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Depression: Functional Medicine Approach

11/8/2014

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SOURCE: Functional Medicine University
Ronald Grisanti, DC, DABCO, DACBN, MS
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Depression is considered the most  dreaded condition of mankind.  What makes depression so awful  is the sad fact that it is the one  disease devoid of hope in the minds of many  who suffer with this global epidemic.

Unlike debilitating diseases like arthritis, which shows it's ugly face by causing pain, depression is a silent enemy afflicting millions every year. My goal in this article is to prepare and educate you on a few of the common triggers of depression.

These are not original thoughts on the subject of depression but are in fact documented peer-reviewed research proving the existence of a world of information kept under "lock and key" contributing to a sea of suffering and mental anguish.

You will soon discover information that will change your life and the life of your family, friends, and patients.

Depression is a national and global epidemic. Just in the United States alone there are over 12 million people who suffer with depression, and that number is rising at an alarming rate. The costs to the American public are enormous.

The following are just a few of the common causes of depression. If you want to get better and bring happiness and joy back into your life, then you owe it to yourself to be absolutely certain that you have each of the following causes thoroughly checked.

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Depression and Thyroid Function
Approximately 10%-15% of patients with depression have a thyroid hormone deficiency. Now I must emphasize to you that the testing of your thyroid MUST include the following: 
  • Thyroid-stimulating hormone (TSH)• Free serum thyroxine (fT4)
  • Free triiodothyroine (fT3)
  • Reverse T3 (rT3)
  • Anti-thyroglobulin antibodies (anti-TG)
  • Anti-thyroid peroxidase antibodies (anti-TPO)

Anything less than this is simply unacceptable. It is well documented that the evaluation of only TSH is inadequate as a means of testing your thyroid. If you have been told by your physician that your thyroid is fine and have not had the above tests ordered, then think again…your physician DOES NOT have all the facts.

Obtaining a comprehensive thyroid panel is essential to rule out thyroid disorder as a possible cause of depression. The medical literature has discovered a link between low T3 and long-standing depression. In fact the common treatment of hypothyroidism with Synthroid (a T4-only thyroid medication) may be contributing to an increase in depressive symptoms due to its inability to address a deficient T3.

A comprehensive thyroid panel will also test the possibility of you suffering from a thyroid auto-immune/depression syndrome. The medical literature has found women with high levels of anti-thyroid peroxidase (anti-TPO) antibodies to be more vulnerable to depression. A recent German study concluded: "in cases of repeated depressive episodes, it seems necessary not only to get lab testing for TSH, T3, and T4 but also to assess the autoimmune status of the thyroid gland (autoantibodies)."

As you have read, it is CRITICAL that you ask your physician to do a comprehensive thyroid panel. DO NOT settle for a TSH test alone. The cause of your depression just may be found with a thyroid problem.
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Depression and Adrenal Function
Depression has been linked to disruptions in the body's stress center -- the hypothalamic pituitary adrenal (HPA) axis. The HPA is a complex communication system between the hypothalmus, the pituitary gland, and the adrenal glands.

The hypothalamus is a region of the brain that controls an immense number of bodily functions including, but not limited to, emotions, behavior, pain, and pleasure. The pituitary gland is again divided into two distinct portions: the anterior (front) pituitary and the posterior (back) pituitary portions. For the sake of this article, I will only discuss the significance of the anterior pituitary and its relation to depression. The anterior pituitary produces six very important hormones.

Each has a different and distinct function necessary for maintaining health and well-being. One hormone of special interest for the topic of depression is called Adrenocorticotropin. Adrenocorticotropin is responsible for causing the adrenal glands to produce the well-known stress hormones called cortisol and DHEA.

Now with some basic physiology under your belt, here is what happens to a person suffering with depression.

First, when a person experiences some powerful depressing thought, the hypothalamus is sent a signal to wake the pituitary up telling it to produce some of its hormones. The hypothalmus is basically a collecting center for information concerned with the well-being of the body, and in turn much of this information is used to stimulate the pituitary to produce its hormones. The one hormone just discussed is called Adrenocorticotropin. This in turn sends a signal to the adrenal glands to produce more and more of its hormones. Adrenal gland secretion of the hormones cortisol and DHEA has been directly tied to stress and other emotional factors.

A strong relationship between the overproduction of cortisol and mood variations has been established in both depressed and healthy individuals. As with many of the body's physiological responses, balance is the key. Overactivity of the body's stress system is associated with anxiety, insomnia, loss of libido, while underactivity is linked to depression with accompanying fatigue, lethargy, and indifference.

Depressed individuals often exhibit trouble in the normal relationship between the hypothalmic, pituitary, and adrenal glands. A hyperactive Hypothalamic-Pituitary-Adrenal axis may likely result in a hypersecretion (too much) of cortisol, which in turn will also result in depressive symptoms.

It is important to know how your hypothalmic pituitary adrenal (HPA) axis is functioning. With that information in hand, your physician will be in a better position to outline a patient specific treatment.

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Nutrient deficiencies, Chemical Toxins and Depression
As the incidence of depression reaches epidemic proportions, I sometimes wonder how one can overlook or may I say ignore the research documenting known causes that can be easily identified and treated.

Another common cause is the relationship between nutrient deficiencies, chemical toxins, and depression. The medical literature is "over-flowing" with peer-reviewed
abstracts proving beyond a shadow of a doubt that depression, nutritional deficiencies, and chemical toxicities are linked.

Our bodies require optimal amounts of trace minerals such as magnesium, zinc, and vanadium (to name a few) to function. Not too much and not too little… just the right balance. Excesses or deficiencies of specific minerals can set off symptoms of
depression. For instance, low levels of zinc are associated with resistant depression. Deficiencies of magnesium can bring on a wide range of psychiatric symptoms related to depression and psychosis. Research has revealed a link between high levels of the mineral vanadium and manic symptoms.
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Chemical Connection: Invisible Brain Toxins
One of the big problems with chemicals is they have this nasty ability to sneak up on you and when you least expect it. Most of the chemical sensitivities sneak up on a person over a period of weeks, months or years slowly damaging your detoxification pathways. It is not unusual for a person to experience a sudden onset of depression when a new carpet is installed or a building is renovated or freshly painted.

Let me explain some basic biochemistry...
In order to detoxify chemical toxins, your body requires adequate amounts of zinc. Zinc runs the enzyme alcohol dehydrogenase and it is this important enzyme that is responsible for detoxifying everyday home and office chemicals. The most
common chemical found in carpets, home furnishings, copy machines, secretarial white-out, commercial floor cleaners, polishers, waxes, glues, adhesives, and other common household and office surroundings is a chemical called trichloroethylene.

You may be asking how trichloroethylene can cause depression.
Let me explain. When you are exposed to this chemical, it is likely that you either inhaled it or absorbed it through your skin. Normally this chemical, like most chemicals, will be neutralized by your body's detoxification system and eliminated.

However, if your body's ability to neutralize chemicals is impaired (possibly a zinc deficiency), the chemical will back up and will accumulate in the brain. When trichloroethylene is stored in the brain it is likely converted to choloral hydrate.
If you are a baby-boomer reading this, you may remember the old "Mickey Finn" or knockout drops. And this is exactly how a person feels who is sensitive to tricholoroethylene. They will feel spacey, dizzy, dopey, unable to concentrate, foggy, and very depressed.

I have simply presented one chemical linked to depression. There are other environmental toxins linked to depression. My goal was to provide another piece of the depression mystery. There is no one treatment that will fix all people. Take ten
people suffering with depression and it is likely the cause and the treatment can be different for all ten. What may help one person may do absolutely no good for five others. With that in mind, it is wise to be certain what may be causing your health
problem. You may indeed be suffering with a zinc deficiency that would interfere with the body's ability to effectively eliminate chemicals off-gassing from your new carpet.

Again, what works for one will undoubtedly fail on another. With that in mind, it is imperative to have a physician who understands the potential causes of a disease and, for the sake of this report, depression.

Your physician MUST conduct a thorough and rather exhaustive interview/consultation with each patient and determine what direction to go in. For one patient, your physician may determine that an evaluation of the thyroid and cortisol levels would be a good start. For another patient, maybe checking for chemical toxicities and nutrient deficiencies would be the way to go. No matter what, the recommending of an anti-depressant without this type of medical detective work is simply not acceptable.

If you think that the cause of your depression is linked to chemical toxicity and/or nutrient deficiencies, then I recommend that you ask your doctor to order the following tests:
  • RBC mineral/toxic chemical assay
  • Toxic Effects Core 
  • Urine Toxic Metals- DMSA Challenge

Depression is disease that claims new victims everyday. The causes of this mental disease can range from thyroid, cortisol deficiencies, to nutrient deficiencies/chemical toxicity exposure.
References
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challenge. Ann Pharmacother. 2000 Oct;34(10):1142-5.
2. Cooke RG, Joffe RT, Levitt AJ. T3 augmentation of antidepressant
treatment in T4-replaced thyroid patients. J Clin Psychiatry. 1992 Jan;53(1):16-8.
3. Weissel M. Administration of thyroid hormones in therapy of psychiatric
illnesses] Acta Med Austriaca. 1999;26(4):129-31.
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hypothyroidism in patients with chronic and treatment-resistant
depression. Aust N Z J Psychiatry. 1996 Apr;30(2):246-52.
5. Haggerty JJ Jr, Prange AJ Jr. Borderline hypothyroidism and depression.
Annu Rev Med. 1995;46:37-46.
6. Joffe RT, Levitt AJ. Major depression and subclinical (grade 2) hypothyroidism.
Psychoneuroendocrinology. 1992 May-Jul;17(2-3):215-21.
7. Pop VJ, Maartens LH, Leusink G, van Son MJ, Knottnerus AA, Ward
AM, Metcalfe R, Weetman AP.Are autoimmune thyroid dysfunction and
depression related? J Clin Endocrinol Metab. 1998 Sep;83(9):3194-7.
8. Konig F, von Hippel C, Petersdorff T, Kaschka W. Thyroid autoantibodies
in depressive disorders Acta Med Austriaca. 1999;26(4):126-8.
9. von Zerssen D, Doerr P, Emrich HM, Lund R, Pirke KM. Diurnal
variation of mood and the cortisol rhythm in depression and normal
states of mind. Eur Arch Psychiatry Neurol Sci. 1987;237(1):36-45.
10. Guechot J, Lepine JP, Cohen C, Fiet J, Lemperiere T, Dreux C. Simple
laboratory test of neuroendocrine disturbance in depression: 11 p.m.
saliva cortisol. Neuropsychobiology. 1987;18(1):1-4.
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G, Dreux C. Physiological and pathological variations in saliva
cortisol. Horm Res. 1982;16(6):357-64.
12. Galard R, Gallart JM, Catalan R, Schwartz S, Arguello JM, Castellanos
JM. Salivary cortisol levels and their correlation with plasma ACTH
levels in depressed patients before and after the DST. Am J Psychiatry.
1991 Apr;148(4):505-8.
13. Goodyer I, Herbert J, Moor S, Altham P. Cortisol hypersecretion in
depressed school-aged children and adolescents. Psychiatry Res. 1991 Jun;37(3):237-44. 
14. Oldehinkel AJ, van den Berg MD, Flentge F, Bouhuys AL, ter Horst GJ, Ormel J. Urinary free cortisol excretion in elderly persons with minor and major depression. Psychiatry Res. 2001 Oct 10;104(1):39-47.
15. Young AH, Gallagher P, Porter RJ. Elevation of the cortisol dehydroepiandrosterone ratio in drug-free depressed patients. Am J Psychiatry. 2002 Jul;159(7):1237-9.
16. Twardowska K, Rybakowski J. Limbic-hypothalamic- pituitary-adrenal axis in depression: literature review] Psychiatr Pol. 1996 Sep- Oct;30(5):741-55.
17. Maes M, Vandoolaeghe E, Neels H, Demedts P, Wauters A, Meltzer HY, Altamura C, Desnyder R. Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness. Biol Psychiatry. 1997 Sep 1;42(5):349-58.
18. Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium deficiency. Int J Psychiatry Med. 1989;19(1):57-63.
19. Naylor GJ, Smith AH, Bryce-Smith D, Ward NI. Tissue vanadium levels in manic-depressive psychosis. Psychol Med. 1984 Nov;14(4):767- 72.
20. McLoughlin IJ, Hodge JS. Zinc in depressive disorder. Acta Psychiatr Scand. 1990 Dec;82(6):451-3.
21. Pfeiffer CC, Braverman ER. Zinc, the brain and behavior. Biol Psychiatry. 1982 Apr;17(4):513- 32.
22. Brodkin CA, Daniell W, Echeverria D, Redlich C, Checkoway H. Concerns and assumptions of labor and management in the dry-cleaning industry. Am J Ind Med. 1999 Oct;36(4):482-3.
23. Echeverria D, White RW, Sampaio C, A behavioral evaluation of PCE exposure in patients and dry cleaners: a possible relationship between clinical and preclinical effects, JOEM, 37:6, 667-680, June 1995
24. Moser VC, Cheek BM, MacPhail RC. A multidisciplinary approach to toxicological screening: III. Neurobehavioral toxicity.J Toxicol Environ Health. 1995 Jun;45(2):173-210.
25. Lemmen CA, Holden CE, Benedek EP. Criminal responsibility and solvent exposure. New Dir Ment Health Serv. 1996 Spring;(69):59-66.
26. Waters EM, Gerstner HB, Huff JE. Trichloroethylene. I. An overview. J Toxicol Environ Health. 1977 Jan;2(3):671-707. Review.
27. Winneke G. Acute behavioral effects of exposure to some organic solvents -psychophysiological aspects. Acta Neurol Scand Suppl. 1982;92:117-29.
28. Kishi R, Harabuchi I, Ikeda T, Katakura Y, Miyake H. Acute effects of trichloroethylene on blood concentrations and performance decrements
in rats and their relevance to humans. Br J Ind Med. 1993 May;50(5):470-80.
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Research Review for November

11/6/2014

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SOURCE: Global Medical Education
Guest Commentary by Angelo Sambunaris, MD

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GME Research Review is a monthly newsletter where internationally recognized experts select, summarize, and provide a clinical commentary on the latest published research in psychiatry. Each summary has been derived from the relevant article’s abstract and the clinical commentary has been provided by our expert.
REVIEW INCLUDES:
  • Adipokines as Emerging Depression Biomarkers:  A Systematic Review and Meta-Analysis
  • Seasonal Variation of Depressive Symptoms in Unipolar Major Depressive Disorder
  • Improvement in Suicidal Ideation after Ketamine Infusion: Relationship to Reductions in Depression and Anxiety
  • Effectiveness of a Smartphone App for Guiding Antidepressant Drug Selection
  • Assessment and Lifestyle Management of Patients with Obesity:  Clinical Recommendations from Systematic Reviews

Adipokines as Emerging Depression Biomarkers:  A Systematic Review and Meta-Analysis
Carvalho, AF, et. al.
Journal of Psychiatric Research 2014

Objectives
Adiponectin, leptin and resistin are hypothesized to play a role in the pathophysiology of major depressive disorder (MDD).   The purpose of this study was to determine if adipokines are biomarkers using a meta-analysis approach across diagnostic studies and intervention studies.

Conclusion
  • Differences in peripheral levels of these hormones are inconsistent across diagnostic and intervention studies.
  • Meta-regression analyses revealed that gender and depression severity explained the heterogeneity observed in adiponectin diagnostic studies, while BMI and the difference in BMI between MDD individuals and controls explained the heterogeneity of leptin diagnostic studies.
  • Subgroup analyses revealed that adiponectin peripheral levels were significantly lower in MDD participants compared to controls when assayed with RIA, but not ELISA.
  • Leptin levels were significantly higher in individuals with mild/moderate depression versus controls.
  • Resistin serum levels were lower in MDD individuals compared to healthy controls (N = 298; Hedge's g = -0.25; P = 0.03).
  • In conclusion, this systematic review and meta-analysis underscored that relevant moderators/confounders (e.g., BMI, depression severity and type of assay) should be controlled for when considering the role of leptin and adiponectin as putative MDD diagnostic biomarkers.

Discussion
Cytokines are immunomodulating agents and some consider adipokines to be cytokines but there is disagreement as to their placement in this category of potential biomarkers as they do not react within the immune system.  The question then is whether they should be considered adipose tissue derived hormones and what roles do these hormones play in depression.  Interestingly, in order for a meta-analysis to occur there should be standardization of the data collection process.  In this case there was variance including diagnosis, treatment interventions, ELISA versus RIA tests, severity of disease, BMI, gender, etc.

The search for biomarkers in the field of depression research is important but uniformity of data collection and size of datasets is critical to the establishment of a biomarker that withstands the rigors of time. The collection of larger datasets with uniform testing of samples might fall under the purview of academic networks or the NIMH rather than relying on interpretation based on meta-analyses of small datasets.   Perhaps RDOC criteria could also play a role in minimizing variance and thus moving the field along. Although the work is important there is need for standardization before interpretations can be made.

Seasonal Variation of Depressive Symptoms in Unipolar Major Depressive Disorder.
Cobb, BS et. al
Complimentary Psychiatry 2014

Objectives
Retrospective and cross-sectional studies of seasonal variation of depressive symptoms in unipolar major depression have yielded conflicting results. This study examined seasonal variation of mood symptoms in a long-term prospective cohort - the Collaborative Depression Study (CDS).


Results
  • A small increase in proportion of time depressed was found in the months surrounding the winter solstice.
  • The greatest symptom burden was seen in December through April with a peak in March.
  • The relative burden of winter depressive symptoms in the first decade demonstrated no relationship to that of the second decade.
  • The onset of new episodes was highest October through January, peaking in January.

Discussion
A very interesting trial with results that would be expected based on one’s clinical experience.  The beauty of this design was borne out of necessity, to find enough patients to follow over a span of ten years or more.  Although the n is small for such a trial the results are still interesting.  There are many other questions to address in a program such as this such as: how many unipolar patients were found to be bipolar and if bipolar which type, I or II; how many were lost to follow-up; what was data on medication compliance versus non-compliance over these winter months.  It would be interesting to see if sub-group analyses provide a clinician with any additional guidance on diagnosis, treatment, and follow-up through the winter months versus summer months for patients with unipolar depression.

Improvement in Suicidal Ideation after Ketamine Infusion: Relationship to Reductions in Depression and Anxiety.
Ballard, ED, et. al.
Journal of Psychiatric Research 2014

Objectives
Suicide is a psychiatric emergency. There are no approved pharmacologic treatments for suicidal ideation.  Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist that rapidly reduces suicidal ideation as well as depression and anxiety, but the dynamic between these symptoms is not known. The aim of this analysis was to evaluate whether ketamine has an impact on suicidal thoughts, independent of depressive and anxiety symptoms.

Results
  • At 230 min post-infusion, correlations between changes in suicidal ideation and depression ranged from 0.23 to 0.44 (p < .05), accounting for up to 19% in the variance of ideation change.
  • Correlations with anxiety ranged from 0.23 to 0.40 (p < .05), accounting for similar levels of variance.
  • Ketamine infusion was associated with significant reductions in suicidal ideation compared to placebo, when controlling for the effects of ketamine on depression (F1,587 = 10.31, p = .001) and anxiety (F1,567 = 8.54, p = .004).

Discussion
Another interesting study emanating from the Zarate lab at NIMH and providing more data in support of  ketamine as a putative approach to the treatment of depression.   The trial size is large although it must be difficult to calculate the power analysis for programs of this specific focus, suicidal ideation.  The objectives note that there are no approved pharmacologic treatments for suicidal ideation.  Many clinicians might beg to differ stating that antidepressants and other psychopharmacologic agents prevent suicide but the key point here is that approval is a regulatory item and the FDA has not given approvals for symptomatology but rather gives approvals for treatments of diagnoses. 

Thus a question is raised as to whether the correlation in this trial between improvement in depression and anxiety was due to changes in somatic anxiety symptoms or due to alleviation of psychic symptoms or due to a simple improvement in depression (sub-items) raises an interesting question.  A new study comparing Ham-A to MADRS would be a possibility but Zarate and colleagues could also remove confusion by focusing on items from the Bech subscale in order to correlate change to strictly depression or other items.  An item analysis would also be beneficial.

So although questions arise as to why the change the data are important as well as the change in the mindset of the FDA allowing symptomatology to be tested rather than a diagnostic entity.

Effectiveness of a Smartphone App for Guiding Antidepressant Drug Selection
Man, C. et. al.
Fam Med 2104 Sep

Objectives
The purpose of this study was to assess the impact of a mobile application on the confidence level of family physicians in treating depression.


Results
  • The average confidence levels in managing depression, starting an antidepressant on a patient with depression, and choosing an initial antidepressant based on patient symptoms increased significantly within the period of smartphone application usage.
  • The average scores on the antidepressant knowledge tests also improved.

Discussion
Computer programs have been used to assist in educational settings and as well as in development and use of algorithms.  In a mobile society the smartphone application fits well into the requirements of the on-the-go physician.  Being readily available and easy to use one would expect it to be an effective tool for both increasing confidence in depression treatment and educating physicians. Future studies on the impact on medical education are warranted.

Assessment and Lifestyle Management of Patients with Obesity:  Clinical Recommendations from Systematic Reviews
Kushner, RF, Ryan, DH
JAMA 2014 

Objectives
To describe current best practices for assessment and lifestyle management of obesity and to demonstrate how the updated Guidelines (2013) for Managing Overweight and Obesity in Adults based on a systematic evidence review sponsored by the National Heart, Lung, and Blood Institute (NHLBI) can be applied to an individual patient.

Results
  • The first step in obesity management is to screen all adults for overweight and obesity. A medical history should be obtained assessing for the multiple determinants of obesity, including dietary and physical activity patterns, psychosocial factors, weight-gaining medications, and familial traits.
  • Emphasis on the complications of obesity to identify patients who will benefit the most from treatment is more useful than using body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) alone for treatment decisions.  The Guidelines (2013) recommend that clinicians offer patients who would benefit from weight loss (either BMI of ≥30 with or without comorbidities or ≥25 along with 1 comorbidity or risk factor) intensive, multicomponent behavioral intervention. Some clinicians do this within their primary care practices; others refer patients for these services.
  • Weight loss is achieved by creating a negative energy balance through modification of food and physical activity behaviors. The Guidelines (2013) endorse comprehensive lifestyle treatment by intensive intervention.
  • Treatment can be implemented either in a clinician's office or by referral to a registered dietitian or commercial weight loss program. Weight loss of 5% to 10% is the usual goal. It is not necessary for patients to attain a BMI of less than 25 to achieve a health benefit.

Discussion
Excellent review.  The Primary Care setting is the first line in healthcare consideration and treatment recommendation with regard to this problem.  Some Primary Care providers may elect to refer patients out for treatment but this review suggests that screening criteria, and the initial discussion, should begin in the PCP setting.
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