related leg amputations in the United States, see?

What about blood-sugar control? The AIM paper addressed that. A few definitions are in order: HbA1c is a blood test that effectively tells what a person’s average blood sugar was like over the past month or two. A HbA1c <7 is considered good, and <8 is considered fair. The AIM paper compared the percentage of American diabetes patients getting HbA1c’s <7 and <8 in the period from 1988 to 1994 (the “pre-metformin era”) to the period from 2005 to 2010. Note that this study covers roughly the same span of time as the NEJM paper, but looks at different kinds of outcomes.

Here goes: HbA1c was <7 in 51% of diabetics in the 1988/94 period and 59% in 2005/10. It was <8 in 67% and 79%, respectively. If we just look at diabetes patients taking medication to control their disease—which gets more to the heart of the question I formulated getting ready for the AARP, are we doing any better with 11 classes of drugs than with 2?—40% achieved a HbA1c <7 in 1988/94 and 55% in 2005/10. And HbA1c <8: 59% and 78%, respectively.

So, to summarize the AIM paper, in all cases we are doing better now. That’s not surprising, that’s what I guessed for the purposes of my talk, but I also surmised in the talk that though we’re doing better, we’re not doing all that much better. And that is what this data shows. For diabetics taking drugs to get under control, the percentage getting under excellent control improved by only about a third (55% divided by 40%), and the percentage achieving at least fair control increased by just about the same degree. That’s good. I’m very happy we’re doing that, but I don’t think a 1/3 improvement is all that impressive stacked up against the fact that the number of classes of drugs for diabetes has quintupled, and some of those newer drugs cost hundreds of dollars per month. (To be fair, not all of those 11 classes were available in the study period ending in 2010, but most were.)

There is something else to consider—prior to 1991 there was no definitive proof that getting the HbA1c to <7 was important. I was in my training in that period before the DCCT trial and I can attest to there having been far less aggressiveness on the part of many physicians’ diabetes management. So, we are seeing a 1/3 improvement in the percentage of diabetics on drugs getting under control, at a time when we have 5X the number of drugs to do the job, and a greater understanding that it is important to try. See what I mean? If you were to factor out the doctors who didn’t even try in 1988, something that might be malpractice today, I bet the improvements would be even less impressive.

What do we learn if we combine the findings of these two papers? Seems to me that we are doing a much better job of preventing most complications, including heart attacks and death from diabetes, at least in the individual diabetic—we’re not doing so good with the population because we’re doing a lousy job of preventing new cases of diabetes, which have soared. Anyway, we’re reducing complications despite less impressive improvements in actual blood-sugar control. Which tells me that it isn’t all about blood sugars.

Glucose control is important but it is not necessarily more important than other challenges diabetes patients face, such as high blood pressure, high cholesterol, insulin resistance, vascular inflammation. I think we’re doing at least as good a job and probably better controlling these things as we are controlling blood sugars. Especially LDL cholesterol, with the introduction of the statin drugs at about this same time in the early 1990s. These are the real lifesavers, I believe. The prevention of heart attack and stroke and amputations in diabetics owes at least as much to better blood pressure and cholesterol medicines as it does to better glucose control.

So what about those 9 newer classes of diabetes drugs? Are they worth the added cost and complexity? You might’ve been expecting me to say no, considering the tone of this posting to this point. But, as I said, it’s not all about blood sugar. Those shinier newer drugs might not be doing that much better for blood sugar, but what they are doing, they are doing in different ways compared to what was available pre-1994 when all we did was increase insulin levels. We’re reducing insulin resistance, systemic inflammation, glucagon levels, appetite stimulation, altering fat-cell metabolism, and cholesterol profiles—all with just our newer diabetes medicines. There may even be a lower overall cancer risk with the newer versus the older drugs.

So, yes, we are better off paying top dollar, when we can afford to, for these newer drugs and drug combinations. Like with anything: you get what you pay for. They may not be showing that much more bang for the buck when it comes to blood sugars, but when you factor in how they do what they do, and the side benefits beyond blood sugar control, it is the best of times for those with diabetes.

Now we need to work on prevention, because it is still the worst of times in that arena.

Dr. Rone Read More 
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Is Vitamin D3 better than D2? Is Dr. Mercola Right?

A patient sent me a letter asking if she should stop taking her ergocalciferol (Vitamin D2) and take Vitamin D3 instead, as she had read an online item from Dr. Mercola about Vitamin D. I read that and also reviewed this subject in a recent major endocrine text and a recent major nutrition text. The endocrine text simply said there was no difference in how D2 and D3 are used by and affect the body and said nothing more about it. The nutrition text presented a large amount of information, in great detail about many studies, less than 20 years old, stating, in effect that there was no difference. It went on however to discuss in just as much detail recent studies, since 2000, suggesting that there might be differences.
--What I came away with is that the subject is very complicated and still up for debate.
--What I can safely say is that there is NOT widespread agreement among medical and nutritional experts that Dr. Mercola's position is correct.
--I can also say that his presentation is overly simplified, and incomplete. There are studies saying what he claims they say, but there are others saying something different and he leaves that part out.
--I should point out that Dr. Mercola is widely considered to be a quack. I am not calling him a quack--I don't know enough about him--some people disagree with me too. I suggest Googling "Dr. Mercola quack" and read that stuff before deciding who to listen to. Also, he is a family practice doctor, not an endocrinologist or nutritionist--that doesn't make him wrong, but it does mean he isn't a board-certified expert on Vitamin D
--Now, he claims D2 doesn't raise Vit D levels as well as D3--I've personally taken both in roughly equal amounts and they've both kept my levels the same and the D2 brought mine up from clearly low levels that I started with. The labs of the patient in question show the same thing, and her PTH and Ca++ levels are normal suggesting her D2 is working.
--Now, I have nothing against D3--I take it--only because it's cheap and available over the counter--not because of any of this.
--my suggestion to this patient, because she is on a very large dose of D2, was that we stick with the 50,000 D2 caps--she'll be taking a lot of pills if we go with the lower doses D3 is available in.
--I offered to let her try weaning the D2 down and if we get her to the point that a once daily D3 would easily do the trick, I'd be happy to switch her. It's always reasonable to try getting away with the least medicine that does the job. Read More 
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All About Hypoparathyroidism Treatment


For routine monitoring of established hypoparathyroidism (hypopara) there is no role for checking parathyroid hormone (PTH.) You obviously would check PTHs at least periodically in the early stages postop to assess for recovery, which is not unusual. And in that phase of the disorder you have to be sure a low PTH is due to real deficiency, not appropriate suppression of PTH in the face of aggressive calcium (Ca++) and vitamin D supplementation. That is, if there is suspicion or evidence of residual PTH production, running the supplements at low doses might be illustrative (that is if the PTH rises and prevents hypocalcemia [low Ca++; hypoCa++] then hypopara is not in fact present).

In straight-forward postsurgical hypopara, I treat with around a 2000-mg total daily dose of Ca++ plus however much calcitriol (this is a form of vitamin D; typically the dose is 0.25 to 0.5 mcg daily, but sometimes more) is needed to adjust the total serum Ca++ to levels in the lower half of the normal range or perhaps even slightly low. Mid-normal or higher Ca++ levels in hypopara patients over the long run can bring on renal failure due to Ca++ collecting in the kidneys and can cause kidney stones (without PTH, Ca++ floods through the kidneys and out in the urine).

Labs I check are Ca++ and phosphorus (phos), period. We don't care what the 25D (storage form of vitamin D) level is because it can't be used in the absence of PTH and we don't care what the 1,25D (active form of vitamin D) level is because the Ca++ tells us all we need to know—provided a decent dose of Ca++ is being taken, a Ca++ lower than the goals discussed above means the 1,25D is too low, and Ca++ higher than goal means the 1,25D is too high.

Ideally phos should be normal of course and with us running the Ca++'s relatively low (thus mitigating the 1,25D effect of raising phos) I don't see a lot of hyperphosphatemia (high phos, or hyperphos). When we do have hyperphos, provided the Ca++/phos product (Ca++ level multiplied by the phos level) is below 55 to 70 there should be no problem. I don't check magnesium or urine Ca++ (remember, keeping the blood Ca++ low normal or low, just enough to prevent symptoms, handles the urinary excretion concerns).


If well monitored, there is probably no harm in combining the two forms of vitamin D, and there might be some value, but it wouldn't typically be necessary. I've never deliberately combined them, and there would be greater risk of vitamin D toxicity (that is, dangerously high Ca++, or hyperCa++). Vitamin D2 and D3, have very long half lives, meaning they take a long time to go away if overdosed, but relatively safe because the body has to activate them, which the kidneys won't do in the face of if the Ca++ is too high. On the other hand, calcitriol is riskier because it's more potent—it can directly raise Ca++ levels whether that would be a good thing for the body or not—the regulatory step of converting 25D to 1,25D in bypassed. But it's in the end relatively safe because its half-life is short—it goes away fast. These "safety features" of each would be maintained in a combination, but there is no way the risk, at least short term, for hyperCa++ would not be greater, so I don't see the benefit outweighing the risk. I'd avoid the combo.

Phosphate binders are mostly used in chronic renal failure--I don't, and have not much heard of them being used in hypopara. And remember, renal failure patients typically have low Ca++'s and their PTHs are typically appropriately high in response to the low Ca++, so that is really a totally different situation from hypopara.

Yes, avoid excess dietary phos, give Ca++ at about 2000mg per day as described, and lower the vitamin D supplement to get the Ca++ low or low normal. That should fix the phos level, and again, if the Ca++ times the phos product is ok, I wouldn't worry about it. Really, I haven't had much problem with hyperphos.

I assume by vitamin D analogues you are referring to the brand name drugs Hectorol and Zemplar. These as well as calcitriol (brand name Rocaltrol) all mimic the effects of 1,25D, the active form of vitamin D in the body. All these drugs lower PTH and raise Ca++ and phos. There may be some differences as to the degree of the effects on calcium and phos, which I can't really give any authoritative information about. I always use calcitriol and haven't used the others, which are more commonly used by nephrologists (kidney specialists). They deal with a different group of patients than I do, mostly renal failure patients who have enormously high PTH levels that need to be brought down.

My use of agents that stimulate the 1,25D receptor, like calcitriol, mostly
involves hypopara (low, rather than high PTH). These people need 1,25D replacement because they lack PTH, which is needed to trigger 25D to 1,25D conversion in the kidneys (storage form to active form). No PTH, no 1,25D, and Ca++ drops dangerously low because of a lack of vitamin D effect on the kidneys and intestine, and lack of PTH effect on kidneys and bone. Phos already may be high owing to the PTH lack (PTH lowers phos) and we have to monitor to be sure the 1,25D doesn't dangerously elevate phos at the same time as it's raising Ca++.

The other commonly used vitamin D supplements (D2 and D3) are forms of 25VitD, the storage form, and have to be converted to 1,25D, which most people with normal parathyroid and kidney function do just fine. D2 and D3, in very large doses, in hypopara, might raise Ca++ and phos a little, but not very efficiently.

In people with intact parathyroid glands and intact kidneys (no renal failure),
who have elevated PTH levels for whatever reason, all these vitamin D forms would
be expected to lower PTH.


The primary driver of PTH release is CA++. So, if CA++ IS low (8.1 and 8.5 in your case, with a lower limit of 8.6), then PTH has to be deficient—it matters not that you have residual function—most do—what matters is PTH is deficient relative to your needs. PTH will always be produced at maximal levels in the face of low Ca++, regardless of calcitriol doses. So if your Ca++ is low, you are deficient, period, and after 4 years recovery is unlikely--not impossible, but very unlikely.

Now, you may be subtly better off for having that residual function—easier to control, more stable—owing to your body perhaps being able to do some fine-tuning to make up for some deficit in your replacement regimen, but in overall terms of how we manage this it doesn't matter.

You might be right that, given residual PTH function, your body might be able to somewhat utilize D3, but to what end? If the object is to lower the calcitriol dose and lessen some perceived adverse effect of calcitriol—remember, D3 works through its conversion to 1,25D, which is the same thing as calcitriol, with the same potential side effects. So why bother? Just take one drug, the more effective one—calcitriol.

I doubt there would be any benefit to lowering your replacement doses to promote PTH recovery. If it was going to recover, those low calciums would have done it already. And there are risks to making your hypoCa++ worse, including seizures, so why take the chance? (below I'm going to talk about weaning calcitriol for the purpose of seeing what your minimum effective treatment regimen is, but not for the purpose of promoting PTH recovery, see?)

On the other hand, if there is some remote chance of recovery, getting you to that minimum effective level of treatment would mean our treatment would interference with that hypothetical recover to the lowest possible degree, while still “taking care of business.”

With respect to your management, based upon data provided—first, it's not clear to me anything has to be changed—the most important parameter to watch is Ca++. It needs to be high enough to prevent symptoms—and you say you don't have symptoms—and it needs to be low enough not to cause kidney stones or renal damage. That is, they should range from mildly low to somewhere in the lower half of the normal range. You're there! Now, if I were going to change anything, I would do the following:

1) Up the Ca++ to 2000 mg from 1200 mg—you don't want to be depending on your dietary Ca++ intake in this situation—it's too variable—taking 2000 mg per day masks fluctuations in day-to-day intake.

2) Take Ca++ with food in at least 2 divided doses, at least 2 hours after your thyroid hormone.

3) Once the Ca++ is at 2000/day, then fine tune the serum Ca++ level using calcitriol. And here's an advantage of taking more calcium—there's no harm in more calcium—it's not that well absorbed anyway—but you've expressed concern about calcitriol side effects (hyperphos for instance). On 2000/day of Ca++, you might be able to back down on the calcitriol.

4) You're already on a very low calcitriol dose—I dose most people daily—if you do go down further, to say twice weekly, it should be for one of two reasons—either your calcium is too high (which it isn’t), or to see if you can wean off it. Some hypopara patients get by with Ca++ only. If on twice weekly calcitriol your Ca++ is above 8 and you have no symptoms, try stopping it (not sure once a week would be a worthwhile step). On the other hand, if Ca++ is below 8, especially if there are symptoms (cramping, spasms), just go back to 3 per week and stay there.

5) If off calcitriol for a week or two, and Ca++ is still above 8 with no symptoms, I probably would then add D3 1000-2000 units/d, which is probably good for most normal people, you certainly would want to do at least that.

6) From that point on—if you get there—monitor Ca++ and 25D and maybe an occasional phos, but if that's normal initially I'd drop it.

Now, assuming you do just stay on Ca++ and some dose of calcitriol—I would monitor Ca++ and phos, period. We covered what the Ca++ goal should be. The phos should be normal, but a slightly high level may be a necessary evil and I wouldn't worry about it. Just make sure the Ca++ level times the phos level is not over 55.

I'm going to end with some constructive criticism. I think you're trying to micromanage this too much. This is very complex—too complex for any of us to fine tune every little link in the chain. My advice is to pay attention to the key end results: symptoms and Ca++ levels. If they're okay, don't worry about PTHs and vitamin D’s (and phos usually isn't an issue either as we've said). Obviously working with an endocrinologist with a lot of experience in this area should be helpful.

A last bit of wisdom:

This is a difficult problem to manage under the best of conditions. It is a complication of surgery best avoided rather than to have to be treated. An experimental human recombinant PTH product may help things in the future, but we aren't there yet. Thus, prevention is key: only do thyroid and parathyroid surgery when it’s absolutely needed, and make sure the best surgeon (that is, a lot of experience in the neck, and proven low complication rates) you have access to is doing the case. (With any luck, the physician referring you for the surgery will be able to tell you who that is.) A couple of years ago one of my patients needed thyroid surgery and I recommended a local community general surgeon I've worked closely with for 16 years and from whom I have rarely if ever seen a Ca++-related surgical complication. She flouted my advice and went instead to a surgeon somebody recommended at a world-class university medical center in the next county, and now I'm managing her permanent postsurgical hypopara, just as you are dealing with.


This is precisely what I mean by micromanaging. I don't believe that in 25 years I have ever checked a 24-hour urine Ca++ in a hypopara patient. I've checked them in hyperpara, and in osteoporosis, but not hypopara. I suppose if you've had multiple kidney stones, or renal insufficiency, you might have reason to be concerned—if not, don't check it. And if you were having kidney stones you could take a thiazide diuretic to lower the urine Ca++. You're forgetting that my protocol mitigates renal Ca++ exposure by setting the serum Ca++ goal low. And I don't believe that in 25 years I've had a hypopara patient have kidney stones either, that I recall anyway.

Say you do as I advise and your urine Ca++ is still high? (which you're telling me is, in fact, the case). In the absence of a clinical problem like renal failure or kidney stones, doesn't matter. Fugggedaboutit!

In focusing on, and worse, acting on the urine Ca++ and serum phos you are making the common error of equating biochemical testing, falling outside the lab's reference range, with a disease that needs to be treated. The two aren't the same thing. I make this point very strongly in The Thyroid Paradox. A lab abnormality is a signal that deserves investigation, it is not a disease; it is not, necessarily, a demand for action. I ignore numerous minor lab abnormalities everyday, every physician does. The job of a quality healthcare practitioner is to evaluate a patient with a history and an exam and--labs!--and perhaps radiology or even tissue pathology studies, and put all that together and decide what is going on, and what if anything to do. The answer might be nothing. Reading a lab report comes no where close to the work that needs to be done.

Hope that helps!

Dr. Rone Read More 
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Healthy Eating Myths

A Dec. 2013 health column in my local paper, The Tennessean, authored by Julian Hayes II, a Nashville fitness and lifestyle coach, was titled: “Nutritional Myths You Can Stop Stressing Over.” Having recently published, What About My Weight? I’m compelled to offer commentary on Mr. Hayes’ myth busting. I’ll take them one at a time, and remember, these are—from the article’s perspective—myths, his position being the opposite of the assertion presented:


Mr. Hayes’ take: Meal timing isn’t important; skipping breakfast is a way to “intermittently fast,” which he cites to be beneficial; feel free to skip it if you want.

My take: There are seeds of truth here but I largely disagree. Let me offer as preface, though, to all my comments—a basic tenet of What About My Weight? is that we are all different. Different weight-loss/control strategies work for different people. So, if whatever you’re doing is working, great! Keep doing it. If it isn’t, try something different: like skipping breakfast or not, depending on where you started.

Anyway, I’m a big believer in breakfast. There is data, at least in diabetics, that blood sugar control and weight loss is aided by eating breakfast, and skipping or limiting supper, in support of the adage, “Eat breakfast like a king, lunch like a prince, and supper like a pauper.” This plan also allows intermittent fasting (little or no intake from lunch to breakfast), and I agree limited fasting is beneficial. It offers an opportunity to lower calorie intake, yes, but there is a more complex aspect. Leptin levels rise (this is a hormone produced by fat tissue) when we eat and store fat. This signals the brain to shut down appetite, so we don’t overeat. Leptin levels fall when we fast, and appetite returns. Modern Western excess-eating habits have created a situation where leptin levels are high all the time (that is, we eat round the clock, never seeing a true fasting state). The brain ignores those constantly high levels and appetite never shuts off; it’s the rising and falling of leptin that is important to appetite control, not absolute levels.

So, Mr. Hayes and I agree that skipping a meal is a good thing. Is breakfast the best one to skip? My own experience is that a big breakfast satisfies to lunch, fueling the most active part of the work day (assuming a tradition 9-to-5-type schedule) without need for snacking. A decent-size lunch does the same for the afternoon, and by the time you’re home relaxing, there isn’t as great a need for all that fuel.

One argument against meal timing is that calorie intake minus output determines body weight—it’s all in the math, and doesn’t matter what hour of the day the calories get consumed. Physiologically, this is true. But I think thoughtful meal-timing can help regulate the appetite, limit snacking as I described above. My strong feeling is that manipulating or “fooling” one’s appetite into eating less is at least as important, perhaps more so, than the math. In other words: if you eat a calorie, it matters not when you ate it, you’ll gain the same weight; meal-timing though might mean you never eat that calorie in the first place. See?


Mr. Hayes’ take: Eating 2000 calories in five meals is the same as eating it in two; quit timing and make your nutrition fit your preferred lifestyle.

My take: We largely agree, and the issues are not dissimilar to the last “myth.” Amongst my pet peeves, though, are experts pontificating about healthy living and healthy nutrition as if there were one set of rules, etched in concrete, for the whole genetically, medically diverse population. Everyone talks up diversity these days, but not so much in this arena. I can’t tell you how many patients I’ve had who are overweight and complaining they can’t lose weight, and in the next breath claim: “I’m eating right,” “I follow a healthy diet,” like any of that mattered. If it isn’t working try something different.

To that end I might say there may be people who for whatever reason get more satisfaction out of frequent small meals and might as a result eat less overall—but I do agree with Mr. Hayes that eating five or six meals a day is not good universal advice. His point about making nutrition fit with one’s preferred lifestyle is good as well, provided that lifestyle isn’t clearly unhealthy, like spending hours in front of the TV curled up with a big bag of Lay’s potato chips. I would add that the best nutritional strategies are ones incorporating one’s dietary preferences, and ethnic food background.


Mr. Hayes’ take: Barring certain health-issues (serious kidney disease would be an example) he advises a high protein intake.

My take: He’s 100 % right on this one. Protein slows absorption of carbs, helping diabetes control and making one feel fuller, longer, and less apt to overeat. Protein, together with resistance training increases muscle mass, and the more muscle you have the more calories you burn at rest. What was that? I said REST. Sure, exercising muscle burns calories, but for most of us—those not out running marathons, for instance—muscle tissue’s greatest contribution to weight control is its contribution to “resting energy expenditure,” which it huge. This point cannot be overemphasized—we all eat more than we need, that is, all mammals do. Overeating is natural, and if the metabolic engine is tuned correctly, resting muscle burns up much of the excess so we don’t gain weight.


Mr. Hayes take: Carbohydrates are necessary.

My take: Again, he’s right—carbs are the body’s major preferred fuel and it doesn’t take a medical degree to know we all need fuel as much as a car does. Furthermore, the brain—the body’s most important organ bar none, burns glucose (the major carb) exclusively. Except under very unusual circumstances, the brain must have glucose. So, no carbs is not an option. However, everybody is different and the devil is in the details. Many people overindulge in carbs and have been, wrongly encouraged to by all the haranguing about the evils of fat for the last 40 years.

One of our biggest nutritional problems, one of the major causes of the obesity and diabetes epidemics is the overconsumption of sugars, especially in the form of sweetened liquids, like sodas, juices, sweet teas. We simply must stop that, must get over our collective sweet tooth. It’s killing us.

And under the category, everybody’s different—some have diabetes, some don’t. A great many more are insulin resistant and at risk of diabetes (most people with a family history of diabetes fall in that category). If you are insulin resistant and/or have type 2 diabetes, the more carbs you eat or drink the higher your blood sugars and insulin levels will be, and high insulin levels begat weight gain. So, for that group, limiting (but not eliminating) carbs may be an important health habit, helping prevent obesity and diabetes. If you’re not one of those people, you can eat more carbs, but I’d still say everybody should limit the sweet beverages.


Mr. Hayes take: This sounds good for people with no social life, yet dinner is a popular time to get together with friends and family.

My take: I’ve indicated already that incorporating one’s preferred lifestyle into a nutritional plan is a good strategy for success. I’ve also pointed out the benefits—for those with diabetes at least, and perhaps others—of eating little or no supper. And while it is true that dinner is a popular time for socializing, that doesn’t make it healthy. On the other hand, I state in my book that were I to eat a substantial meal in the evening, I might want it to be higher in carbs/glycemic index. My rationale being that higher protein/fat meals during the day will be more satisfying and lessen the urge to snack—while at night those more filling meals might promote acid reflux and abdominal fullness that might interfere with sleep.

So, I agree with Mr. Hayes that there is no specific need to avoid carbs at night, but except for certain special occasions out, I do think the notion of limiting any type of calorie intake at night (not just carbs) has merit.


Mr. Hayes take: No one-size-fits-all diet; the best diet is one fitting your schedule, causes little stress, and you can stick to.

My take: I agree. Any attempt to give universal healthy-eating advice is complete folly and a major flaw with much nutritional pontification, including by doctors.

I disagree that schedule, stress inducement, and ease of adherence are absolute definers of the best diet. My definition of the “perfect diet” for a given individual is the one that works—the proof is in the pudding. If one starts with a diet that fits schedules, is unstressful, is easy to stick with, and that diet achieves one’s health and weight goals—great! If that diet doesn’t work, though, move on from there. The solution might not be easy—many worthwhile things aren’t.

My conclusions: We disagree in a few details, but overall Mr. Hayes’ view of nutrition is very insightful, nay, revolutionary, because, to quote his preamble to the column: “The image of getting in shape and eating healthy has become rigid and narrow minded.” And, “The tunnel-vision approach is outdated. You have options.” There is way too much posturing and pontificating by everyone—physicians, nutritionists, semi-quackish alternative-medicine providers, the government, the media, the public. I had a patient tell me she was following some diet plan and very successfully was losing weight. Then her friend told her, no, no, no, you have to cut carbs, or something or other. My patient listened and started regaining her weight. I told her, go back to what you were doing that was working and stop listening to oversimplified advice. One of the biggest challenges, I think, we have to overcome in the skillful practice of the art and science of medicine and healing, is our tendency toward hubris. Toward thinking we, any of us, can master the awesome complexity of human physiology. We can scratch the surface and often help our fellow man, but we mustn’t think any of this is simple, or completely manipulatable. Read More 
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