Life, Longevity, & Anti-Aging Coaching

Month: April 2020

Light Therapy for Peri/Menopausal Thyroid Problems.

Light therapy

Light therapy helps thyroid function: it assists inreversing hypothyroidism by modifying gonadotropin hormone release (32).  Gonadotropins are hormones that, in women, stimulate the release of follicle stimulating hormones (FSH) and luteinizing hormones (LH) from the pituitary gland.  In the female body, LH stimulates the production of testosterone, which is then converted to estrogen.  FSH stimulates the egg follicles to mature, these follicles will eventually produce progesterone and small amounts of estrogen.  Human gonadotropin(hCG) hormones are weak stimulators of thyrotropin or TSH.  Human gonadotropin hormones stimulate a substance called adenosine monophosphate or cAMP (89) that then produces more thyroid stimulating hormone.  In both humans and animals hCG has been shown in studies to stimulated thyroid activity.  For instance, when people have overly high levels of hCG they are often diagnosed with hyperthyroidism (89). 

This link between sex hormones and thyroid functioning in women should not be overlooked.  Women are up to 20 times more likely to develop Hashimoto’s thyroiditis.  This condition is linked to disruptions in sex hormones.  Progesterone deficiency, often experienced in the menopausal transition, is interrelated with estrogen dominance (too much estrogen in comparison to the amount of progesterone).  This condition is linked to thyroid problems.  Estrogen increases the production of a protein made in the liver that inactivates thyroid hormone, called thyroid binding globulin or TBH (90).  The end result of such an imbalance is a slow down of the metabolism and increased weight and body fat.  Conversely, progesterone improves thyroid hormone activity by lowering the production of thyroid binding globulin.  When thyroid hormones are active, the body’s metabolism is stimulated, energy levels are improved, more fat is burned, and weight is better managed (91).  And, if estrogen dominance goes unchecked, hypothyroidism can be the result.  There are several shared symptoms of estrogen dominance and hypothyroidism (fatigue, headache, hair loss, reduced sex drive, and weight problems).  Estrogen dominance is also considered a symptom of thyroid insufficiencies (92).  So, these two conditions, which overlap, can be mistaken for one another (95). 

Hypothyroidism is associated with depression in research where other factors, like economics, race, age, and education levels, have been ruled out (93).  When progesterone drops and estrogen goes up or is imbalanced (normal estrogen, but not as much or no progesterone) thyroid binding globulin (TBG) goes up.  In response to elevated TBG, thyroid hormone T3 production is slowed.  So, it becomes less available to cells, disrupting their functioning.  This is one way in which progesterone deficiency disrupts limbic system functioning.  There are thyroid hormone receptors on brain cells (102), and if the brain is deprived of thyroid hormones mood states and cognition can become compromised (103), especially in the limbic system (104).  The limbic system is an area of the brain that includes the amygdala, hypothalamus, thalamus, hippocampus and other structures.  These structures are involved in regulating mood, as well as motivation, learning, and memory.  Making things worse, when T3 goes down, production of neurotransmitters serotonin and norepinephrine also drops.  As these neurochemicals are involved in mood and though process, the result can be low mood, depression, and a lack of interest in pleasure, called anhedonia (94).

Keep in mind that thyroid disruptions can also impact sex hormones.  Thyroid hormone T3 can galvanize the release of progesterone from luteal cells (100).  Progesterone production mainly takes place during or slightly after ovulation.  It happens in the ovaries, specifically in the corpus luteum, which is a temporary structure and the remains of an ovarian follicle, after it has released a mature ovum or egg.  So, if women have trouble ovulating, they will have trouble producing enough progesterone.  This is another reason that the menopausal transition is associated with thyroid problems. 

Thyroid problems are also connected to the inflammatory response and the oxidative stress underlying it.  Thyroid hormones are meant to play a protective role regarding damage due to inflammation and oxidative stress.  But, if the thyroid is not functioning properly, this can’t happen.  So, hypothyroidism can amplify oxidative stress, which can magnify inflammation, which can then suppress sex hormone production, causing yet more thyroid issues (101) and problems producing neurochemicals.

Melatonin, which is improved with light therapy, also impacts thyroid health.  Both melatonin and thyrotropin releasing hormone or TRH are produced by the pineal gland.  TRH stimulates the production of thyroid stimulating hormone or TSH.  TSH then galvanizes the production of thyroid hormone.  So, melatonin can directly stimulate TSH production (87).  In a study of women lacking proper estrogen/progesterone production, those who took 3mg of melatonin for three to six months were shown to increase thyroid hormone levels (88).

Light therapy improves vitamin D production.  Vitamin D deficiency is associated with thyroid disease (96).  It one study, 72% of subjects with autoimmune thyroid disease had D deficiency (97).  In another study, on Hashimoto’s thyroiditis, 85% of subjects had low levels of D, and high levels of anti-thyroid antibodies (98).  And, it follows that vitamin D can help to treat thyroid problems.  In one study, those patients who received 1,200 to 4,000 international units or IUs of vitamin D per day over a period of four months showed lower levels of anti-thyroid antibodies at the end of the treatment (98).  Keep in mind that this is above the recommended daily allowance of 600 IUs.  Regarding thyroid stimulating hormone specifically, in a study of hypothyroidism and vitamin D, those who took supplements for 12 weeks showed improved levels of thyroid stimulating hormone.  Keep in mind that there was no change to thyroid hormones T3, thyroxin, T4, or triiodothyronine (99).

Depression is connected to sex hormone dysregulation.  In the female body, LH stimulates the production of testosterone, which is then converted to estrogen.  FSH stimulates the egg follicles to mature, these follicles will eventually produce progesterone and small amounts of estrogen.  Female sex hormones are neuromodulators, they play a significant role in controlling the dopamine neurons, called nigrostriatal, found in the area of the brain linked to cognitive processes, called the Substantia nigra.  In animal studies (female rats and primates) subjects who had their ovaries removed experienced a 30%, or higher, loss of dopamine cells (35).  This is very important as neurotransmitter dopamine is produced in these cells.  So, sex hormones, by way of the Substantia nigra, are central to cognition, emotion, and movement.  The neurons in the Substantia nigra travel to the frontal lobes (attention and executive function) and the area of the brain associated with motor control.  If there is a death of neurons in the Substantia nigra, cognitive problems, and loss of motor control, will result (36).  Further, estrogen also intensifies the effects of norepinephrine (adrenaline in the brain) and serotonin.  It does this partly by decreasing the monoamine oxidase (MAO) activity in the central nervous system (CNS).  MAO breaks down serotonin and norepinephrine, so estrogen slows this process down, leaving the neurotransmitters active longer.  This may explain the antidepressant like effect of melatonin (if given/taken at the right time of day) in perimenopausal and menopausal women (32). In a human study of natural morning light, it was found that post menopausal women who had less morning window covering and more morning light experienced less depressed mood (37). 

This information is for educational and informational purposes only.  It is not to take the place of medical advice or treatment.   Seek out a qualified health care provider if you have questions or need help.  Dr. Grant is not responsible for any possible health consequences of anyone who follows or reads the information in this content.  Everyone, but especially those taking medication (over the counter or prescription) should talk with a physician before undertaking any changes to their lifestyle or diet (including taking supplements).

Information is copy written.

References:

32   Zimmermann, R.C., & Olcese, J.M., (2007).  Melatonin, in Treatment of the Postmenopausal Woman, Basic      and Clinical Aspects, (third ed), 2007.  Academic Press. Elsevier Inc., Amsterdam, Netherlands.  DOI:  10.1016/B978-0-12-369443-0.x5000-5.   Accessed at:    https://www.sciencedirect.com/tompics/neuroscience/melatonin.

35   Leranth, C., Roth, R.H., Elsworth, J.D., Naftolin, F., Horvath, T.L., & Redmond, D. E., (2000).  Estrogen is  essential for maintaining nigrostriatal dopamine neurons in primates: implications for Parkinson’s  disease and memory.  Journal of Neuroscience 20:8604-8609.

36   Rutgers’s University Website: Memory Loss and the brain.  The newsletter of the memory disorders project at   Rutgers’s University.  webpage: Glossary Substantia nigra.  Accessed on: Jan 03, 2018.  Accessed at:   www.memorylossonline.com

37   Youngstedt, S.D., Leung, A., Kripke, D.F., & Langer, R.D., (2004).  Association of morning illumination and window covering with mood and sleep among post menopausal women.  Sleep and Biological Rhythms 2(3):174-183.  DOI:10.1111/j.1479-8425.2004.00139.x.

87   Sakamoto, S., Nakamura, K.,Inoue, K., & Sakai, T., (2000).  Melatonin stimulates thyroid stimulating hormone accumulation in the thyrotropes of the rat pars tuberalis.  Hstochem Cell Biol., 114(3): 213-218.  DOI:         10.1007/s004180000188.

88   Bellipanni, G., Di Marzo, F., Blasi, F., & Di Marzo, A., (2005).  Effects of melatonin in premenopausal and menopausal women: our personal experience.  Ann N Y Acad Sci., 1057:393-402.  DOI: 10.1196/annals.1356.030.

89   Hershman, J.M., (1999).  Human chorionic gonadotropin and the thyroid: hyperemesis gravidarum and trophoblastic tumors. Thyroid, 9(7): 653-657.  DOI: 10.1089/thy.1999.9.653.

90   Ben-Rafael, Z., Struass, J.F., Arendash-Durand, B., Mastroianni, L. Jr., & Flickinger, G.L., (1987).  Changes in thyroid function tests and sex hormone binding globulin associated with treatment by gonadotropin.       Fertility and Sterility., 48(2):318-320. DOI: 10.1016/S0015-0282(16)59363-7.  Accessed at:          http://europepmc.org/abstract/med/3111894.

91   Taylor medical group website.  Webpage:  estrogen and progesterone: two important hormones.  Accessed at:         https://taylormedicalgroup.net/healthtopics/estrogen-and-progesterone.

92   Santin, A. P., & Furlanetto, T. W., (2011).  Role of estrogen in thyroid function and growth regulation.  Journal of Thyroid Research., 2011, 875125. DOI: https://doi.org/10.4061/2011/875125.

93    Zavareh, A.T., Jomhouri, R., Bejestani, H.S., Arshad, M., Daneshmand, M., Ziaei, H., Babadi, N., & Amiri, M., (2016).  Depression and hypothyroidism in a population-based study of Iranian women.  Rom J Intern Med.,             54(4):2170221.  DOI: 10.1515/rjim-2016-0033.

94   Santin, A. P., & Furlanetto, T. W., (2011).  Role of estrogen in thyroid function and growth regulation.  Journal of thyroid research, 2011, 875125.  DOI: https://doi.org/10.4061/2011/875125

95   Kumar, P., & Magon, N., (2012).  Hormones in pregnancy.  Niger Med J., 53(4): 179-183.  DOI: 10.4103/0300-     1652.107549.

96   Yavropoulou, M.P., Panagiotou, G., Topouridou, K., Karayannopoulou, G., Koletsa, T., Zarampoukas, T., Goropoulos, A., Chatzaki, E., Yovos, J.G., & Pazaitou-Panyiotou, K., (2017).  Vitamin D receptor and progesterone receptor protein and gene expression in papillary thyroid carcinomas: associations with histological features. Journal of Endocrinological Investigation., 40(12):1327-1335. DOI: 10.1007/s40618-        017-0700-4.  Accessed at;  https://www.ncbi.nlm.nih.gov/pubmed/28589382

97   Kivity, S., Agmon-Levin, N., Zisappl, M. et al., (2011).  Vitamin D and autoimmune thyroid diseases. Cell Mol Immunol., 8, 243–247.  Accessed at: https://doi.org/10.1038/cmi.2010.73.

98   Mazokopakis, E.E., Papadomanolaki, M.G., Tsekouras, K.C., Evangelopoulos, A.D., Kotsiris, D.A., & Tzortzinis, A.A., (2015).   Is Vitamin D Related to Pathogenesis and Treatment of Hashimoto’s Thyroiditis? Hell J Nucl      Med.,      18(3):222-7.  PMID: 26637501.

99   Simsek Y, Cakir I, Yetmis M, et al., (2016).  Effects of Vitamin D Treatment on Thyroid Autoimmunity.  J Res Med Sci., 21:85.  DOI:10.4103/1735-1995.192501.

100   Datta M, Roy P, Banerjee J, Bhattacharya S., (1998).  Thyroid hormone stimulates progesterone release from         human   luteal cells by generating a proteinaceous factor.  Journal of Endocrinology., 158(3):319-25.      Accessed at: https://www.ncbi.nlm.nih.gov/pubmed/9846161.

101   Mancini, A., Di Segni, C., Raimondo, S., Olivieri, G., Silvestrini, A., Meucci, E., & Currò, D., (2016).  Thyroid Hormones, Oxidative Stress, and Inflammation.  Mediators of inflammation, 2016: 6757154.                https://doi.org/10.1155/2016/6757154.

102   Schroeder, A.C., & Privalsky, M.L., (2014).  Frontiers in Endocrinology, 5: 40.  DOI: 10.3389/fendo.2014.00040.

103 1   Dais, J.D., & Tremont, G., (2007).  Neuropsychiatric aspects of hypothyroidism and treatment reversibility. Minerva Endocrinol., 32(1): 46-65. 

104   Bauer, M., London, E., Silverman, D.H., Rasgon, N., Kirchheiner, J., &Whybrow, P.C., (2003).  Thyroid, brain      and mood odulation in affective disorder: insights from molecular research and functional brain imaging.  Pharmacopsychiatry, 33(supp 3): s215-s221.  DOI: 10.1055/s-2003-45133.

For more information on light therapy go to: http://lifeisbeautifullifecoach.com/light-therapy-an-overview/

This information is for educational and informational purposes only. Contact a certified health care provider if you need help.

Red light for Improved Dental Health.

Dental health: may benefit from light therapy devices. Blue LED or dental halogen curing lamps are specifically designed to fit into the mouth. Periodontal disease leads not only to loss of gum recession and tooth loose, but are associated with other, systemic, diseases. These devices can kill certain bactria found in the mouth (actinomycetemcomitans, Fusobactrium nucleatum, and Porphyromonas gingivalis) in 15 to 60 seconds, but only if in a certain state (biofilm) in other states (planktonic state “2) it is helpful in reducing pathogens only (21). Keep in mind that blue light may activate reactive oxygen species after gum surgery, which could be damaging to gum tissue after surgery specifically.

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This information is for educational and informational purposes only. Please see a qualified medical professional if you need help.

Light Therapy for Diabetic Pain.

Light therapy can help treat diabetic peripheral neuropathy. This is considered to be the disease or dysfunction of peripheral nerves, causing numbness or weakness. It does this by improving plantar sensitivity, or sensitivity to touch of the plantar area of the food, which is usually decreased in diabetics. Light therapy was shown to help with (short-term) improvements to tactile sensitivity (16). It has also been used, in conjunction with muscle stretching exercise, to treat myofascial trigger points. It (830 m) also helps improve circulation and joint range of motion, pressure sensitivity, and pain in patients with osteoarthritis of the knee (10).

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THIS INFORMATION IS FOR EDUCATIONAL AND ENTERTAINMENT PURPOSES ONLY. PLEASE CONSULT A MEDICAL PROFESSIONAL FOR HELP IF NEEDED.

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