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Long Term Weight Loss for Thyroid Patients: Hormonal Factors That Affect Diets An Interview with Kent Holtorf, MD By Mary Shomon Thyroid Disease Expert; & “Long Term Weight Loss-More Than Will Power?” by Ken Holtorf in

Long Term Weight Loss for Thyroid Patients: Hormonal Factors That Affect Diets
An Interview with Kent Holtorf, MD

By Mary Shomon
Thyroid Disease Expert

– Kent Holtorf, MD
Kent Holtorf, MD is a California-based expert on hormonal medicine. Kent Holtorf, MD
Updated December 16, 2014.

Written or reviewed by a board-certified physician. See’s Medical Review Board.

Kent Holtorf, MD has a long history of working with patients who have hormone imbalances — including thyroid, adrenal, and reproductive hormones. He runs the Holtorf Medical Group in California, where he specializes in complex endocrine dysfunction, including hypothyroidism, adrenal insufficiency, and insulin resistance.
Dr. Holtorf has been working with a number of his patients — many of whom have an underactive thyroid — who have found it difficult or seemingly impossible to lose weight. What he discovered is that while there are many factors involved in the inability to lose weight, almost all the overweight and obese patients he treats have demonstrable metabolic and endocrinological dysfunctions that are major contributors to the weight challenges of these patients. In particular, Dr. Holtorf has, based on some of the latest research, focused on evaluating two key hormones — leptin and reverse T3 (rT3)– and treating any identified irregularities to help his patients lose weight.

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I’m pleased to be able to bring you this interview with Dr. Kent Holtorf, discussing his approaches to help thyroid patients achieve long-term weight loss.

Mary Shomon: You have said that you feel that two key hormones — leptin and reverse T3 — are playing a key role in regulating weight and metabolism. Can you tell us a bit about leptin, first, and what it has to do with weight loss challenges?

Kent Holtorf, MD: The hormone leptin has been found to be a major regulator of body weight and metabolism. Leptin is secreted by fat cells and the levels of leptin increase with the accumulation of fat. The increased leptin secretion that occurs with increased weight normally feeds-back to the hypothalamus as a signal that there are adequate energy (fat) stores. This stimulates the body to burn fat rather than continue to store excess fat, and stimulates thyroid releasing hormone (TRH) to increase thyroid stimulating hormone (TSH) and thyroid production.

Studies are finding, however, that the majority of overweight individuals who are having difficulty losing weight have varying degrees of leptin resistance, where leptin has a diminished ability to affect the hypothalamus and regulate metabolism. This leptin resistance results in the hypothalamus sensing starvation, so multiple mechanisms are activated to increase fat stores, as the body tries to reverse the perceived state of starvation.

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The mechanisms that are activated include diminished TSH secretion, a suppressed T4 to T3 conversion, an increase in reverse T3, an increase in appetite, an increase in insulin resistance and an inhibition of lipolysis (fat breakdown).

These mechanisms may be in part due to a down-regulation of leptin receptors that occurs with a prolonged increase in leptin.

The result? Once you are overweight for an extended period of time, it becomes increasingly difficult to lose weight.

Mary Shomon: You’ve said that you feel that leptin levels above 10 may warrant treatment. Can you explain a bit more about leptin levels?

Kent Holtorf, MD: Most underweight or normal weight individuals will have leptin levels below 10, although most major labs will use a reference range of 1 to 9.5 for men and 4 to 25 for women. (It must be remembered that this range includes 95% of so-called normal people and includes many who are overweight.) Almost all patients who are of healthy weight will have a leptin less than 10.

Mary Shomon: How do you treat leptin resistance in your practice?

Kent Holtorf, MD: Treatment can be focus on treating the elevated leptin — leptin resistance. An elevated leptin also indicates, however, that the TSH is an unreliable marker for tissue thyroid levels, as the TSH is often suppressed, along with significantly reduced T4-to-T3 conversion. In short, if your leptin is elevated, you have reduced tissue thyroid levels. Also, almost all diabetics are leptin resistant, which has been shown to reduce T4-to-T3 conversion in diabetics by as much as 50% without an increase in TSH, making it very difficult for type II diabetics to lose weight.

Because there is poor T4-to-T3 conversion, timed-released T3 is the optimal treatment — although T4/T3 combination medications such as natural desiccated thyroid (NDT) can be used.

We check the resting metabolic rate (RMR) in our patients, and interestingly, those with elevated leptin levels indicative of leptin resistance have RMRs that are consistently below normal. These patients are often burning 500 to 600 calories less each day than someone of equal body mass.

Thus, to have a reasonable chance of losing weight, these patients can either try and reduce calories by 500 to 600 calories a day (just to keep from gaining weight), exercise for an hour or two a day (just to keep from gaining weight) or normalize the thyroid and metabolism.

Humans are a very successful species because we can store energy (fat) very well. There are many mechanisms to gain weight and leptin resistance is just one of them, so we use a multisystem approach; there is no one magic bullet, although any one treatment can have a dramatic effect on a particular patient.

In addition to optimizing the thyroid (remember, giving thyroid hormone to lose weight is not appropriate, but that’s not what we are doing, here we are correcting a deficiency), Symlin (pramlintide) and/or Byetta (exenatide) can be very effective for many. Human Chorionic Gonadrotropin (HCG) is another potential option that works for some. While I’ve found that the antidepressant Wellbutin (bupropion) does not work well for weight loss, a combination of Wellbutrin and low-dose naltrexone (LDN) is having some surprisingly good results. Topamax (topiramate) is an option for some but is not always well tolerated. Standard appetite suppressants, which boost metabolism, can be used, especially if the RMR is low.


Kent Holtorf Headshot
Medical Director, Holtorf Medical Group

Long Term Weight Loss – More Than Will Power?

Obesity has become a major health epidemic and has dramatically increased over the last decades. Studies show that approximately one-third of the U.S. population is classified as obese and over two-thirds are significantly overweight. While the cause is multifactorial, studies are clear that almost all overweight individuals have metabolic and endocrinological dysfunction that is causing or contributing to their inability to lose weight.

It is not simply a problem that individuals are taking in more calories than they are consuming or lack of exercise or willpower, but rather it is a complex vicious-cycle of endocrinological and metabolic dysfunction. Contemporary medicine has failed to address these dysfunctions in overweight individuals and doctors and patients continue to believe that all cases are a matter of willpower and lifestyle. Thus, it is no surprise that obesity is reaching epidemic proportions.

Research is demonstrating that dysregulation of two key hormones may be a cause or major contributor of weight gain or inability to lose weight in the majority of overweight people. The first is leptin and the second is reverse T3. The exciting part is that doctors can now test for the presence of these physiologic barriers to weight loss and prescribe appropriate treatments with potentially dramatic results.


The hormone leptin has been found to be a major regulator of body weight and metabolism. The body secretes leptin as weight is gained to signal the brain (specifically the hypo¬thalamus) that there are adequate energy (fat) stores. The hypothalamus should then stimulate metabolic processes that result in weight loss, including a reduction in hunger, an increased satiety with eating, an increase in resting metabolism and an increase in lipolysis (fat breakdown). New research has found that this leptin signaling is dysfunctional in the majority of people who have difficultly losing weight or are unable to lose weight.

The problem is not in the production of leptin, but rather, studies show that the ma¬jority of overweight individuals who are having difficulty losing weight have a leptin resistance, where the leptin is unable to produce its normal effects to stimulate weight loss. This leptin resistance is sensed as starvation, so multiple mechanisms are activated to increase fat stores, rather than burn excess fat stores. Leptin resistance also stimulates the formation of reverse T3, which blocks the effects of thyroid hormone on metabolism (discussed below).

Testing: A leptin level can be ordered by your physician. If greater than 10, it demonstrates there is a degree of leptin resistance contributing to an inability to lose weight. The higher the number the more significant the leptin resistance.

Treatment: There are currently two medications are shown to be able to treat leptin resistance and can result in significant weight loss. One is Symlin and the other is Byetta. These are currently approved for the treatment of diabetes but can be prescribed “off-label” for the treatment of leptin resistance. They are showing significant promise in the non-diabetic population with the ability to produce dramatic weight loss in a large percentage of overweight patients. The amount of weight loss varies according to the study design, but a significant percent of patients are experiencing weight loss, despite little or no change in diet.

The leptin resistance is not permanent and is shown to improve with weight loss so diet and exercise can be beneficial. The “catch-22″ is, however, that it is difficult to lose weight with leptin resistance. High carbohydrate diets and in particular high-fructose corn syrup is shown to significantly increase leptin resistance and is a likely mechanism that high fructose corn syrup is associated with obesity, especially in children. Avoidance of high fructose corn syrup and carbohydrates would be recommended for those with high leptin levels.

Reverse T3

It is well known that thyroid hormones regulate metabolism and that low thyroid hormone production (hypothyroidism) causes low metabolism, but it has only recently been understood that thyroid production can be fine but there can a problem of activation of the hormones inside the cells that can be a major cause of low metabolism.

The thyroid gland secretes an inactive thyroid hormone called thyroxine, also known as T4. This is regulated by thyroid stimulation hormone (TSH) produced by the brain (specifically the pituitary). Normally, the inactive T4 is converted inside the cell to the active thyroid hormone called triiodothyronine (also known as T3). Most doctors will check TSH and T4 levels to see if thyroid levels are normal.

The studies are showing that it is not the production of thyroid that is the problem, but rather it is problem inside the cell that the inactive T4 is not converted to T3 but rather to a mirror image of T3 called reverse T3. The reverse T3 has the opposite effect of T3, blocking the effects of T3 and lowering rather than increasing metabolism.

It is an evolutionary fall-back that was useful in times of famine or in hibernating animals to lower metabolism. Studies are showing that stress and dieting (especially yo-yo dieting) can set this hormone into action as well as chronic illness such as diabetes, chronic fatigue syndrome and fibromyalgia.

The production of reverse T3 is found to be a major method by which the body ‘tries” to regain any lost weight with dieting. As soon as the body senses a reduction in calories, the production of reverse T3 is stimulated to lower metabolism. With chronic dieting or stress, the body often stays in this “starvation mode” with elevated levels of reverse T3 and decreased levels of T3, which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).

Testing: There has been a long held belief by endocrinologists and other physicians that adequate thyroid levels can be determined by testing the TSH and T4 levels. Studies are showing that such standard testing will miss 80% of thyroid dysfunction so most endocrinologists and other doctors will tell their patients that their thyroid is fine based on this usual testing. The doctors must run a free T3/reverse T3 ratio. Generally, a healthy person will have a ratio greater than 2 so a person with a ratio less than 2 should also be considered a candidate for thyroid supplementation. Many endocrinologist and physicians are not yet aware of the significance or ability to run this ratio so it may take some searching.

Treatment: The standard treatment of hypothyroidism involves the supplementation with T4, including Synthroid and Levoxyl. These are not effective to remedy such a situation because the problem is not the amount of T4 but rather the excess conversion of T4 to reverse T3, blocking effects of the active T3. One must bypass the abnormality by supplementing with physiologic doses of T3, not T4 (preferably timed released T3). It is not appropriate to give thyroid hormone for weight loss, but rather to correct an abnormality diagnosed by appropriate blood tests.

In summary, emerging evidence demonstrates that a significant number of overweight patients have a metabolic problem rather than a problem of willpower or lifestyle. Identification and correction of these metabolic abnormalities, including leptin resistance and cellular thyroid dysfunction, can result in dramatic long term successful weight loss.

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