Taking homeopathy seriously
02/02/11 12:55
The debate over homeopathy rages on! I just read this article in the Huffington Post in which Nobel Prize winner Luc Montagnier (the virologist who discovered the AIDS virus) explains why he supports homeopathy. The article cites a fair bit of research into homeopathy, which makes for a great read if you want to learn more. Thanks Theresa Jahn, ND for sending me the link!
The article makes some great points in favour of homeopathy that I wanted to highlight:
Reading through the comments on this article, I also found a link to this page on frequently asked questions about homeopathy. This is a really detailed Q&A on all the most-asked questions about homeopathy and is a great place to start if you want to learn about this wonderful modality. Enjoy!
The article makes some great points in favour of homeopathy that I wanted to highlight:
- “Most clinical research conducted on homeopathic medicines that has been published in peer-review journals have shown positive clinical results,(3, 4) especially in the treatment of respiratory allergies (5, 6), influenza, (7) fibromyalgia, (8, 9) rheumatoid arthritis, (10) childhood diarrhea, (11) post-surgical abdominal surgery recovery, (12) attention deficit disorder, (13) and reduction in the side effects of conventional cancer treatments. (14).”
- “In addition to clinical trials, several hundred basic science studies have confirmed the biological activity of homeopathic medicines. One type of basic science trials, called in vitro studies, found 67 experiments (1/3 of them replications) and nearly 3/4 of all replications were positive. (15, 16).”
- Homeopathy “gained widespread popularity in the U.S. and Europe during the 19th century due to the impressive results people experienced in the treatment of epidemics that raged during that time, including cholera, typhoid, yellow fever, scarlet fever, and influenza.”
- “High dilutions of something are not nothing. They are water structures which mimic the original molecules."
Reading through the comments on this article, I also found a link to this page on frequently asked questions about homeopathy. This is a really detailed Q&A on all the most-asked questions about homeopathy and is a great place to start if you want to learn about this wonderful modality. Enjoy!
Comments
Homeopathy: cure or con?
14/01/11 12:02
Tonight CBC Marketplace will air a report called Cure or Con? on homeopathy. Even though the report has not aired yet, there are lots of comments! From what I can tell from their preview, I doubt that these journalists have actually investigated homeopathy in-depth and that their “research” is likely a waste of time and money. I look forward to watching it to see what they have done.
I use homeopathy as part of my practice with great results and have written blogs about it on this site. If you are interested in learning more about homeopathy, start with my blog Homeopathy primer. For information about research into homeopathy, check out Homeopathy literature review.
What most people consider research is often only the tip of the iceberg as far as information goes. True “evidence-based medicine” encompasses clinical experience as well! Check out my blog Is evidence-based medicine compatible with naturopathic principles for a more a discussion on this topic and my blog Mythology of science-based medicine for even more insight into medical research.
I use homeopathy as part of my practice with great results and have written blogs about it on this site. If you are interested in learning more about homeopathy, start with my blog Homeopathy primer. For information about research into homeopathy, check out Homeopathy literature review.
What most people consider research is often only the tip of the iceberg as far as information goes. True “evidence-based medicine” encompasses clinical experience as well! Check out my blog Is evidence-based medicine compatible with naturopathic principles for a more a discussion on this topic and my blog Mythology of science-based medicine for even more insight into medical research.
The secrets of sleep
28/06/10 11:23
Fascinating National Geographic article about sleep. Also, check out my previous blog on Sleep and Metabolic Syndrome.
Homeopathy literature review
18/02/10 09:37
Homeopathy is often criticized for having little research evidence available. This blog is a compilation of what I have learned in examining research evidence for homeopathy published in conventional medical journals. For more info on homeopathy, please see a previous blog entitled “Homeopathy primer.”
One of the major reasons that the results of most mainstream research on homeopathy are often inconclusive because the methods used usually do not honour the principles of homeopathy and therefore the research does not actually evaluate the practice of homeopathy. Aphorism 104 in the Organon explains how a practitioner can take and treat a case homeopathically:
“Once the totality of symptoms that principally determine and distinguish the disease case … has been exactly recorded, the most difficult work is done … He can then select … a well-aimed, similar, artificial disease potence, in the form of a homeopathically chosen medicinal means, to oppose the total disease image (1).”
Unfortunately, remedies are often not prescribed individually and are instead selected based on typical clinical presentation of pathology.
A meta-analysis published by Shang et al. in the Lancet in 2005 compared placebo-controlled homeopathy trials to conventional medicine trials matched by disorder and type and determined that “the clinical effects of homoeopathy, but not those of conventional medicine, are unspecific placebo or context effects (2).” The homeopathy trials were categorized classical, clinical, or complex homoeopathy (or as isopathy). Specifically,
“Classical homoeopathy was defined as comprehensive homoeopathic history-taking, followed by the prescription of a single individualised remedy, possibly with subsequent change of remedy in response to changing symptoms. If no comprehensive homoeopathic history was taken and all patients received a single, identical remedy, interventions were classified as clinical homoeopathy (2).”
Only “classical” homeopathy trials actually reflect the use of remedies according to homeopathic principles as set out in the Organon. “Clinical” homeopathy is the substitution of homeopathic remedies for conventional medicine and therefore not the practice of homeopathy. Of 110 homeopathy trials analyzed, only 18 were categorized as “classical” while 48 “clinical” homeopathy trials were analyzed. The selection of trials for this analysis therefore precluded results that would accurately evaluate the effects of homeopathic treatment.
Rutten and Stolper analyzed post-publication data from the Shang paper and concluded that:
“Re-analysis of Shang's post-publication data did not support the conclusion that homeopathy is a placebo effect. The conclusion that homeopathy is and that conventional is not a placebo effect was not based on comparative analysis and not justified because of heterogeneity and lack of sensitivity analysis. If we confine ourselves to the predefined hypotheses and the part of the analysis that is indeed comparative, the conclusion should be that quality of homeopathic trials is better than of conventional trials, for all trials (p=0.03) as well as for smaller trials (p=0.003) (3).”
A review by Lüdtke and Rutten also came to this conclusion. Their meta-analysis determined that “homeopathy had a significant effect beyond placebo (OR=0.76; 95% CI: 0.59-0.99; p=0.039) (4).” and that, “Shang's negative results were mainly influenced by one single trial (4).” They concluded: “Shang's results and conclusions are less definite than had been presented (4).”
Linde et al. published a review of randomized controlled trials of individualized homeopathy in the Lancet in 1998. In this review, the team clarified that, “in individualized homeopathy the choice of the remedy for treatment is not based on a conventional diagnosis but on the match of the patient’s particular symptoms with the ‘remedy picture (5)’” and also conceded that, “no attempt was made to assess the ‘homeopathic’ quality of the trials. The reviewer’s knowledge and experience homeopathy are insufficient for such judgments (5).” While recognizing their limited comprehension of homeopathy, Linde et al. reviewed 32 studies, providing detailed information about each study’s methodology, including whether remedies were indeed prescribed homeopathically:
“In 20 trials, the choice of the remedy seemed to be unrestricted (approach 1), in 2 trials patients were included only if they matched the remedy picture of one of a preset range of remedies (approach 2), in 7 studies patients were included (without taking into account "homeopathic" aspects) and then the best fitting remedy had to be chosen from a range of predefined remedies was prescribed (approach 3), and in 3 trials only one remedy was applied and patients were entered only if they matched the remedy picture (approach 4) (5).”
Only 19 trials provided “sufficient data for meta-analysis (5),” although not all of these trials were of high methodological quality nor did all of them use individualized therapy. Of 12 trials categorized as “likely to have good methodological quality” or “unlikely to have major flaws,” all except two favoured homeopathy over placebo (5). Of these 12 highest quality trials, seven were individualized, and all except one favoured homeopathy. This review relied on the data from the 19 trials (both individualized and otherwise) and concluded: “while overall the results indicate that individualized homeopathy is superior to placebo, the methodologically better trials have less positive results and confirmatory independent replications are lacking. The evidence from these trials that individualized is clearly more efficacious than placebo is, therefore, not fully convincing (5).”
This review, which recognized individualization of treatment in homeopathy, is a step in the right direction. Conducting useful research on homeopathy within the conventional medical paradigm requires a greater understanding of the system of medicine being investigated in order to truly evaluate the use of homeopathy as a treatment modality.
Finally, a long-term observational study by Witt et al. assessed perceived change in complaint severity and quality of life at baseline, and after 2 and 8 years in 3,709 patients treated with homeopathy. In this study, physicians were free to choose treatment which “usually included the prescription of homeopathic medicines according to homeopathic principles, but also could include the onset, change, or withdrawal of a conventional medicine, referrals to specialists, or admission to a hospital (6).” At eight years, 32.9% of patients were still receiving homeopathic treatment, 29.2% of patients stopped treatment due to perceived major improvements in health, 26.0% stopped treatment because they did not feel homeopathy helped enough, 7.1% of patients stopped treatment for reasons unrelated to efficacy of therapy, and 3.6% stopped treatment without reason (6). The researchers concluded that, “patients who seek homeopathic treatment are likely to improve considerably, although this effect must not be attributed to homeopathic treatment alone. These effects persisted for 8 years (6).”
1. Hahnemann S. Organon of the Medical Art. Palo Alto: Birdcage Books; 1996, p. 141.
2. Shang A, Huwiler-Müntener K, Nartey L, Jüni P, Dörig S, Sterne JA, Pewsner D, Egger M. Are the clinical effects of homoeopathy placebo effects? Comparative study of placebo-controlled trials of homoeopathy and allopathy. Lancet. 2005 Aug 27-Sep 2;366(9487):726-32.
3. Rutten AL, Stolper CF. The 2005 meta-analysis of homeopathy: the importance of post-publication data. Homeopathy. 2008 Oct;97(4):169-77.
4. Lüdtke R, Rutten AL. The conclusions on the effectiveness of homeopathy highly depend on the set of analyzed trials. J Clin Epidemiol. 2008 Dec;61(12):1197-204. Epub 2008 Oct 1. Review.
5. Linde K, Melchart D. Randomized controlled trials of individualized homeopathy: a state-of-the-art review. J Altern Complement Med. 1998 Winter;4(4):371-88. Review.
6. Witt CM, Lüdtke R, Mengler N, Willich SN. How healthy are chronically ill patients after eight years of homeopathic treatment?--Results from a long term observational study. BMC Public Health. 2008 Dec 17;8:413.
One of the major reasons that the results of most mainstream research on homeopathy are often inconclusive because the methods used usually do not honour the principles of homeopathy and therefore the research does not actually evaluate the practice of homeopathy. Aphorism 104 in the Organon explains how a practitioner can take and treat a case homeopathically:
“Once the totality of symptoms that principally determine and distinguish the disease case … has been exactly recorded, the most difficult work is done … He can then select … a well-aimed, similar, artificial disease potence, in the form of a homeopathically chosen medicinal means, to oppose the total disease image (1).”
Unfortunately, remedies are often not prescribed individually and are instead selected based on typical clinical presentation of pathology.
A meta-analysis published by Shang et al. in the Lancet in 2005 compared placebo-controlled homeopathy trials to conventional medicine trials matched by disorder and type and determined that “the clinical effects of homoeopathy, but not those of conventional medicine, are unspecific placebo or context effects (2).” The homeopathy trials were categorized classical, clinical, or complex homoeopathy (or as isopathy). Specifically,
“Classical homoeopathy was defined as comprehensive homoeopathic history-taking, followed by the prescription of a single individualised remedy, possibly with subsequent change of remedy in response to changing symptoms. If no comprehensive homoeopathic history was taken and all patients received a single, identical remedy, interventions were classified as clinical homoeopathy (2).”
Only “classical” homeopathy trials actually reflect the use of remedies according to homeopathic principles as set out in the Organon. “Clinical” homeopathy is the substitution of homeopathic remedies for conventional medicine and therefore not the practice of homeopathy. Of 110 homeopathy trials analyzed, only 18 were categorized as “classical” while 48 “clinical” homeopathy trials were analyzed. The selection of trials for this analysis therefore precluded results that would accurately evaluate the effects of homeopathic treatment.
Rutten and Stolper analyzed post-publication data from the Shang paper and concluded that:
“Re-analysis of Shang's post-publication data did not support the conclusion that homeopathy is a placebo effect. The conclusion that homeopathy is and that conventional is not a placebo effect was not based on comparative analysis and not justified because of heterogeneity and lack of sensitivity analysis. If we confine ourselves to the predefined hypotheses and the part of the analysis that is indeed comparative, the conclusion should be that quality of homeopathic trials is better than of conventional trials, for all trials (p=0.03) as well as for smaller trials (p=0.003) (3).”
A review by Lüdtke and Rutten also came to this conclusion. Their meta-analysis determined that “homeopathy had a significant effect beyond placebo (OR=0.76; 95% CI: 0.59-0.99; p=0.039) (4).” and that, “Shang's negative results were mainly influenced by one single trial (4).” They concluded: “Shang's results and conclusions are less definite than had been presented (4).”
Linde et al. published a review of randomized controlled trials of individualized homeopathy in the Lancet in 1998. In this review, the team clarified that, “in individualized homeopathy the choice of the remedy for treatment is not based on a conventional diagnosis but on the match of the patient’s particular symptoms with the ‘remedy picture (5)’” and also conceded that, “no attempt was made to assess the ‘homeopathic’ quality of the trials. The reviewer’s knowledge and experience homeopathy are insufficient for such judgments (5).” While recognizing their limited comprehension of homeopathy, Linde et al. reviewed 32 studies, providing detailed information about each study’s methodology, including whether remedies were indeed prescribed homeopathically:
“In 20 trials, the choice of the remedy seemed to be unrestricted (approach 1), in 2 trials patients were included only if they matched the remedy picture of one of a preset range of remedies (approach 2), in 7 studies patients were included (without taking into account "homeopathic" aspects) and then the best fitting remedy had to be chosen from a range of predefined remedies was prescribed (approach 3), and in 3 trials only one remedy was applied and patients were entered only if they matched the remedy picture (approach 4) (5).”
Only 19 trials provided “sufficient data for meta-analysis (5),” although not all of these trials were of high methodological quality nor did all of them use individualized therapy. Of 12 trials categorized as “likely to have good methodological quality” or “unlikely to have major flaws,” all except two favoured homeopathy over placebo (5). Of these 12 highest quality trials, seven were individualized, and all except one favoured homeopathy. This review relied on the data from the 19 trials (both individualized and otherwise) and concluded: “while overall the results indicate that individualized homeopathy is superior to placebo, the methodologically better trials have less positive results and confirmatory independent replications are lacking. The evidence from these trials that individualized is clearly more efficacious than placebo is, therefore, not fully convincing (5).”
This review, which recognized individualization of treatment in homeopathy, is a step in the right direction. Conducting useful research on homeopathy within the conventional medical paradigm requires a greater understanding of the system of medicine being investigated in order to truly evaluate the use of homeopathy as a treatment modality.
Finally, a long-term observational study by Witt et al. assessed perceived change in complaint severity and quality of life at baseline, and after 2 and 8 years in 3,709 patients treated with homeopathy. In this study, physicians were free to choose treatment which “usually included the prescription of homeopathic medicines according to homeopathic principles, but also could include the onset, change, or withdrawal of a conventional medicine, referrals to specialists, or admission to a hospital (6).” At eight years, 32.9% of patients were still receiving homeopathic treatment, 29.2% of patients stopped treatment due to perceived major improvements in health, 26.0% stopped treatment because they did not feel homeopathy helped enough, 7.1% of patients stopped treatment for reasons unrelated to efficacy of therapy, and 3.6% stopped treatment without reason (6). The researchers concluded that, “patients who seek homeopathic treatment are likely to improve considerably, although this effect must not be attributed to homeopathic treatment alone. These effects persisted for 8 years (6).”
1. Hahnemann S. Organon of the Medical Art. Palo Alto: Birdcage Books; 1996, p. 141.
2. Shang A, Huwiler-Müntener K, Nartey L, Jüni P, Dörig S, Sterne JA, Pewsner D, Egger M. Are the clinical effects of homoeopathy placebo effects? Comparative study of placebo-controlled trials of homoeopathy and allopathy. Lancet. 2005 Aug 27-Sep 2;366(9487):726-32.
3. Rutten AL, Stolper CF. The 2005 meta-analysis of homeopathy: the importance of post-publication data. Homeopathy. 2008 Oct;97(4):169-77.
4. Lüdtke R, Rutten AL. The conclusions on the effectiveness of homeopathy highly depend on the set of analyzed trials. J Clin Epidemiol. 2008 Dec;61(12):1197-204. Epub 2008 Oct 1. Review.
5. Linde K, Melchart D. Randomized controlled trials of individualized homeopathy: a state-of-the-art review. J Altern Complement Med. 1998 Winter;4(4):371-88. Review.
6. Witt CM, Lüdtke R, Mengler N, Willich SN. How healthy are chronically ill patients after eight years of homeopathic treatment?--Results from a long term observational study. BMC Public Health. 2008 Dec 17;8:413.
Is evidence-based medicine compatible with naturopathic principles?
08/02/10 17:50
One of the most common criticisms of natural medicine is that it lacks supportive evidence. This is simply not true! In many cases, there is as much or more research evidence for natural medicine as conventional medicine. However, there are also areas in which the research evidence is sparse or incomplete. The purpose of this blog is to clarify the true meaning of evidence-based medicine (EBM) and explore its role in contributing to natural medicine.
Evidence-based medicine (EBM) is defined as the “conscientious, explicit and judicious use of current best evidence in making decisions about care of individual patients (1).” Furthermore:
“The practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research. By individual clinical expertise we mean the proficiency and judgment that individual clinicians acquire through clinical experience and clinical practice (1).”
This definition of evidence-based medicine does not conflict with the principles of naturopathic medicine. Naturopathic medicine is based on a large body of evidence gathered through systematic research and knowledge gained through clinical experience. Its principles support the application of this information to devise the most effective treatment for our patients.
However, the colloquial understanding of EBM supports randomized, double blind, placebo-controlled studies as gold standard of knowledge and leaves little room for other forms of research or for clinical experience.
Conventionally understood EBM is limited in encouraging health care that adheres to naturopathic principles. First, EBM does not recognize holistic treatment of individuals, and in fact seeks to boil down complex information to a simple conclusion recognizing only how the majority of subjects respond to a single intervention. Not only does this ignore the knowledge that could be gained through examining all the subjects in a study and why they each responded in the way that they did, but also is not necessarily applicable to real life health care since patients are nearly never under controlled conditions and subject to only one intervention. Naturopathic doctors are interested in treating real patients in the real world and therefore in gathering knowledge in any area that will serve this purpose. In many cases, this knowledge includes clinical observation and experience with real patients.
Second, funding committed to research is not allocated based on what areas of knowledge are the most interesting, warrant the most investigation, or even may be the most beneficial to the public. Most research is conducted by pharmaceutical companies on products they hope to bring to market in order to earn profits for shareholders. Unfortunately, this capitalist drive behind health knowledge is not conducive to researching how low-cost treatments such as diet and lifestyle changes can be far more effective than any drug. It is also not conducive to gaining knowledge through “failed” experiments, such as when pharmaceutical research does not yield results favourable to the drug being researched. Currently, pharmaceutical companies are not required to publish such research, although there is a movement to change this, thankfully. Naturopathic doctors are interested in achieving results, even if there is no particular product to sell.
Finally, naturopathic doctors also act as teachers, seeking to empower patients with information so that they can care for themselves. EBM places power in a faceless research environment, removing it from clinicians with decades of experience, and therefore also removing it from individual patients who may know their unique needs best.
Therefore, while the official definition of EBM does fit with naturopathic principles, the applied definition, in terms of how the health care system actually operates, does not.
For more information and more of my thoughts on conventional medical research, please see my previous blog Mythology of science-based medicine.
1. Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS. Evidence based medicine: what it is and what it isn't. BMJ. 1996;312 (7023):71–2.
Evidence-based medicine (EBM) is defined as the “conscientious, explicit and judicious use of current best evidence in making decisions about care of individual patients (1).” Furthermore:
“The practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research. By individual clinical expertise we mean the proficiency and judgment that individual clinicians acquire through clinical experience and clinical practice (1).”
This definition of evidence-based medicine does not conflict with the principles of naturopathic medicine. Naturopathic medicine is based on a large body of evidence gathered through systematic research and knowledge gained through clinical experience. Its principles support the application of this information to devise the most effective treatment for our patients.
However, the colloquial understanding of EBM supports randomized, double blind, placebo-controlled studies as gold standard of knowledge and leaves little room for other forms of research or for clinical experience.
Conventionally understood EBM is limited in encouraging health care that adheres to naturopathic principles. First, EBM does not recognize holistic treatment of individuals, and in fact seeks to boil down complex information to a simple conclusion recognizing only how the majority of subjects respond to a single intervention. Not only does this ignore the knowledge that could be gained through examining all the subjects in a study and why they each responded in the way that they did, but also is not necessarily applicable to real life health care since patients are nearly never under controlled conditions and subject to only one intervention. Naturopathic doctors are interested in treating real patients in the real world and therefore in gathering knowledge in any area that will serve this purpose. In many cases, this knowledge includes clinical observation and experience with real patients.
Second, funding committed to research is not allocated based on what areas of knowledge are the most interesting, warrant the most investigation, or even may be the most beneficial to the public. Most research is conducted by pharmaceutical companies on products they hope to bring to market in order to earn profits for shareholders. Unfortunately, this capitalist drive behind health knowledge is not conducive to researching how low-cost treatments such as diet and lifestyle changes can be far more effective than any drug. It is also not conducive to gaining knowledge through “failed” experiments, such as when pharmaceutical research does not yield results favourable to the drug being researched. Currently, pharmaceutical companies are not required to publish such research, although there is a movement to change this, thankfully. Naturopathic doctors are interested in achieving results, even if there is no particular product to sell.
Finally, naturopathic doctors also act as teachers, seeking to empower patients with information so that they can care for themselves. EBM places power in a faceless research environment, removing it from clinicians with decades of experience, and therefore also removing it from individual patients who may know their unique needs best.
Therefore, while the official definition of EBM does fit with naturopathic principles, the applied definition, in terms of how the health care system actually operates, does not.
For more information and more of my thoughts on conventional medical research, please see my previous blog Mythology of science-based medicine.
1. Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS. Evidence based medicine: what it is and what it isn't. BMJ. 1996;312 (7023):71–2.
Mythology of science-based medicine
12/01/10 16:30
This blog emerged after reading several different articles about the state of conventional medical care and some of the misperceptions surrounding efficacy of conventional medical treatments.
First, an article titled The Mythology of Science-Based Medicine provides examples of conventional medical interventions considered to be safe, valid, or effective when in fact they lack scientific basis or have been proven ineffective. This article provides links to sources and some responses from the authors and other medical experts in the comments. Here is an addendum to that article further addressing comments.
Second, an article titled How Common Are Medical Mistakes? which delves into the startling fact that the third leading cause of death of Americans is iatrogenic causes, meaning caused by doctors, medical treatment, or diagnostic procedures.
Finally, a few of my thoughts on this topic:
The “gold-standard” of medical research is the double-blind randomized controlled trial, which attempts to isolate the effect of a single intervention and control all other factors (including many features of patients such as pre-existing conditions, medications, lifestyle, diet, etc.) This makes sense in a research context but has little bearing on reality, in which medical interventions are used in conjunction with other treatments in a wide variety of patients. It is important to understand that a clinical trial is only the first step in evaluating treatment. It provides information on how something works and verifies safety in the short-term but is most definitely not a verdict on the effectiveness in the real world. This can only truly be gauged in the context of an uncontrolled patient population over time.
Something important to note about bypass surgery and angioplasty is that while they do not extend life (which is the case for many common medical treatments), this is not the only important measure to consider! Quality of life is also incredibly important and these procedures can make a major difference here. Patients with cardiovascular disease who in the past would not have these options would be severely limited by the inability to engage in even the most basic everyday activities but would also not be ill enough that they would pass away. These procedures have allowed many patients to return to a more normal level of activity and participation in life which is invaluable, even if their lifespan remains the same.
Regarding antidepressants, it should not be surprising that they are not very effective except in cases of severe depression. In most cases, antidepressants are the sole treatment prescribed despite mountains of evidence that combining them with other treatments (most notably psychotherapy) is far more effective. For many patients with depression, there are valid reasons to feel depressed, such as grief, declining health, emotional stressors, post-partum changes, etc. Depression is a natural human response to life’s ups and downs. Unfortunately most of us are just not equipped to accept and work through life’s challenges on our own. Psychotherapy can be enormously helpful in arming patients with coping and self-care skills. There are also many patients for whom antidepressants are very useful in boosting them up enough so that they can actively seek other treatments to address the underlying causes of depression, but the key here is that the cause must be addressed and corrected. Otherwise antidepressants either just don’t cut it or simply mask a problem that will re-emerge once the patient discontinues the medication. This is common considering the many uncomfortable and intolerable side-effects of these medications. There are so many proven and safe treatments for depression (such as nutrition, exercise, supplements, lifestyle changes, homeopathy, therapy) that can be used in place of or in conjunction with antidepressants to achieve much better outcomes.
First, an article titled The Mythology of Science-Based Medicine provides examples of conventional medical interventions considered to be safe, valid, or effective when in fact they lack scientific basis or have been proven ineffective. This article provides links to sources and some responses from the authors and other medical experts in the comments. Here is an addendum to that article further addressing comments.
Second, an article titled How Common Are Medical Mistakes? which delves into the startling fact that the third leading cause of death of Americans is iatrogenic causes, meaning caused by doctors, medical treatment, or diagnostic procedures.
Finally, a few of my thoughts on this topic:
The “gold-standard” of medical research is the double-blind randomized controlled trial, which attempts to isolate the effect of a single intervention and control all other factors (including many features of patients such as pre-existing conditions, medications, lifestyle, diet, etc.) This makes sense in a research context but has little bearing on reality, in which medical interventions are used in conjunction with other treatments in a wide variety of patients. It is important to understand that a clinical trial is only the first step in evaluating treatment. It provides information on how something works and verifies safety in the short-term but is most definitely not a verdict on the effectiveness in the real world. This can only truly be gauged in the context of an uncontrolled patient population over time.
Something important to note about bypass surgery and angioplasty is that while they do not extend life (which is the case for many common medical treatments), this is not the only important measure to consider! Quality of life is also incredibly important and these procedures can make a major difference here. Patients with cardiovascular disease who in the past would not have these options would be severely limited by the inability to engage in even the most basic everyday activities but would also not be ill enough that they would pass away. These procedures have allowed many patients to return to a more normal level of activity and participation in life which is invaluable, even if their lifespan remains the same.
Regarding antidepressants, it should not be surprising that they are not very effective except in cases of severe depression. In most cases, antidepressants are the sole treatment prescribed despite mountains of evidence that combining them with other treatments (most notably psychotherapy) is far more effective. For many patients with depression, there are valid reasons to feel depressed, such as grief, declining health, emotional stressors, post-partum changes, etc. Depression is a natural human response to life’s ups and downs. Unfortunately most of us are just not equipped to accept and work through life’s challenges on our own. Psychotherapy can be enormously helpful in arming patients with coping and self-care skills. There are also many patients for whom antidepressants are very useful in boosting them up enough so that they can actively seek other treatments to address the underlying causes of depression, but the key here is that the cause must be addressed and corrected. Otherwise antidepressants either just don’t cut it or simply mask a problem that will re-emerge once the patient discontinues the medication. This is common considering the many uncomfortable and intolerable side-effects of these medications. There are so many proven and safe treatments for depression (such as nutrition, exercise, supplements, lifestyle changes, homeopathy, therapy) that can be used in place of or in conjunction with antidepressants to achieve much better outcomes.
Sleep and metabolic syndrome
24/11/09 10:56
I wrote a research paper looking the relationship between sleep duration and metabolic syndrome and this blog is a summary of what I learned. References are listed at the end and can be found on PubMed.
Metabolic syndrome is a group of metabolic risk factors used to identify individuals at risk for cardiovascular disease (1). A correlation between sleep duration and the development of metabolic syndrome has been observed.
The National Cholesterol Education Program (NCEP) Adult Treatment Panel III diagnosis of metabolic syndrome requires the presence of three or more of the following features (1):
1. Waist circumference:
- Men: Greater than or equal to 102cm (40in)
- Women: Greater than or equal to 88cm (35in)
2. Triglycerides: Greater than or equal to 1.7mmol/L (150 mg/dL)
3. HDL cholesterol:
- Men: Less than 1.0mmol/L (40mg/dL)
- Women: Less than 1.3mmol/L (50mg/dL)
4. Blood pressure: Greater than or equal to 130/85 mmHg or medicated for hypertension
5. Fasting blood glucose: Greater than or equal to 5.6mmol/L (100mg/dL) or medicated for hyperglycemia
First-line treatment focuses on lifestyle factors such as dietary modification and increased physical activity (1). However, given that “‘normal’ average sleep duration has decreased from about 9 h per night in 1910 to about 7.5 h currently, (2)” and mounting evidence that sleep deprivation causes physiological changes that lead to metabolic syndrome, sleep deprivation is another important lifestyle factor to consider.
Short sleep duration (less than 6 hours per night) is associated with the highest risk for metabolic syndrome, but long sleep duration (more than 8 or 9 hours per night) is also associated with increased risk. The lowest risk was seen in subjects sleeping 7-8 hours per night (3,4).
With regards to abdominal obesity, “very short and short sleepers were at least 1.6 times more likely to meet criteria for abdominal obesity … compared with individuals who slept 7 to 8 hours per night (4).”
There is also a correlation between insulin resistance and sleep duration, both short and long: “with the reference group, the odds of meeting the glucose criterion were at least 1.7 times greater in the very short (< 6 hours) and long (> 8 hours) sleeper groups (4).” It is also likely that insulin resistance due to altered metabolism resulting from inadequate sleep develops gradually over years. One study restricted sleep in healthy young men to four hours per night for six nights and found that sleep debt led to impaired carbohydrate tolerance. Decreased morning insulin sensitivity was observed after 6 days of sleep restriction compared to when subjects were fully rested (6). “These results suggest that insulin sensitivity was lower on the 6th than on the 5th day of sleep restriction and thus that insulin resistance may develop progressively with increasing exposure to partial sleep loss (5).”
The Sleep Heart Health Study found that sleep duration was associated with risk of hypertension, with those sleeping less than 6 and 6-7 hours and those sleeping 8-9 and 9 or more hours demonstrating increased risk (6). A longitudinal analyses of the first National Health and Nutrition Examination Survey demonstrated that sleep durations of “< or =5 hours per night were associated with a significantly increased risk of hypertension … in subjects between the ages of 32 and 59 years (7).”
The studies discussed above have also found a relationship between increased sleep and metabolic syndrome. When examined more closely in one study, relationships between long sleep duration and metabolic syndrome and elevated glucose “were no longer significant with adjustment for use of antihypertensive medication, which has been shown to impact fasting blood glucose levels (4).” There is also a relationship between long sleep duration and sleep apnea, suggesting that “long sleep duration is a proxy for sleep disordered breathing and that sleep apnea drives the relationship between long sleep duration and health outcomes (4).”
Sleep quality is also an important factor to consider. An observational, cross-sectional study demonstrated that “poor global sleep-quality scores on the Pittsburgh Sleep Quality Index were related significantly to the presence of the metabolic syndrome (8).”
Studies relating sleep duration to metabolic changes are often confounded by pre-existing conditions (such as diabetes or hypertension), lifestyle habits (such as smoking, diet, alcohol intake, and caffeine intake), and other factors affecting sleep (such as sleep apnea). It is therefore important that studies of sleep duration take these factors into account and control for them as much as possible in order to establish a clear relationship between sleep and health outcomes. One researcher has challenged the above conclusions by offering three criticisms. First, “few obese adults/children are short sleepers, and few short sleeping adults/children are obese or suffer obesity-related disorders (9).” Second, the clinical risk only emerges from very short or long sleep duration and develops over many years, so while acute sleep restriction does lead to leads to glucose intolerance and metabolic syndrome “this is too little sleep and cannot be sustained beyond a few days (9).” Finally, he offers an alternative explanation for the relationship between sleep and metabolism: “habitually insufficient sleep could contribute towards obesity, metabolic syndrome, etc., via sleepiness-related inactivity and excess energy intake (9).”
It seems obvious that sleep is an important factor in health, but it is often overlooked by both conventional and naturopathic practitioners. Based on the studies discussed, the optimal sleep duration is between 7-8 hours per night. Many patients fail to prioritize sleep or have trouble falling asleep easily, both issues that can be greatly aided by naturopathic interventions. Sleep quality is also an important consideration and naturopathic doctors are also well equipped to make recommendations in this area.
1. MD Consult. Metabolic Syndrome. Accessed 18 Nov 2008. Available at: http://www.mdconsult.com.
2. Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999 Oct 23;354(9188):1435-9.
3. Choi KM, Lee JS, Park HS, Baik SH, Choi DS, Kim SM. Relationship between sleep duration and the metabolic syndrome: Korean National Health and Nutrition Survey 2001. Int J Obes (Lond). 2008 Jul;32(7):1091-7. Epub 2008 May 13.
4. Hall MH, Muldoon MF, Jennings JR, Buysse DJ, Flory JD, Manuck SB. Self-reported sleep duration is associated with the metabolic syndrome in midlife adults. Sleep. 2008 May 1;31(5):635-43.
5. Knutson KL, Spiegel K, Penev P, Van Cauter E. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007 Jun;11(3):163-78. Epub 2007 Apr 17. Review.
6. Gottlieb DJ, Redline S, Nieto FJ, Baldwin CM, Newman AB, Resnick HE, Punjabi NM. Association of usual sleep duration with hypertension: the Sleep Heart Health Study. Sleep. 2006 Aug 1;29(8):1009-14.
7. Gangwisch JE, Heymsfield SB, Boden-Albala B, Buijs RM, Kreier F, Pickering TG, Rundle AG, Zammit GK, Malaspina D. Short sleep duration as a risk factor for hypertension: analyses of the first National Health and Nutrition Examination Survey. Hypertension. 2006 May;47(5):833-9. Epub 2006 Apr 3.
8. Jennings JR, Muldoon MF, Hall M, Buysse DJ, Manuck SB. Self-reported sleep quality is associated with the metabolic syndrome. Sleep. 2007 Feb 1;30(2):219-23.
9. Horne JA. Short sleep is a questionable risk factor for obesity and related disorders: statistical versus clinical significance. Biol Psychol 2008;77:266-76.
Metabolic syndrome is a group of metabolic risk factors used to identify individuals at risk for cardiovascular disease (1). A correlation between sleep duration and the development of metabolic syndrome has been observed.
The National Cholesterol Education Program (NCEP) Adult Treatment Panel III diagnosis of metabolic syndrome requires the presence of three or more of the following features (1):
1. Waist circumference:
- Men: Greater than or equal to 102cm (40in)
- Women: Greater than or equal to 88cm (35in)
2. Triglycerides: Greater than or equal to 1.7mmol/L (150 mg/dL)
3. HDL cholesterol:
- Men: Less than 1.0mmol/L (40mg/dL)
- Women: Less than 1.3mmol/L (50mg/dL)
4. Blood pressure: Greater than or equal to 130/85 mmHg or medicated for hypertension
5. Fasting blood glucose: Greater than or equal to 5.6mmol/L (100mg/dL) or medicated for hyperglycemia
First-line treatment focuses on lifestyle factors such as dietary modification and increased physical activity (1). However, given that “‘normal’ average sleep duration has decreased from about 9 h per night in 1910 to about 7.5 h currently, (2)” and mounting evidence that sleep deprivation causes physiological changes that lead to metabolic syndrome, sleep deprivation is another important lifestyle factor to consider.
Short sleep duration (less than 6 hours per night) is associated with the highest risk for metabolic syndrome, but long sleep duration (more than 8 or 9 hours per night) is also associated with increased risk. The lowest risk was seen in subjects sleeping 7-8 hours per night (3,4).
With regards to abdominal obesity, “very short and short sleepers were at least 1.6 times more likely to meet criteria for abdominal obesity … compared with individuals who slept 7 to 8 hours per night (4).”
There is also a correlation between insulin resistance and sleep duration, both short and long: “with the reference group, the odds of meeting the glucose criterion were at least 1.7 times greater in the very short (< 6 hours) and long (> 8 hours) sleeper groups (4).” It is also likely that insulin resistance due to altered metabolism resulting from inadequate sleep develops gradually over years. One study restricted sleep in healthy young men to four hours per night for six nights and found that sleep debt led to impaired carbohydrate tolerance. Decreased morning insulin sensitivity was observed after 6 days of sleep restriction compared to when subjects were fully rested (6). “These results suggest that insulin sensitivity was lower on the 6th than on the 5th day of sleep restriction and thus that insulin resistance may develop progressively with increasing exposure to partial sleep loss (5).”
The Sleep Heart Health Study found that sleep duration was associated with risk of hypertension, with those sleeping less than 6 and 6-7 hours and those sleeping 8-9 and 9 or more hours demonstrating increased risk (6). A longitudinal analyses of the first National Health and Nutrition Examination Survey demonstrated that sleep durations of “< or =5 hours per night were associated with a significantly increased risk of hypertension … in subjects between the ages of 32 and 59 years (7).”
The studies discussed above have also found a relationship between increased sleep and metabolic syndrome. When examined more closely in one study, relationships between long sleep duration and metabolic syndrome and elevated glucose “were no longer significant with adjustment for use of antihypertensive medication, which has been shown to impact fasting blood glucose levels (4).” There is also a relationship between long sleep duration and sleep apnea, suggesting that “long sleep duration is a proxy for sleep disordered breathing and that sleep apnea drives the relationship between long sleep duration and health outcomes (4).”
Sleep quality is also an important factor to consider. An observational, cross-sectional study demonstrated that “poor global sleep-quality scores on the Pittsburgh Sleep Quality Index were related significantly to the presence of the metabolic syndrome (8).”
Studies relating sleep duration to metabolic changes are often confounded by pre-existing conditions (such as diabetes or hypertension), lifestyle habits (such as smoking, diet, alcohol intake, and caffeine intake), and other factors affecting sleep (such as sleep apnea). It is therefore important that studies of sleep duration take these factors into account and control for them as much as possible in order to establish a clear relationship between sleep and health outcomes. One researcher has challenged the above conclusions by offering three criticisms. First, “few obese adults/children are short sleepers, and few short sleeping adults/children are obese or suffer obesity-related disorders (9).” Second, the clinical risk only emerges from very short or long sleep duration and develops over many years, so while acute sleep restriction does lead to leads to glucose intolerance and metabolic syndrome “this is too little sleep and cannot be sustained beyond a few days (9).” Finally, he offers an alternative explanation for the relationship between sleep and metabolism: “habitually insufficient sleep could contribute towards obesity, metabolic syndrome, etc., via sleepiness-related inactivity and excess energy intake (9).”
It seems obvious that sleep is an important factor in health, but it is often overlooked by both conventional and naturopathic practitioners. Based on the studies discussed, the optimal sleep duration is between 7-8 hours per night. Many patients fail to prioritize sleep or have trouble falling asleep easily, both issues that can be greatly aided by naturopathic interventions. Sleep quality is also an important consideration and naturopathic doctors are also well equipped to make recommendations in this area.
1. MD Consult. Metabolic Syndrome. Accessed 18 Nov 2008. Available at: http://www.mdconsult.com.
2. Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999 Oct 23;354(9188):1435-9.
3. Choi KM, Lee JS, Park HS, Baik SH, Choi DS, Kim SM. Relationship between sleep duration and the metabolic syndrome: Korean National Health and Nutrition Survey 2001. Int J Obes (Lond). 2008 Jul;32(7):1091-7. Epub 2008 May 13.
4. Hall MH, Muldoon MF, Jennings JR, Buysse DJ, Flory JD, Manuck SB. Self-reported sleep duration is associated with the metabolic syndrome in midlife adults. Sleep. 2008 May 1;31(5):635-43.
5. Knutson KL, Spiegel K, Penev P, Van Cauter E. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007 Jun;11(3):163-78. Epub 2007 Apr 17. Review.
6. Gottlieb DJ, Redline S, Nieto FJ, Baldwin CM, Newman AB, Resnick HE, Punjabi NM. Association of usual sleep duration with hypertension: the Sleep Heart Health Study. Sleep. 2006 Aug 1;29(8):1009-14.
7. Gangwisch JE, Heymsfield SB, Boden-Albala B, Buijs RM, Kreier F, Pickering TG, Rundle AG, Zammit GK, Malaspina D. Short sleep duration as a risk factor for hypertension: analyses of the first National Health and Nutrition Examination Survey. Hypertension. 2006 May;47(5):833-9. Epub 2006 Apr 3.
8. Jennings JR, Muldoon MF, Hall M, Buysse DJ, Manuck SB. Self-reported sleep quality is associated with the metabolic syndrome. Sleep. 2007 Feb 1;30(2):219-23.
9. Horne JA. Short sleep is a questionable risk factor for obesity and related disorders: statistical versus clinical significance. Biol Psychol 2008;77:266-76.
Thyroid, iodine, and breast health
03/07/09 10:53
This blog was originally published on December 2, 2008 here.
I wrote a research paper looking the relationships between thyroid function, breast pathologies, and the role of iodine supplementation. This blog is a summary of what I learned. References are listed at the end and can be found on PubMed.
First, thyroid. There is an observed correlation between thyroid dysfunction and breast cancer (1,2,3), particularly hypothyroidism (3,4). Decreased function of the thyroid gland and rising TSH are also associated with a doubling in the risk of development of fibrocystic breast disease (5).
Next, iodine and breasts. Both breast tissue and thyroid tissue concentrate iodine (6) and deficiency of iodine causes “atypical tissue and physiologic changes in both” (7). One researcher noted that “geographic differences in the rates of breast, endometrial, and ovarian cancer appear to be inversely correlated with dietary iodine intake” (8). For example, in Japan seaweed (high in both iodine and selenium) is a major part of the diet and may play a role in the low incidence of both benign and malignant breast disease in that country (9).
A study on rats demonstrated a reduction in breast cancer incidence with iodine treatment (10). With regard to fibrocystic breast disease, randomized, double-blind, placebo-controlled, multicenter clinical trials (the gold-standard of conventional medicine!) have demonstrated that supplementation with iodide/iodine significantly reduced breast pain, tenderness, and nodularity (11,12).
So how does this work? One theory is that iodine deficiency leads to a state of excess estrogen (13), increasing the risk of a whole host of cancers. Iodine is also believed to suppress tumour growth (14), induce tumour cell death (15), and regulate genes that influence hormone metabolism, cell cycle, growth, and differentiation (16).
Why is this useful information? Everything in the body is connected, particularly the endocrine system. So, when something is going wrong in one area, like thyroid function, there are likely also going to be issues either immediately or down the road with another area, particularly reproductive organs. The causal mechanisms are not clear yet, but it is prudent to assess breast health when patients present with thyroid dysfunction and vice versa. There is evidence to suggest that iodine is effective nutritional treatment for fibrocystic breast disease and it may also be useful in reproductive cancers. Molecular iodine, rather than iodide, was found to be most effective and have the least adverse effects on the thyroid (12).
There is lots of other interesting information that I was not able to get to, such as a deeper look at the interaction of sex hormones with thyroid function and other influences on hormonal balance, such as sleep. Maybe one day I’ll have time to do more research and I’ll post an update!
References:
1. Turken O, NarIn Y, DemIrbas S, Onde ME, Sayan O, KandemIr EG, YaylacI M, Ozturk A. Breast cancer in association with thyroid disorders. Breast Cancer Res. 2003;5(5):R110-3. Epub 2003 Jun 5. PMID: 12927040
2. Saraiva PP, Figueiredo NB, Padovani CR, Brentani MM, Nogueira CR. Profile of thyroid hormones in breast cancer patients. Braz J Med Biol Res. 2005 May;38(5):761-5. Epub 2005 May 25. PMID: 15917958
3. Giani C, Fierabracci P, Bonacci R, Gigliotti A, Campani D, De Negri F, Cecchetti D, Martino E, Pinchera A. Relationship between breast cancer and thyroid disease: relevance of autoimmune thyroid disorders in breast malignancy. J Clin Endocrinol Metab. 1996 Mar;81(3):990-4.
4. Kuijpens JL, Nyklíctek I, Louwman MW, Weetman TA, Pop VJ, Coebergh JW. Hypothyroidism might be related to breast cancer in post-menopausal women. Thyroid. 2005 Nov;15(11):1253-9. PMID: 16356089
5. Mardaleishvili KG, Nemsadze GG, Metreveli DS, Roinishvili TL. [About correlation of dysfunction of the thyroid gland with fibrocystic diseases in women] Georgian Med News. 2006 Nov;(140):30-2. Russian.
6. Patrick L. Iodine: deficiency and therapeutic considerations. Altern Med Rev. 2008 Jun;13(2):116-27. Review. PMID: 18590348
7. Eskin BA, Grotkowski CE, Connolly CP, Ghent WR. Different tissue responses for iodine and iodide in rat thyroid and mammary glands. Biol Trace Elem Res. 1995 Jul;49(1):9-19. PMID: 7577324
8. Stadel BV. Dietary iodine and risk of breast, endometrial, and ovarian cancer. Lancet. 1976 Apr 24;1(7965):890-1. PMID: 58152
9. Cann SA, van Netten JP, van Netten C. Hypothesis: iodine, selenium and the development of breast cancer. Cancer Causes Control. 2000 Feb;11(2):121-7. Review. PMID: 10710195
10. García-Solís P, Alfaro Y, Anguiano B, Delgado G, Guzman RC, Nandi S, Díaz-Muñoz M, Vázquez-Martínez O, Aceves C. Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion. Mol Cell Endocrinol. 2005 May 31;236(1-2):49-57. Epub 2005 Apr 13. PMID: 15922087
11. Kessler JH. The effect of supraphysiologic levels of iodine on patients with cyclic mastalgia. Breast J. 2004 Jul-Aug;10(4):328-36. PMID: 15239792
12. Ghent WR, Eskin BA, Low DA, Hill LP. Iodine replacement in fibrocystic disease of the breast. Can J Surg. 1993 Oct;36(5):453-60. PMID: 8221402
13. Stadel BV. Dietary iodine and risk of breast, endometrial, and ovarian cancer. Lancet. 1976 Apr 24;1(7965):890-1. PMID: 58152
14. Funahashi H, Imai T, Tanaka Y, Tobinaga J, Wada M, Morita T, Yamada F, Tsukamura K, Oiwa M, Kikumori T, Narita T, Takagi H. Suppressive effect of iodine on DMBA-induced breast tumor growth in the rat. J Surg Oncol. 1996 Mar;61(3):209-13. PMID: 8637209
15. Shrivastava A, Tiwari M, Sinha RA, Kumar A, Balapure AK, Bajpai VK, Sharma R, Mitra K, Tandon A, Godbole MM. Molecular iodine induces caspase-independent apoptosis in human breast carcinoma cells involving the mitochondria-mediated pathway. J Biol Chem. 2006 Jul 14;281(28):19762-71. Epub 2006 May 5. PMID: 16679319
16. Stoddard FR 2nd, Brooks AD, Eskin BA, Johannes GJ. Iodine alters gene expression in the MCF7 breast cancer cell line: evidence for an anti-estrogen effect of iodine. Int J Med Sci. 2008 Jul 8;5(4):189-96. PMID: 18645607
I wrote a research paper looking the relationships between thyroid function, breast pathologies, and the role of iodine supplementation. This blog is a summary of what I learned. References are listed at the end and can be found on PubMed.
First, thyroid. There is an observed correlation between thyroid dysfunction and breast cancer (1,2,3), particularly hypothyroidism (3,4). Decreased function of the thyroid gland and rising TSH are also associated with a doubling in the risk of development of fibrocystic breast disease (5).
Next, iodine and breasts. Both breast tissue and thyroid tissue concentrate iodine (6) and deficiency of iodine causes “atypical tissue and physiologic changes in both” (7). One researcher noted that “geographic differences in the rates of breast, endometrial, and ovarian cancer appear to be inversely correlated with dietary iodine intake” (8). For example, in Japan seaweed (high in both iodine and selenium) is a major part of the diet and may play a role in the low incidence of both benign and malignant breast disease in that country (9).
A study on rats demonstrated a reduction in breast cancer incidence with iodine treatment (10). With regard to fibrocystic breast disease, randomized, double-blind, placebo-controlled, multicenter clinical trials (the gold-standard of conventional medicine!) have demonstrated that supplementation with iodide/iodine significantly reduced breast pain, tenderness, and nodularity (11,12).
So how does this work? One theory is that iodine deficiency leads to a state of excess estrogen (13), increasing the risk of a whole host of cancers. Iodine is also believed to suppress tumour growth (14), induce tumour cell death (15), and regulate genes that influence hormone metabolism, cell cycle, growth, and differentiation (16).
Why is this useful information? Everything in the body is connected, particularly the endocrine system. So, when something is going wrong in one area, like thyroid function, there are likely also going to be issues either immediately or down the road with another area, particularly reproductive organs. The causal mechanisms are not clear yet, but it is prudent to assess breast health when patients present with thyroid dysfunction and vice versa. There is evidence to suggest that iodine is effective nutritional treatment for fibrocystic breast disease and it may also be useful in reproductive cancers. Molecular iodine, rather than iodide, was found to be most effective and have the least adverse effects on the thyroid (12).
There is lots of other interesting information that I was not able to get to, such as a deeper look at the interaction of sex hormones with thyroid function and other influences on hormonal balance, such as sleep. Maybe one day I’ll have time to do more research and I’ll post an update!
References:
1. Turken O, NarIn Y, DemIrbas S, Onde ME, Sayan O, KandemIr EG, YaylacI M, Ozturk A. Breast cancer in association with thyroid disorders. Breast Cancer Res. 2003;5(5):R110-3. Epub 2003 Jun 5. PMID: 12927040
2. Saraiva PP, Figueiredo NB, Padovani CR, Brentani MM, Nogueira CR. Profile of thyroid hormones in breast cancer patients. Braz J Med Biol Res. 2005 May;38(5):761-5. Epub 2005 May 25. PMID: 15917958
3. Giani C, Fierabracci P, Bonacci R, Gigliotti A, Campani D, De Negri F, Cecchetti D, Martino E, Pinchera A. Relationship between breast cancer and thyroid disease: relevance of autoimmune thyroid disorders in breast malignancy. J Clin Endocrinol Metab. 1996 Mar;81(3):990-4.
4. Kuijpens JL, Nyklíctek I, Louwman MW, Weetman TA, Pop VJ, Coebergh JW. Hypothyroidism might be related to breast cancer in post-menopausal women. Thyroid. 2005 Nov;15(11):1253-9. PMID: 16356089
5. Mardaleishvili KG, Nemsadze GG, Metreveli DS, Roinishvili TL. [About correlation of dysfunction of the thyroid gland with fibrocystic diseases in women] Georgian Med News. 2006 Nov;(140):30-2. Russian.
6. Patrick L. Iodine: deficiency and therapeutic considerations. Altern Med Rev. 2008 Jun;13(2):116-27. Review. PMID: 18590348
7. Eskin BA, Grotkowski CE, Connolly CP, Ghent WR. Different tissue responses for iodine and iodide in rat thyroid and mammary glands. Biol Trace Elem Res. 1995 Jul;49(1):9-19. PMID: 7577324
8. Stadel BV. Dietary iodine and risk of breast, endometrial, and ovarian cancer. Lancet. 1976 Apr 24;1(7965):890-1. PMID: 58152
9. Cann SA, van Netten JP, van Netten C. Hypothesis: iodine, selenium and the development of breast cancer. Cancer Causes Control. 2000 Feb;11(2):121-7. Review. PMID: 10710195
10. García-Solís P, Alfaro Y, Anguiano B, Delgado G, Guzman RC, Nandi S, Díaz-Muñoz M, Vázquez-Martínez O, Aceves C. Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion. Mol Cell Endocrinol. 2005 May 31;236(1-2):49-57. Epub 2005 Apr 13. PMID: 15922087
11. Kessler JH. The effect of supraphysiologic levels of iodine on patients with cyclic mastalgia. Breast J. 2004 Jul-Aug;10(4):328-36. PMID: 15239792
12. Ghent WR, Eskin BA, Low DA, Hill LP. Iodine replacement in fibrocystic disease of the breast. Can J Surg. 1993 Oct;36(5):453-60. PMID: 8221402
13. Stadel BV. Dietary iodine and risk of breast, endometrial, and ovarian cancer. Lancet. 1976 Apr 24;1(7965):890-1. PMID: 58152
14. Funahashi H, Imai T, Tanaka Y, Tobinaga J, Wada M, Morita T, Yamada F, Tsukamura K, Oiwa M, Kikumori T, Narita T, Takagi H. Suppressive effect of iodine on DMBA-induced breast tumor growth in the rat. J Surg Oncol. 1996 Mar;61(3):209-13. PMID: 8637209
15. Shrivastava A, Tiwari M, Sinha RA, Kumar A, Balapure AK, Bajpai VK, Sharma R, Mitra K, Tandon A, Godbole MM. Molecular iodine induces caspase-independent apoptosis in human breast carcinoma cells involving the mitochondria-mediated pathway. J Biol Chem. 2006 Jul 14;281(28):19762-71. Epub 2006 May 5. PMID: 16679319
16. Stoddard FR 2nd, Brooks AD, Eskin BA, Johannes GJ. Iodine alters gene expression in the MCF7 breast cancer cell line: evidence for an anti-estrogen effect of iodine. Int J Med Sci. 2008 Jul 8;5(4):189-96. PMID: 18645607