The role of Oxytocin from Birth to Old Age

The Role of Oxytocin from Birth to Old Age

Jorge D. Flechas M.D., M.P.H., H(MD)

This paper offers an introduction to the hormone oxytocin and its many physiological functions.


Oxytocin Physiology

Oxytocin (OT) is synthesized as a nine-amino-acid neuropeptide inside the neurons of the hypothalamic periventricular nuclei (PVN) and the supraoptic nuclei (SON). Oxytocin is also produced in peripheral tissues such as the placenta, the corpus luteum, the testes, the heart, the adrenals, the pancreas, and other tissues.

1 The neurons make oxytocin as part of a peptide precursor. By enzyme activity, the prohormone is cleaved and amidated as it is transported down the axon.

2 Oxytocin is attached to a neurophysin I (a transport protein that is stimulated into production by estrogen) and to OT- extended form (OT-X), which is oxytocin with a C-terminal three-amino-acid extension.

3 The prohormone undergoes proteolysis by several convertase enzymes as it travels down the axon.

These enzymes are present in the oxytocin neurosecretory vesicles. By the time the prohormone reaches the terminal end of the axon, oxytocin is released as its nine-amino-acid neuropeptide into the body or into the brain. It has been documented that oxytocin receptors can be found in the brain and that these receptors occur in areas throughout the brain, not just in one region. However, the oxytocin receptors are found in higher concentrations in some areas of the brain, including the amygdala, the hippocampus, the septum, the PVN, the brainstem area, and the posterior dorsal horn cells of the spine.2,4-8 Oxytocin receptors have also been identified in other parts of the body, including the kidney, heart, thymus, pancreas, and adipocytes.1 It is now known that the axons that distribute oxytocin from the PVN and SON go from the hypothalamus to many regions of the brain such as the brainstem and the spinal cord areas.9 Papers have been published documenting that oxytocin modulates neural circuitry for social cognition and fear in humans.10 Oxytocin is known to have antinociceptive and analgesic properties as well as anxiolytic and antidepressant effects, which makes this neuropeptide of interest especially in the field of fibromyalgia research.10 The fact that oxytocin has been found in high concentrations in the posterior dorsal horn cells of the spine suggests that the periventriculo-spinal pathway is particularly related to specific groups of sympathetic and parasympathetic neurons and to the marginal zone, which is involved in the relay of ascending nociceptive information through the spinal thalamic tract.

11 A mother releases oxytocin when she is nursing her child or when she hears the baby crying.12,13 One has to be concerned about the presence of silicone breast implants since the ability of the brain to communicate with the breast tissue is inhibited by nerves that were cut at the time of surgery. Silicone implant surgery often results in a loss of feeling and sensation in the nipples, and the nipples help provide information to the brain for release of oxytocin. The loss of breast tissue that occurs with many breast cancer surgeries also presents concerns as this loss results in the removal of a major pathway for the stimulation of oxytocin production. For years, a decrease in breast milk in lactating mothers has been noted to occur in the presence of stress, anger and fear. An increase in milk production has been seen in the presence of acetylcholine and in the presence of inositol, a carbohydrate alcohol that is found in rice. Oxytocin functions to contract smooth muscle cells by binding to heptahelical G protein receptors. When oxytocin binds to these receptors, inositol triphosphate and diacylglycerol are formed. These compounds increase intracellular calcium and activate protein kinase C (which plays a role in phosphorylating membrane calcium channels), and thereby further increase the levels of intracellular calcium. The increased influx of calcium results in the binding of calcium to calmodulin in muscle cells, which activates myosin, and thus, results in the contraction of endometrial and myoepithelial cells.14

Oxytocin is inhibited by stress, opioid peptides, opioids, fear and anger.10,15-21 Extrauterine actions of oxytocin were first discovered during an early medical conference on oxytocin in South America where it was reported that oxytocin helps control the peripheral circulation.22


Oxytocin at the Time of Birth

It has been reported that the oxytocin inside the fetal brain is responsible for helping a mother go into labor. In rats there is evidence of a signaling system between the mother and the fetus aimed at preparing fetal neurons for delivery. In immature neurons, GABA is the primary excitory neural transmitter. Shortly before delivery, there is a transient reduction in the intracellular chloride concentration and an excitory-to-inhibitory switch of GABA actions occurs. These events are triggered by oxytocin, a maternal hormone that is essential for labor. In vivo administration of an oxytocin receptor antagonist before delivery prevented the switch of the GABA actions in the fetal neurons and aggravated the severity of anoxic episodes experienced by the newborn. Thus, oxytocin inhibits fetal neurons and increases the resistance to insults during delivery23,24

Oxytocin and Stem Cells

Oxytocin induces differentiation of the P19 embryonic stem cells to cardiomyocytes.25-28 Oxytocin is known to stimulate stem cells inside the bone marrow to make more bone tissue.27 Oxytocin also inhibits proliferation of human breast cancer lines.29

Oxytocin Acts as a Paracrine Hormone

As a neuropeptide, oxytocin helps in partition and lactation. Oxytocin plays a pivotal role in memory processing, regulation of body temperature, blood pressure control, brain development, maternal behavior and sexual behavior.1 Oxytocin behaves as a paracrine hormone at the level of the ovary, the testes, the adrenals, the retina, the pineal gland, the thymus, the uterus, the placenta, and the prostate.30- 34 As a paracrine ovarian hormone, there is a rise in the amount of oxytocin around the time of ovulation, and this rise lasts approximately 4 days. There is a second minor increase in oxytocin levels during the luteal phase. Oxytocin is known to be luteolytic. Oxytocin can stimulate motility of the reproductive tract and oxytocin downregulates progesterone production by the corpus luteum.35-39 Oxytocin is produced in the placenta as well as in the decidua of the uterus.40-44 Oxytocinase (also known as cystine aminopeptidase) is also produced in the placenta to deactivate oxytocin during pregnancy and thus keep the uterus from going into premature labor. But as labor begins, the level of oxytocinase decreases, thereby allowing oxytocin to initiate the contractions of labor and delivery.45-47 In males, oxytocin is also produced in the leydig cells of the testes. Oxytocin stimulates tubular activity, and this, in turn, is related to androgen production.48-57 Oxytocin modulates testosterone steroidogenesis and increases activity of 5 alpha-reductase, which converts testosterone to DHT.48, 57, 58

Several different mechanisms operate to destroy oxytocin in the bloodstream. The main mechanism is a peptidase that has the ability to destroy oxytocin. Other agents that work to destroy oxytocin in the bloodstream include an enzyme called cystine aminopeptidase, also known as oxytocinase, found in the placenta; a peptidase called glutothyone hormone transhydrogenase, found in the liver; amiopeptidase, found in the liver, kidney, pituitary, and cerebral cortex; and an enzyme called trypsin-chymotrypsin-like enzyme, found in the liver, kidney, uterus, and cerebral cortex.

Oxytocin and Thyroid Function

Oxytocin is known to stimulate the making of the sodium iodide symporter.59 The symporter is a channel through which the body has the ability to increase the absorption of iodine into the cells. Both oxytocin and prolactin stimulate the sodium iodide symporter system.

Oxytocin as an Adrenal Hormone

When given from an external source oxytocin will decrease cortisol production via inhibition of ACTH production from the hypothalamus.60 The more oxytocin given, the less cortisol is produced by the adrenals.

Oxytocin as a Pancreatic Hormone

Oxytocin stimulates the pancreas to make glucagon and to help control blood sugars.61-65

Oxytocin as a Prostate Hormone

Oxytocin helps in the maintenance of prostatic tone. Oxytocin helps in the contraction of the prostate at the time of orgasm.31,54,57,66

Oxytocin as a Molecular Mimic

Oxytocin has the ability to do what is called molecular mimicry. That is, oxytocin can look like many other hormones inside the body and can mimic some of their functions. For instance, oxytocin can mimic interleukin (IL)-2.67-72 Thymic nursing cells will use oxytocin to process T-cells for their future work. It is of interest that thymic nursing cells are constantly screening all lymphocytes that are processed and become T-cells for reactivity to oxytocin. If a thymic nursing cell finds a T-cell that has the ability to react to oxytocin, the T-cell is immediately destroyed by the thymic nursing cells so that no white blood cells produced by the T-cell system of the thymus has the ability to react against oxytocin. Not only can oxytocin behave like IL-2, it can behave like insulin with one-fifth the activity of the insulin molecule,73 like arginine vasopressin to vasodilate blood vessels inside the brain,74 and like an opioid with the ability to kill pain via the central nervous system.75-78

Oxytocin’s Role in Certain Diseases

Low levels of oxytocin have been found when certain illnesses are present. In Prader-Willi Syndrome there are reduced numbers of oxytocin-producing neurons inside the hypothalamus. Children with autism have been found to have low levels of oxytocin. In actuality, these children are making OT-X (oxytocin extended form). Children with autism do not have the enzyme that is necessary for the breaking up of the oxytocin peptide union, and as a result, very little oxytocin is present inside the blood stream. However, there is plenty of OT-X. The peptide on the oxytocin molecule is on the C-terminal end, where we find the peptides being glycine or glycine-lysine or glycine-lysine and arginine. Once more, these amino-acids have to be disassociated from the oxytocin molecule. The disassociation occurs in the presence of an enzyme that is not being produced in the autistic child, or, if present, is produced in very low levels.79-80 Since oxytocin blood levels are very low in the presence of autism, one would have to wonder if many of the symptoms of autism are not in actuality oxytocin deficiency. A closer look at mounting research studies reveal that low levels of oxytocin are associated with increased risk of certain medical conditions and life events, including:

  •  Prader Willi syndrome 85-87
  •  Autism88
  •  Low estrogen states89
  •  Low thyroid (T3) levels67
  •  Depression90
  •  AIDS91
  •  CMV infection16
  •  Multiple sclerosis92
  •  Fibromyalgia93
  •  Chronic stress situations94
  •  Chronic opioid use51
  •  Parkinson’s disease95
  •  Loneliness96
  •  Anxiety disorders97
  •  Some types of schizophrenia98

Oxytocin Production: Stimulants and Suppressants

There are several things that serve to increase oxytocin levels in the body. Stimulators of oxytocin production in both males and females include estrogen, histamine, physical touch, acetylcholine, tactile genital stimulation, and intercourse.99-106 The stimulating influence of estrogen explains why women tend to have higher levels of oxytocin than men and why estrogen deprivation in women decreases oxytocin levels. In the book, Harrison’s Principles of Internal Medicine (1998 14th edition, page 2011) the following statement was made: “The manipulation or distention of the female genital tract artificially or during partition is a very strong stimulus for oxytocin production in the brain. The same is true when the breasts are suckled. Touch deprivation, alcohol consumption, chronic pain, and habitual use of narcotics all downregulate oxytocin production.” In premenopausal women, hugging their husbands or partners stimulates the body to produce higher levels of oxytocin.107 Oxytocin is a vasodilator, and hence lowers the blood pressure in women.

Oxytocin and Arginine Vasopressin in Human Emotions and Behaviors

Both oxytocin and arginine vasopressin (AVP) increase the need for social contact and contribute to positive social behavior, increase social bonding, decrease anxiety, increase the desire for single rather than multiple partner selection, increase sexual behavior, improve memory processes (oxytocin primarily improves the memory that is attached to emotion), and upregulate parasympathetic autonomic functions. Oxytocin reduces stress, contributes to relaxation and a sense of well-being, decreases aggression (more so in men than in women), decreases glucocorticoid release, increases sensory processing, increases the desire for touching, and increases the bonding between mates and between parents and children. It is released in a pulsatile manner (this is what increases uterine contractions during birth and body contractions during orgasm). Oxytocin is felt to be a key player in sexual and reproductive behavior since it is involved from the start of the falling-in-love process, to the conception of children, to the sustaining of a lasting and beneficial relationship. It is oxytocin that instills trust, loyalty and devotion – all key ingredients in a happy and fulfilling relationship. Oxytocin induces parenting behavior, promotes affectionate behavior, and in some cases, has been linked to obsessive compulsive disorder.

AVP increases blood pressure, increases territorial and flight or fight behaviors (more so in men than in women), modulates corticoid release, is a component of the stress response, increases reward and limbic processing, and is an oxytocin agonist / partial antagonist.108

Oxytocin as a Biological Probe

Oxytocin can be used as a biological probe in the medical office. Oxytocin can be used to probe the phosphatidylinositol pathway to see if it is intact.109-111 The phosphatidylinositol pathway is necessary to night vision, and it is crucial to the proper functioning of the natural killer (NK) cells of the immune system. This pathway is the major path for the body to respond to oxytocin. The nasal spray form of oxytocin is often used to stimulate women to produce milk when trying to nurse their children. If a woman uses oxytocin nasal spray and has no increase in her milk production, one must consider a breakdown of the phosphatidylinositol pathway. Oxytocin used as a probe can also help determine the source of decreased sex drive in both men and women. The female sex drive is controlled by DHEA, and the male sex drive is controlled primarily by testosterone, which cannot be produced without DHEA.112 Since DHEA is necessary for oxytocin to function properly in the body, oxytocin can be used as a probe for DHEA insufficiency. Observable signs of an oxytocin insufficiency, and hence, of a DHEA insufficiency, include cold extremities (one of the first descriptions given about oxytocin back in 1959 was its ability to control the microcirculation in the peripheral tissues) and a pale skin color.113 However, an injection of oxytocin will provide a better indicator. The oxytocin injection is given intramusclarly using 10 units/cc with 1?4 cc lidocaine. Oxytocin has a pH of approximately 4.5, which causes pain when injected alone, so the use of lidocaine helps take the sting out of the injection. Since oxytocin is a vasodilator, within 15 minutes, the hands should warm and the ears should turn red if there is sufficient DHEA to enable proper functioning of the oxytocin. The rest of the body may also turn pink or red in response to the oxytocin if DHEA levels are sufficient. Typically, DHEA blood levels of over 200 mcg/dl are adequate for a clinical response to the oxytocin injection and for normal sex drive (DHEA levels less than 150mcg/dl can result in decreased sex drive). If there is no response to the oxytocin injection, a DHEA insufficiency should be considered, and blood work should be done to confirm this suspicion. If the blood work does indeed reveal a DHEA insufficiency, the patient is typically started on 25 mg/day DHEA if the patient’s age is less than 50 and on 50 mg/day if the patient’s age is 50 or above. Often, 2,000 mg/day of inositol is prescribed along with the DHEA. Both DHEA and inositol promote the development of the phosphatidylinositol pathway. The patient can be rechallenged with the oxytocin/lidocaine injection after 3 months of taking DHEA and inositol. Once there is sufficient DHEA for oxytocin to function properly, sexual desire and performance should be enhanced in both the male and the female.

Oxytocin and Sexual Behavior

In the female brain oxytocin facilitates female sexual maturation through a glia-2-neuron signaling pathway.114 The female brain is marinated in the presence of estrogen, progesterone, and oxytocin, with oxytocin being the number one neural peptide inside the brain. The male brain is marinated in testosterone, mularian inhibitory substance and AVP. Oxytocin rises in response to touch (more in females than in the males), and oxytocin can increase the desire for cuddling. In both men and women, oxytocin levels go up with sexual response.115,116 In men, the surge of oxytocin that occurs with an orgasm will make most of them sleepy and will decrease their interest in sex. In some humans it can impair memory, which is why lovemaking can wipe out the impact of an argument. This also explains why oxytocin has been used in treatment for post traumatic stress disorder (PTSD) over the last 20-30 years.117 In women, oxytocin may cause sexual desire to increase.

Oxytocin and Sexual Performance

Women who are multiorgasmic have much higher levels of plasma oxytocin and have a more subjective intensity of orgasm.118 Oxytocin is commercially available (via a prescription) in the form of injectibles, time-released tablets (10 and 20 units), sublingual tablets (10 to 40 units) and as a nasal spray. If oxytocin is administered to a woman, there will be an increased receptivity to sex, and with appropriate stimulation, she should respond within one hour. Some female patients have reported an increase in the number of multiple orgasms (usually within 3 hours of oxytocin exposure). Oxytocin has been found to be the main hormone responsible for erection in males. Reports from the field show that men who take the sublingual tablets are able to have an erection within 15 minutes. In both sexes oxytocin controls the arousal mechanism. From a clinical standpoint, patients have reported that oxytocin supplementation therapy (10 units IM with 1?4 cc lidocaine) produces more intense orgasms for both men and women of all ages. In patients above age 35, DHEA replacement therapy may also be necessary (see above). Other noteworthy facts include the following: oxytocin given intramuscularly to a non- pregnant uterus does not give uterine cramps; oxytocin stimulates the production of vaginal secretions; oxytocin increases penile sensitivity; oxytocin can cause some uterine contractions during orgasm.

Oxytocin and Sexual Dysfunction

In America, orgasmic disorder occurs in 11% of all women and is seen often in patients taking selective serotonin reuptake inhibitors (SSRIs). When male rats were given fluoxetine, researchers documented inhibited sexual performance. The same response has been noted in humans. However, when these same rats were given oxytocin, the ejaculatory response was restored.119 120

Oxytocin and Aging

Levels of estrogen, thyroid hormone, and dopamine, all of which stimulate the synthesis of oxytocin, decrease with age. The number of neurons that make oxytocin does not decrease with aging, but several of the major stimulants to oxytocin production do decline during the aging process.121, 122


Oxytocin has traditionally been given primarily for labor and delivery. In a study of premenopausal women, hugging their partner produced higher levels of oxytocin. Since oxytocin is a vasodilator, it lowered the blood pressure in this group of women. Women who are multiorgasmic have much higher levels of plasma oxytocin and have a more subjective intensity of orgasm. From a clinical standpoint, patients’ feedback indicates that oxytocin hormone replacement therapy can produce more intense orgasms for women of all ages and can, in some women, produce more orgasms. In patients above age 35, DHEA replacement therapy may be necessary. Oxytocin exposure to a non-pregnant woman with a uterus, does not give uterine cramps. Oxytocin stimulates the production of vaginal secretions.123 From the time oxytocin is given until the time the orgasm occurs is about one hour; for women who are multiorgasmic, the time from exposure to oxytocin until the start of this event is about three hours. Oxytocin can make a person desire to cuddle more. In men, oxytocin will make some of them sleepy and have loss of interest in sex. In women exposed to oxytocin, sexual desire goes up. Oxytocin promotes touching, promotes bonding between mates, in parents and children. It is involved in the birthing process and breastfeeding, decreases cognition in some individuals, and may or may not impair memory. Oxytocin is secreted by multiple organs in the body – not just the posterior pituitary. Oxytocin has a synergistic relationship with estrogen. It is pulsatile and can be difficult to measure. Oxytocin and dopamine modulate each other. Oxytocin increases the skin desire to be touched. Oxytocin spikes at the time of an orgasm, increases sexual receptivity, speeds ejaculation, increases penile sensitivity, and can cause some uterine contractions during orgasm and during labor. Oxytocin rises in response to touch in the female, but this response is not frequently seen in the male. Oxytocin promotes touching, induces parenting behavior, and promotes affection behavior. Oxytocin has been used to induce labor, to reduce postpartum bleeding, and to treat schizophrenia.81-84 Since oxytocin blood levels are very low in the presence of autism, one would have to wonder if many of the symptoms of autism are in actuality oxytocin deficiency. In fact, the autistic child might provide us with the definition of an oxytocin deficiency, which to date has not been defined by traditional endocrinology.



  1. Kiss A, Mikkelsen JD. Oxytocin–anatomy and functional assignments: a minireview. Endocr Regul. 2005;39:97-105.
  2. Gimpl G, Postina R, Fahrenholz F, Reinheimer T. Binding domains of the oxytocin receptor for the selective oxytocin receptor antagonist barusiban in comparison to the agonists oxytocin and carbetocin. Eur J Pharmacol. 2005;510:9-16.
  3. Gainer H, Jeong SW, Witt DM, Chin H. Strategies for cell biological studies in oxytocinergic neurons. Adv Exp Med Biol. 1995;395:1-8.
  4. Condes-Lara M, Gonzalez NM, Martinez-Lorenzana G, Delgado OL, Freund-Mercier MJ. Actions of oxytocin and interactions with glutamate on spontaneous and evoked dorsal spinal cord neuronal activities. Brain Res. 2003;976:75-81.
  5. Condes-Lara M, Rojas-Piloni G, Martinez-Lorenzana G, Lopez-Hidalgo M, Rodriguez-Jimenez J. Hypothalamospinal oxytocinergic antinociception is mediated by GABAergic and opiate neurons that reduce A-delta and C fiber primary afferent excitation of spinal cord cells. Brain Res. 2009;1247:38- 49.
  6. Robinson DA, Wei F, Wang GD et al. Oxytocin mediates stress-induced analgesia in adult mice. J Physiol. 2002;540(Pt 2):593-606.
  7. Rojas-Piloni G, Lopez-Hidalgo M, Martinez-Lorenzana G, Rodriguez-Jimenez J, Condes-Lara M. GABA-mediated oxytocinergic inhibition in dorsal horn neurons by hypothalamic paraventricular nucleus stimulation. Brain Res. 2007;1137:69-77.
  8. Rojas-Piloni G, Martinez-Lorenzana G, DeLaTorre S, Condes-Lara M. Nociceptive spinothalamic tract and postsynaptic dorsal column neurons are modulated by paraventricular hypothalamic activation. Eur J Neurosci. 2008;28:546-558.
  9. Swanson LW, Hartman BK. Biochemical specificity in central pathways related to peripheral and intracerebral homeostatic functions. Neurosci Lett. 1980;16:55-60.
  10. Kirsch P, Esslinger C, Chen Q, et al. Oxytocin modulates neural circuitry for social cognition and fear in humans. J Neurosci. 2005;25:11489-11493.
  11. Swanson LW, McKellar S. The distribution of oxytocin- and neurophysin-stained fibers in the spinal cord of the rat and monkey. J Comp Neurol. 1979;188:87-106.
  12. Fabian M, Forsling ML, Jones JJ, Lee J. Oxytocin assay with the rat mammary gland in vivo and in vitro. J Physiol. 1968;195:5P.
  13. Forsling ML, Reinhardt V, Himmler V. Neurohypophysial hormones and prolactin release. J Endocrinol. 1974;63:579-580.
  14. Van Kesteren RE, Smit AB, Dirks RW, De With ND, Geraerts WP, Joosse J. Evolution of the vasopressin/oxytocin superfamily: characterization of a cDNA encoding a vasopressin-related precursor, preproconopressin, from the mollusc Lymnaea stagnalis. Proc Natl Acad Sci. 1992;89:4593-4597.
  15. Aulsebrook LH, Holland RC. Central inhibition of oxytocin release. Am J Physiol. 1969;216:830-842.
  16. Oxytocin could be new social-phobic treatment. Health News. 2006;12:10-11.
  17. Aono T. [Hormonal control of lactation]. Nippon Sanka Fujinka Gakkai Zasshi. 1990;42:867-872.
  18. Baumgartner T, Heinrichs M, Vonlanthen A, Fischbacher U, Fehr E. Oxytocin shapes the neural circuitry of trust and trust adaptation in humans. Neuron 2008;58:639-650.
  19. Mathew SJ, Price RB, Charney DS. Recent advances in the neurobiology of anxiety disorders:     implications for novel therapeutics. Am J Med Genet C Semin Med Genet. 2008;148C:89-98.
  20. Onaka T. Neural pathways controlling central and peripheral oxytocin release during stress. J Neuroendocrinol. 2004;16:308-312.
  21. Pittman QJ, Spencer SJ. Neurohypophysial peptides: gatekeepers in the amygdala. Trends Endocrinol Metab. 2005;16:343-344.
  22. Haigh AL, Kitchin AH, Pickford M. The effect of oxytocin on hand blood flow in man following the administration of an oestrogen and isoprenaline. J Physiol. 1963;169:161-166.
  23. Khazipov R, Tyzio R, Ben-Ari Y. Effects of oxytocin on GABA signalling in the foetal brain during delivery. Prog Brain Res. 2008;170:243-257.
  24. Tyzio R, Cossart R, Khalilov I, et al. Maternal oxytocin triggers a transient inhibitory switch in GABA signaling in the fetal brain during delivery. Science 2006;314:1788-1792.
  25. Bouchard F, Paquin J. Skeletal and cardiac myogenesis accompany adipogenesis in P19 embryonal stem cells. Stem Cells Dev. 2009;18:1023-1032.
  26. Danalache BA, Paquin J, Donghao W, et al. Nitric oxide signaling in oxytocin-mediated cardiomyogenesis. Stem Cells. 2007;25:679-688.
  27. Elabd C, Basillais A, Beaupied H, et al. Oxytocin controls differentiation of human mesenchymal stem cells and reverses osteoporosis. Stem Cells. 2008;26:2399-2407.
  28. Paquin J, Danalache BA, Jankowski M, McCann SM, Gutkowska J. Oxytocin induces differentiation of P19 embryonic stem cells to cardiomyocytes. Proc Natl Acad Sci. 2002;99:9550-9555.
  29. Cassoni P, Sapino A, Negro F, Bussolati G. Oxytocin inhibits proliferation of human breast cancer cell lines. Virchows Archiv. 1994;425:467-472.
  30. Liedman R, Hansson SR, Igidbashian S, Akerlund M. Myometrial oxytocin receptor mRNA concentrations at preterm and term delivery – the influence of external oxytocin. Gynecol Endocrinol. 2009;25:188-193.
  31. Nicholson HD. Oxytocin: a paracrine regulator of prostatic function. Rev Reprod. 1996;1:69-72
  32. Roser JF. Regulation of testicular function in the stallion: an intricate network of endocrine, paracrine  and autocrine systems. Anim Reprod Sci. 2008;107:179-196.
  33. Rossoni E, Feng J, Tirozzi B, Brown D, Leng G, Moos F. Emergent synchronous bursting of oxytocin neuronal network. PLoS Comput Biol. 2008;4:e1000123.
  34. Stormshak F. Biochemical and endocrine aspects of oxytocin production by the mammalian corpus  luteum. Reprod Biol Endocrinol. 2003;1:92.
  1. Amico JA, Zeleznik AJ. Ovarian oxytocin and neurophysin concentrations in the cynomolgus monkey (Macaca fascicularis). Endocr Res. 1990;16:17-30.
  1. Auletta FJ, Jones DS, Flint AP. Does the human corpus luteum synthesize neurohypophysial      hormones? J Endocrinol. 1988;116:163-165.
  1. Auletta FJ, Paradis DK, Wesley M, Duby RT. Oxytocin is luteolytic in the rhesus monkey (Macaca mulatta). J Reprod Fertil. 1984;72:401-406.
  1. Behrens O, Maschek H, Kupsch E, Fuchs AR. Oxytocin receptors in human ovaries during the     menstrual cycle. Adv Exp Med Biol. 1995;395:485-486.
  1. Cooke ID. The corpus luteum. Hum Reprod. 1988;3:153-156.
  2. Chibbar R, Miller FD, Mitchell BF. Synthesis of oxytocin in amnion, chorion, and decidua may    influence the timing of human parturition. J Clin Invest. 1993;91:185-192.
  1. Fuchs AR, Fuchs F. Endocrinology of human parturition: a review. Br J Obstet Gynaecol            1984;91:948-967.
  1. Fuchs AR, Fuchs F, Husslein P, Soloff MS. Oxytocin receptors in the human uterus during           pregnancy and parturition. Am J Obstet Gynecol. 1984;150:734-741.
  1. Mauri A, Argiolas A, Ticconi C, Piccione E. Oxytocin in human intrauterine tissues at parturition. Reprod Fertil Dev. 1995;7:1481-1484.
  1. Mitchell BF. Oxytocin synthesis and metabolism in human decidua. Reprod Fertil Dev. 1995;7:319-
  2. Ferrier BM, Hendrie JM, Branda LA. Plasma oxytocinase: the synthesis and biological properties of the first product of the degradation of oxytocin by this enzyme. Can J Biochem. 1974;52:60-66.
  1. Gazarek F, Pohanka J, Talas M et al. Plasma oxytocin and oxytocinase levels in third trimester of pregnancy and at labour. Endocrinol Exp. 1976;10:283-287.
  1. Iwasaki K, Hirata T, Tsuchiya S, Murai K. [Proceedings: Blood oxytocin concentration and           oxytocinase activity in pregnant women]. Nippon Naibunpi Gakkai Zasshi. 1974;50:605.
  1. Adashi EY, Tucker EM, Hsueh AJ. Direct regulation of rat testicular steroidogenesis by neurohypophysial hormones. Divergent effects on androgen and progestin biosynthesis. J Biol Chem. 1984;259:5440-5446.
  2. Assinder SJ, Rezvani A, Nicholson HD. Oxytocin promotes spermiation and sperm transfer in the mouse. Int J Androl. 2002;25:19-27.
  3. Ellis LC, Groesbeck MD, Farr CH, Tesi RJ. Contractility of seminiferous tubules as related to sperm transport in the male. Arch Androl. 1981;6:283-294.
  4. Evans JJ. Oxytocin in the human regulation of derivations and destinations. Eur J Endocrinol. 1997;137:559-571.
  5. Frayne J, Nicholson HD. Effect of oxytocin on testosterone production by isolated rat Leydig cells is mediated via a specific oxytocin receptor. Biol Reprod. 1995;52:1268-1273.
  6. Goverde HJ, Bisseling JG, Wetzels AM, et al. A neuropeptide in human semen: oxytocin. Arch Androl. 1998;41:17-22.
  7. Ivell R, Balvers M, Rust W, Bathgate R, Einspanier A. Oxytocin and male reproductive function. Adv Exp Med Biol. 1997;424:253-264.
  8. Jenkins JS, Nussey SS. The role of oxytocin: present concepts. Clin Endocrinol (Oxf). 1991;34:515- 525.
  9. Melin P. Spermatogenesis and sperm output in rabbits after long-term treatment with oxytocin. Acta Endocrinol (Copenh). 1971;66:515-528.
  10. Nicholson HD, Jenkin L. Oxytocin and prostatic function. Adv Exp Med Biol. 1995;395:529-538.
  11. Nicholson HD, Guldenaar SE, Boer GJ, Pickering BT. Testicular oxytocin: effects of intratesticular oxytocin in the rat. J Endocrinol. 1991;130:231-238.
  1. Arturi F, Ferretti E, Presta I et al. Regulation of iodide uptake and sodium/iodide symporter       expression in the mcf-7 human breast cancer cell line. J Clin Endocrinol Metab. 2005;90:2321-2326.
  1. Coiro V, Passeri M, Davoli C, et al. Oxytocin Reduces Exercise-Induced ACTH and Cortisol Rise in Man. Acta Endocrinoligial (Copenh). 1988;119:405-412.
  1. Kiss A, Mikkelsen JD. Oxytocin anatomy and functional assignments: a minireview. Endocr Regul. 2005;39:97-105.
  1. Lippert TH, Mueck AO, Seeger H, Pfaff A. Effects of oxytocin outside pregnancy. Horm Res.        2003;60:262-271.
  1. Yibchok-Anun S, Hsu WH. Effects of arginine vasopressin and oxytocin on glucagon release from clonal alpha-cell line In-R1-G9: involvement of V1b receptors. Life Sci. 1998;63:1871-1878.
  1. Lee B, Yang C, Chen TH, al-Azawi N, Hsu WH. Effect of AVP and oxytocin on insulin release:     involvement of V1b receptors. Am J Physiol. 1995;269:E1095-E1100.
  1. Bobbioni-Harsch E, Frutiger S, Hughes G, et al. Physiological concentrations of oxytocin powerfully stimulate insulin secretionin vitro. Endocrine. 1995;3:55-59.
  1. Nicholson HD, Whittington K. Oxytocin and the human prostate in health and disease. Int Rev Cytol. 2007;263:253-286.s
  1. Argiolas A, Gessa GL, Melis MR, Stancampiano R, VACCARI A. Effects of Neonatal and Adult     Thyroid Dysfunction on Thymic Oxytocin. Neuroendocrinology. 1990;52:556-559.
  1. Elands J, Resink A, De Kloet ER. Neurohypophyseal Hormone Receptors in the Rat Thymus,        Spleen, and Lymphocytes. Endocrinology. 1990;126:2703-2711.
  1. Geenen V, Legros JJ, Franchimont P, Baudrihaye M, Defresne MP, Boniver J. The Neuroendocrine Thymus: Coexistence of Oxytocin and Neurophysin in the Human Thymus. Science. 1986;232:508-511. 512.
  2. Geenen V, Cormann-Goffin N, Martens H, et al. Thymic neurohypophysial-related peptides and T cell selection. Regulatory Peptides. 1993;45:273-278.
  1. Marten H, Goxe B, Geenen V. The thymic repertoire of neuroendocrine self-antigens: physiological implications in T-cell life and death. Immunology Today. 1996;17:312-317.
  1. Wiedmeier SE, Araneo BA, Huang K, Daynes RA. Thymic modulation of IL-2 and IL-4 synthesis by peripheral T cells. Cell Immunol. 1991;135:501-518.
  1. Hanif K, Goren HJ, Hollenberg MD, Lederis K. Oxytocin Action – Mechanisms for Insulin-Like Activity in Isolated Rat Adipocytes. Molecular Pharmacology. 1982;22:381-388.
  1. Suzuki Y, Satoh SI, Kimura M et al. Effects of vasopressin and oxytocin on canine cerebral            circulation in vivo. J Neurosurg. 1992;77:424-431.
  1. Uryvaev I, Petrov GA. [Decreased pain sensitivity in man after treatment with superlow doses of oxytocin]. Biull Eksp Biol Med. 1996;122:487-489.
  2. Hiltz RE, Gupta PK, Maher KA, et al. Low Threshold of Visceral Nociception and significant Objective Upper Gastrointestinal Pathology in Patients with Fibromyalgia Syndrome. Arthritis & Rheumatism. 1993;36:93.
  3. Louvel D, Delvaux M, Felez A, et al. Oxytocin increases thresholds of colonic visceral perception in patients with irritable bowel syndrome. 1996;39:741-747.
  4. Ohlsson B, Truedsson M, Bengtsson M, et al. Effects of long-term treatment with oxytocin in chronic constipation; a double blind, placebo-controlled pilot trial. Neurogastroenterol Motil. 2005;17:697- 704.
  5. Green L, Fein D, Modahl C, Feinstein C, Waterhouse L, Morris M. Oxytocin and autistic disorder: alterations in peptide forms. Biol Psychiatry. 2001;50:609-613.
  6. Modahl C, Green L, Fein D, et al. Plasma oxytocin levels in autistic children. Biol Psychiatry. 1998;43:270-277.
  7. Bakharev VD, Tikhomirov SM, Lozhkina TK. [Psychotropic properties of oxytocin]. Probl Endokrinol (Mosk). 1984;30:37-41.
  8. Bujanow W. Hormones in the treatment of psychoses. Br Med J. 1972;4:298.
  9. Bujanow W. Letter: Is oxytocin an anti-schizophrenic hormone? Can Psychiatr Assoc J.               1974;19:323.
  1. Marazziti D, Catena DM. The role of oxytocin in neuropsychiatric disorders. Curr Med Chem.    2008;15:698-704.
  1. Martin A, State M, Anderson GM, et al. Cerebrospinal fluid levels of oxytocin in Prader-Willi       syndrome: a preliminary report. Biol Psychiatry. 1998;44:1349-1352.
  1. Swaab DF. Prader-Willi syndrome and the hypothalamus. Acta Paediatr Suppl. 1997;423:50-54.
  2. Swaab DF, Purba JS, Hofman MA. Alterations in the hypothalamic paraventricular nucleus and its oxytocin neurons (putative satiety cells) in Prader-Willi syndrome: a study of five cases. J Clin Endocrinol Metab. 1995;80:573-579.
  1. Panksepp J. Commentary on the Possible Role of Oxytocin in Autism. Journal of Autism and

                     Developmental Disorders. 1993;23:567-569.

  1. Amico JA, Seif SM, Robinson AG. Oxytocin in human plasma: correlation with neurophysin and  stimulation with estrogen. J Clin Endocrinol Metab. 1981;52:988-993.
  1. Evans JJ. Oxytocin in the human regulation of derivations and destinations. Eur J Endocrinol.   1997;137:559-571.
  1. Purba JS, Hofman MA, Portegies P, Troost D, Swaab DF. Decreased Number of Oxytocin Neurons in the Paraventricular Nucleus of the Human Hypothalamus in AIDS. Brain. 1993;116:795-809.
  1. Moller A, Hansen BL, Hansen GN, Hagen C. Autoantibodies in sera from patients with multiple sclerosis directed against antigenic determinants in pituitary growth hormone-producing cells and in structures containing vasopressin/oxytocin. J Neuroimmunol. 1985;8:177-184.
  1. Anderberg UM, Uvnas-Moberg K. Plasma oxytocin levels in female fibromyalgia syndrome patients.  Z Rheumatol. 2000;59:373-379.
  1. Kalin NH, Gibbs DM, Barkskdale CM, Shelton SE, Carnes M. Behavorial Stress Decreases Plasma  Oxytocin Concentrations in Primates. Life Sciences. 1985;36:1267-1280.
  1. van Wimersma Greidanus TB, van de Heijning BJ. Opioid control of vasopressin and oxytocin    release. Regul Pept. 1993;45:183-186.
  1. Lucht MJ, Barnow S, Sonnenfeld C et al. Associations between the oxytocin receptor gene (OXTR) and affect, loneliness and intelligence in normal subjects. Prog Neuropsychopharmacol Biol sychiatry. 2009;33:860-866.
  1. Scantamburlo G, Hansenne M, Fuchs S, et al. Plasma oxytocin levels and anxiety in patients with major depression. Psychoneuroendocrinology. 2007;32:407-410.
  1. Goldman M, Marlow-O’Connor M, Torres I, Carter CS. Diminished plasma oxytocin in schizophrenic  patients with neuroendocrine dysfunction and emotional deficits. Schizophr Res. 2008;98:247-255.
  1. Bealer SL, Crowley WR. Stimulation of central and systemic oxytocin release by histamine in the paraventricular hypothalamic nucleus: evidence for an interaction with norepinephrine.         Endocrinology. 1999;140:1158-1164.
  1. Altura BM. Sex and estrogens and responsiveness of terminal arterioles to neurohypophyseal     hormones and catecholamines. J Pharmacol Exp Ther. 1975;193:403-412. 51
  1. Amico JA, Ervin MG, Leake RD, Fisher DA, Finn FM, Robinson AG. A novel oxytocin-like and vasotocin-like peptide in human plasma after administration of estrogen. J Clin Endocrinol Metab. 1985;60:5-12.
  2. Fox CA. Recent studies in human coital physiology. J Clin Endocrinol Metab. 1973;2:527-543.
  3. Kroeger M. Oxytocin: key hormone in sexual intercourse, parturition, and lactation. Birth Gaz.   1996;13:28-30.
  1. Todd K, Lightman SL. Oxytocin release during coitus in male and female rabbits: effect of opiate receptor blockade with naloxone. Psychoneuroendocrinology. 1986;11:367-371.
  1. Cunningham Jr. ET, Sawchenko PE. Reflex Control of Magnocellular Vasopressin and Oxytocin   Secretion. Tins 1991;14:406-411.
  1. Grewen KM, Girdler SS, Amico J, Light KC. Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact. Psychosom Med. 2005;67:531-538.
  1. Light KC, Grewen KM, Amico JA. More frequent partner hugs and higher oxytocin levels are linked to lower blood pressure and heart rate in premenopausal women. Biol Psychol. 2005;69:5-21.
  1. Esch T, Stefano GB. The Neurobiology of Love. Neuro Endocrinol Lett. 2005;26:175-192.
  2. Anwer K, Oberti C, Perez GJ, et al. Calcium-activated K+ channels as modulators of human        myometrial contractile activity. Am J Physiol. 1993;265:C976-C985.
  1. Atke A, Sjoholm P, Hansen CO, Vilhardt H. Activation of inositol phosphates in the myometrium. Ann N Y Acad Sci. 1993;689:473-474.
  1. Flint AP, Leat WM, Sheldrick EL, Stewart HJ. Stimulation of phosphoinositide hydrolysis by oxytocin and the mechanism by which oxytocin controls prostaglandin synthesis in the ovine endometrium.  Biochem J. 1986;237:797-805.
  1. Cramarossa L, Caruso AA. [Replacement therapy in adrenopause. Dehydroepiandrosterone and aging]. Recenti Prog Med. 2001;92:68-73.
  2. Pickford M. Some Extra-uterine Actions of Oxytocin. In: Caldeyro-Barcia R, ed. Oxytocin,            Proceedings of an International Symposium held in Montevideo, 1959. London: Symposium      Publications Division, Pergamon Press; 1959:68-83.
  1. Parent AS, Rasier G, Matagne V, et al. Oxytocin facilitates female sexual maturation through a glia-to-neuron signaling pathway. Endocrinology. 2008;149:1358-1365.
  1. Carmichael MS, Humbert R, Dixen J, Palmisano G, Greenleaf W, Davidson JM. Plasma oxytocin increases in the human sexual response. J Clin Endocrinol Metab. 1987;64:27-31.
  1. Carmichael MS, Warburton VL, Dixen J, Davidson JM. Relationships among cardiovascular,        muscular, and oxytocin responses during human sexual activity. Arch Sex Behav. 1994;23:59-79.
  1. Olff M, Langeland W, Witteveen A, Denys D. A psychobiological rationale for oxytocin in the      treatment of posttraumatic stress disorder. CNS Spectr. 2010;15:522-530.
  1. Carmichael MS, Warburton VL, Dixen J, Davidson JM. Relationships among cardiovascular,       muscular, and oxytocin responses during human sexual activity. Arch Sex Behav. 1994;23:59-79.
  1. Cantor JM, Binik YM, Pfaus JG. Chronic fluoxetine inhibits sexual behavior in the male rat: reversal with oxytocin. Psychopharmacology (Berl). 1999;144:355-362.
  1. Landry M, Frasier M, Chen Z, et al. Fluoxetine treatment of prepubescent rats produces a selective functional reduction in the 5-HT2A receptor-mediated stimulation of oxytocin. Synapse. 2005;58:102-109
  2. Chiodera P, Volpi R, Capretti L, et al. Oxytocin response to challenging stimuli in elderly men. Regul Pept. 1994;51:169-176.
  1. Hofman MA. Lifespan changes in the human hypothalamus. Exp Gerontol. 1997;32:559-575.
  2. Anderson-Hunt M, Dennerstein L. Increased female sexual response after oxytocin. BMJ.           1994;309:929.


The effects of Hormones on Breast Cancer

The Effects of Hormones on Breast Cancer: How to Use Them to Reduce the Risk

Khalid Mahmud, M.D., FACP, ABAAM
Medical Director, Innovative Directions in Health;
Former Medical Director of Oncology, North Memorial Medical Center (Minneapolis, Minnesota USA)


Conventional practice of medicine has done very little to prevent breast cancer – the one disease women dread the most. The usual emphasis is on self-exam and mammogram, which is early detection, not prevention. By the time cancer is found on a mammogram it, as a rule, has been slowly growing for up to 15 years. Many factors influence the appearance and growth of cancer cells positively or negatively, and these factors could be manipulated to inhibit the initiation and growth of tiny cancers during this period of time. Hormones are one such factor. The aim of this paper is to consider how different hormones affect breast cancer and how to use them to reduce its risk.


Conventional practice of medicine has done very little to prevent breast cancer – the one disease women dread the most. The usual emphasis is on self-exam and mammogram, which is early detection, not prevention. By the time cancer is found on a mammogram it, as a rule, has been slowly growing for up to 15 years. Many factors influence the appearance and growth of cancer cells positively or negatively, and these factors could be manipulated to inhibit the initiation and growth of tiny cancers during this period of time. Hormones are one such factor (Table 1). The following is a discussion of how different hormones affect breast cancer and how to use them to reduce its risk.

Table 1. Hormones that affect breast cancer


Estradiol (E2) and Estrone (E1)

It is well known that these two strong estrogens stimulate the growth of breast cancer cells. They do so by acting on the estrogen receptor alpha (ER-alpha) on these cancer cells (Figure 1). ER-negative breast cancer cells are not affected by these hormones.

Figure 1. Cancer Promotion by Estradiol (E2) and Estrone (E1)

Progesterone, Progestins Testosterone

Thyroid (Tri-iodothyronine) Human growth hormone

The Importance of E1 and E2 Manufactured by the Breast Fat Cells

Although it is commonly recognized that postmenopausal women with breast cancer tend to have higher blood levels of estrogens,1 what is generally not appreciated is the fact that post-menopausal women have much higher levels of these estrogens in the breast – 10 to 50 times higher than in the blood.2, 3 Fat cells, around a post-menopausal breast cancer, have been found to have high aromatase activity, generating estrogen locally to fuel the growth of cancer. (Figure 2).4 The blood level is merely a reflection of the estrogen being generated by the aromatase in the fatty tissues, such as the breast, and not directly involved in stimulating the cancer.

Figure 2. Breast fat cells producing estrogen to fuel cancer growth.

Does Estrogen Treatment for Menopause Increase Risk of Breast Cancer?

Scientific evidence does not support the notion that estrogen treatment for menopause increases the risk of breast cancer. The Women’s Health Initiative (WHI) and Women’s Health Initiative Lund Area, Sweden (WHILA) studies revealed that post-menopausal women receiving estrogen only (without Provera) did not have any increase in the occurrence of breast cancer.5, 6 Only women who had received Provera (PremPro) had an increased risk of breast cancer. In fact, a Swiss HRT study of 23,000 women who were using more natural forms of estrogen (estradiol and estriol) showed an actual 25% decrease in breast cancer risk.7 Furthermore, results of two studies of estrogen use in women with prior history of breast cancer showed a decrease in recurrence rate compared with control subjects.8, 9 The obvious explanation for these findings is that a modest increase in E2 in the blood with estrogen administration does not make any difference to the estrogen level in the breast, which is locally produced and many times higher than what is in the blood. In addition, a study of baboons has revealed that in ovariectomized females (similar to post-menopausal women) estrogen administration causes a sharp and significant drop in the breast tissue aromatase level,10 which should decrease the risk of cancer. This finding suggests that, like in other endocrine systems, the breast fat cells are affected by a negative feedback loop, so that externally administered estrogen actually acts as an ‘aromatase inhibitor’ in the breast, thus explaining the decrease in breast cancer in the larger studies mentioned above.

It should be mentioned that the greatest reduction in breast cancer occurred in the Swiss study where most women received E2 and E3 in more natural forms. The protection has been less obvious in the Premarin studies. This may have to do with the fact that Premarin blocks glutathione S-transferase, an important phase 2 enzyme in the detoxification of carcinogens.11

16 Alpha-Hydroxyestrone (16 alpha-OHE)

16 alpha-hydroxyestrone is an estrogen metabolite that stimulates the growth of breast cancer cells, and has been shown to increase the risk of breast cancer in several studies.12, 13 16 alpha-OHE levels can be lowered by eating less foods containing animal fat and eating more vegetables, particularly the cruciferous varieties, such as broccoli, brussels sprouts, cabbage, and cauliflower.


Estriol (E3)

There is considerable evidence suggesting that estriol (E3) is protective against breast cancer. Estriol is a weak estrogen that binds to ER-alpha, thus keeping the stronger cancer promoting estrogens, E1 and E2, away from the cancer cells.14 Estriol levels decrease in menopause. Asian women have higher estriol levels than Western women and a lower rate of breast cancer. Women with breast cancer tend to have lower levels of this estrogen.15 Henry Lemmon, a gynecologic oncologist at the University of Nebraska spent years studying estriol. He was able to prevent the induction of carcinogen and radiation induced breast cancer in animals by using estriol.16.  Pregnancy is associated with very high levels of estriol and provides protection against breast cancer. A 40-year follow up of 15,000 pregnant women showed that those with the highest pregnancy levels of estriol had a 58% lower rate of breast cancer compared with those that had the lowest levels.17 In the Swiss study cited above, many women received estriol.

Based on such evidence, it makes a great deal of sense to include estriol in hormone replacement therapy preparations. Unfortunately, pharmaceutical estrogen preparations have always excluded estriol.

I believe Biest [E2, 20% + E3 80%] to be the most logical estrogen preparation for women in menopause. Biest should act as an aromatase inhibitor in the breast tissue as well as block ER-alpha to the action of E2. I use Biest cream rather than oral preparations because, unlike oral estrogens,  transdermal preparations do not increase clotting factors and CRP,18 thus reducing the risk of thromboembolism and cardiovascular events. I teach patients to adjust the amount they use and to use just enough to control hot flashes without developing any breast tenderness.

2-Hydroxyestrone (*2-OHE)

2-hydroxyestrone is a good estrogen metabolite. Acting as a week estrogen, it blocks ER-alpha.19 Several studies have shown its protective action, especially the ORDET study (Hormones and Diet in the Etiology of Breast Cancer), an Italian study of 10,760 women.20 2-OHE levels can be increased by eating more vegetables and fruits and less animal fat. Indole 3-Carbinol, an extract of broccoli, has been shown to increase its levels and is a popular supplement for the prevention of breast cancer. I use it in heavy-set women who do not consume enough vegetables.


I believe that progesterone is an anti-cancer hormone. As well as having anti-breast cancer properties it also has an overall anti-cancer effect. Let us look at the evidence:

  1. In 1981, researchers at Johns Hopkins University reported a 13-33 year follow up on approximately 1000 infertile women. These women were divided into two groups: progesterone deficient women and an all-other-cause of infertility group. The progesterone deficient women had five times more breast cancer than the all-other-causes group. Furthermore, the death rate from all types of cancers was ten times higher in the progesterone deficient group than the other group. 21
  1. Fromby and Wiley from the Sansum Medical Research Institute, California, have performed and reported studies demonstrating that progesterone upregulates p53 (tumor suppressor gene) and downregulates bcl-2 and survivin (tumor promoter genes) in progesterone receptor-positive breast cancer cells, thus resulting in apoptosis of cancer cells.22, 23 These findings have been corroborated by other researchers and reported in the International Journal of Cancer.24
  1. Application of progesterone gel to breast has been shown to reduce mitotic activity in the breast  glands.25
  1. A National Cancer Institute study revealed that premenopausal women with the highest third week-of-cycle progesterone levels had a 60% decrease in subsequent breast cancer compared with those who had the lowest levels.26 A French study from International Agency for Cancer

Research showed the same results.27

  1. Breast cancer surgery studies reveal that surgical treatment during the follicular part of menstrual cycle (low progesterone levels) results in higher metastases and death rate compared to surgery during the luteal part (higher progesterone levels) of the menstrual cycle.28
  1. A large 2005 French study of 54,548 menopausal women revealed that women who took estrogen and Provera had a 40% increase in breast cancer. However, those who took estrogen and natural progesterone had a 10% decrease.29

It must be emphasized that only natural bioidentical progesterone has these anti-cancer effects, not the artificial progestins such as Provera (Medroxyprogesterone). Unfortunately, the majority of medical literature does not distinguish between bioidentical and artificial progesterone. Many practitioners of medicine tend to brush these differences aside with statements like: “a hormone is a hormone is a hormone – they are all the same.” To understand such beliefs, one has to go back into the history of steroid hormone discovery and synthesis (Figure 3).

In the 1930s, Russel Marker, a brilliant scientist at Penn State University, set out on a quest to manufacture exact replicas of human steroid hormones by a process of degeneration of similar molecules in plants. Eventually he found one such molecule in the Mexican Yam that could be chemically degraded to produce an exact copy of human progesterone. His discovery was ridiculed in the United States, so he moved in with a small Mexican lab and started producing bioidentical progesterone on a large scale. Subsequently, other bioidentical hormones, such as testosterone and estrogen could be produced.






Medroxyprogesterone (PROVERA)

Russel Marker



Norethindrone (Ortho Micronor)

Progesterone O

T estosterone


OH (Estriol)



Figure 3. Natural and artificial hormones.

When the large US drug companies got into the action, there was no profit motive in marketing the bioidentical, or real hormones, as these hormones could not be patented. The drug houses therefore modified the molecules to create artificial hormones, which are patentable drugs, and marketed those to US physicians as hormones. They called drugs like Provera “Progestins” and made the physicians believe that it was the same thing as progesterone. Similarly, Premarin, a horse estrogen was marketed as a replacement for human estrogen despite the fact that the molecules are very different.

The pharmaceutical companies should have known that a minimal change in the natural molecule – like the minimal change that turns progesterone into testosterone, and testosterone into estrogen – changes the entire action and function of the molecule, and that these molecules act in the human body only by attaching to their specific and exact receptors (Figure 4). Yet, they proceeded to blur the difference between the real and the artificial and proceeded to market these substances to US doctors and US women.

Figure 4. Steroid hormones working in the nucleus of the cell.

Many billions of dollars worth of these “hormones” were sold to women for many years until the WHI studies showed that these drugs resulted in increased cardiovascular complications, strokes, dementia, and breast cancer. Most of these complications appear to be related to Provera (medroxy- progesterone), which has been demonstrated to cause endothelial damage, inflammation, and insulin resistance,30-32 all of which increase the risk of cardiovascular problems, strokes, dementia, and cancer. Real progesterone is protective against these problems.

It must be mentioned that the same companies also manufacture real, “bioidentical”, hormones under government regulations, and sell them to compounding pharmacists who can mix and dispense these according to physician’s orders for individual patients, and much less expensively. It is up to the physicians to learn how to prescribe the real hormones. Unfortunately, most physicians do not have the time or the desire to do so.


Testosterone exerts a direct anti-breast cancer effect. An NIH study clearly demonstrated that testosterone reduced the ER-alpha activity on breast cells in monkeys and reduced the proliferation rate of the cells.33 Researchers at the University of Calabria in Italy have shown that testosterone inhibits breast cancer cells through its own androgen receptor, AR.34 A recent report on 624 breast cancer patients at the National Cancer Institute has indicated that testosterone or DHEA levels did not increase the risk of breast cancer.35

However, it is important to point out that testosterone can get converted into estrogen by aromatase in the breast tissue, and some reports suggest that women with higher estrogen plus testosterone have more breast cancer. So, what is the bottom line? I believe that menopausal women should receive testosterone, if their levels are low and symptomatic, but only in small doses, and in the form of testosterone creams. I monitor their testosterone levels and make every effort not to exceed their levels beyond the 60th percentile. I do not believe in giving women testosterone injections as they lead to high peak levels of testosterone and potentially high conversion to estrogen in the fatty tissues such as the breast.


breast cancers transplanted on to mice.38 Patients with low DHEA levels and breast cancer have more metastases.39 Low DHEA levels have been associated with higher breast cancer risk in pre-menopausal women, conversely, high DHEA levels have been associated with more post-menopausal breast cancer.40 It has been shown that if one infuses a large amount of DHEA into Petri dishes containing breast cancer cells, after about 4 days some of it eventually gets converted into estrogen, which can stimulate breast cancer cells.41 I recommend that women with low DHEA levels receive DHEA, but with caution, and only with blood level monitoring to ensure that you do not to exceed the 60th percentile of the reference range.


Melatonin is not just a sleep hormone. It plays a major role in the integrity of the neuroendocrine and immune systems. Melatonin levels begin to drop after the age of 15. By the time we reach our 60th birthday we have only one-tenth of our youth levels of melatonin.

Melatonin has multiple anti-cancer effects (Figure 5). It upregulates p53 and p21 tumor suppressor genes and reduces the concentration of ER-alpha on the tumor cells.42 Linoleic acid (LA) can promote cancer cell growth. Melatonin has been shown to block the entry of LA into cancer cells.43, 44 Melatonin protects cells against the effect of radiation.45 It also increases superoxide dismutase (SOD), glutathione, and catalase levels in cells, thus protecting them from cancer promoting free radicals.46 Melatonin also has anti-inflammatory properties,47 and thus may also help to prevent cancer by combating inflammation.

Blind women have higher levels of melatonin and a significantly lower rate of breast cancer than non-blind women.48 Conversely, night shift workers such as nurses, radio-telephone operators, and flight attendants tend to have lower melatonin levels and higher rates of breast cancer.49 Some studies have now appeared showing that the addition of melatonin to conventional treatments of cancer result in superior results.50 I believe melatonin should be given to all women having sleep difficulties, especially those at higher risk for breast cancer.

DHEA inhibits the growth of breast cancer cells in mice.36, 37 It also inhibits the growth of human

Free Radicals LA* Inflammation Radiation Cancer Cell


Mechanisms of Melatonin Anti-Cancer Action

*LA: Linoleic Acid *ER-a: Estrogen Reception-alpha

Figure 5. Inhibitory effects of melatonin on breast cancer.

Oxytocin is the pituitary hormone that lets the milk down in lactating mothers. It also has anti- cancer effects. It contracts the milk ducts thus propelling the free radical laden fluid out of the ducts. Free radicals in this fluid have been implicated in the initiation and stimulation of cancer.51 Oxytocin inhibits many types of cancer cells through its own oxytocin receptor (OR) on these cells.52 It also inhibits ER-alpha.53 Studies from many countries have shown that breastfeeding reduces the risk for breast cancer.54 Most likely this benefit is due to higher oxytocin levels during lactation. It makes a great deal of sense to breastfeed babies as long as possible, not just for breast cancer prevention but also for many other benefits to mother and child.

Oxytocin is not only increased with breastfeeding but also with breast and nipple stimulation. A

10-minute stimulation increases oxytocin levels by 100%.55 Alcohol tends to block this release of oxytocin. Frequent breast and nipple stimulation, performed hygienically, seems to make sense and may reduce the risk of breast cancer.56


By acting as a growth factor insulin promotes cancer cells by increasing levels of tyrosine kinase.57 A Vanderbilt study has shown that women with higher insulin levels are more likely to develop breast cancer.58 Whilst other studies have demonstrated that breast cancer patients with high insulin levels have more metastases.59 Finally, the large Nurses Health Study has revealed a higher incidence of breast cancer in the presence of diabetes.60 I believe insulin resistance (metabolic syndrome) should be managed and controlled before the onset of frank diabetes. It will not only reduce breast cancer and other cancers, but also reduce hyperlipidemias, hypertension, and cardiovascular events. I use agents like chromium or metformin in addition to appropriate nutrition and exercise to achieve these ends.

Tri-iodothyronine (T3)

T3 has many unappreciated anti-cancer effects. As we age our natural killer (NK) cells (the first  defense against cancer cells) decline. T3 increases NK cell activity.61 It increases interleukin-2 (IL-2), an important cytokine in the defense against cancer, which has been used effectively in many cancer treatment protocols.62 Tenacin C, a proliferative protein in cancer cells, is inhibited by T3.63 Cyclin D1 and Cyclin T1 genes are turned on in breast cancer cells. T3 suppresses these genes.64 It has been shown to directly inhibit MCF-7 (common type of breast cancer cells) in tissue cultures,65 to decrease aromatase in breast cancer cells,66 and to increase oxytocin production which inhibits cancer cells.67 T3 also increases sex hormone binding globulin (SHBG), which has an anti-breast cancer effect.68 T3 is also involved in DNA repair, which is important for our defense against cancer.69 Hypothyroidism is associated with increased breast cancer risk.70 It is T3 and not T4 or TSH that has anti-cancer activity. Unfortunately, most physicians check TSH and maybe T4, but not T3. Synthroid contains T4 only, and does not increase T3 adequately in many patients. Armour thyroid has both T3 and T4 in more natural proportions. I prefer to give my patients Armour thyroid, and I monitor their T3 levels regularly.

Human Growth Hormone (HGH)

HGH increases the production of insulin-like growth factor (IGF), which, like insulin, can stimulate  the growth of cancer cells.71, 72 However, HGH has many anti-cancer actions (Figure 6). HGH administration increases IGFBP-3, a protein which binds IGF. IGFBP-3 inhibits estrogen-induced  proliferation of breast cancer cells as well as promoting apoptosis of cancer cells.73 HGH repairs DNA damage inflicted to cells by carcinogens and radiation.74 It increases the activity of NK cells.75 It stimulates the thymus gland and modulates the secretion of thymic hormones, improving the overall immune response.76, 77 Its effect on the function of monocytes is inhibitory to cancer cells.78 Nuclear Factor Kappa B (NFKB) is a proliferator of cancer cells. HGH inhibits NFKB in cancer cells by increasing glutathione.79 It also increases levels of vitamin D, which has been shown to be inhibitory to cancer cells.80 Low-dose HGH therapy, unlike high-dose HGH therapy, has been shown to reduce visceral fat and actually improve insulin resistance,81 which should have an anti-cancer effect.
Unfortunately, the academia accentuates the one cancer stimulatory effect of HGH, but fails to mention any thing about its multiple anti-cancer effects. Studies of HGH administration to adults have not shown cancer as a risk.82 Recently, a western clinic that had treated some 2000 adults with HGH over several years communicated the results at the annual A4M meeting. There had been only one case of cancer. Acromegalics with sky-high HGH levels do not have increased rates of cancer; except for a somewhat higher risk for colon cancer.83 They do not have any increase in the rate of breast cancer. I do not believe that HGH therapy should be withheld for fear of cancer if clear cut indications for such therapy exist.

Figure 6. Effects of HGH on Breast Cancer.


Many factors influence the appearance and growth of cancer cells positively or negatively, and these factors can be manipulated to inhibit the initiation and growth of tiny cancers during this period of time. There are a number of things that you can do to help reduce your patient’s risk of developing breast cancer:

  • For HRT use only bioidentical hormones
  • For estrogen use Biest [4:1 ratio of E3 to E2]. Monitor patient and blood levels. Control hot flashes, but avoid breast tenderness. If breast tenderness develops back off on the dose. It may mean that the breast is not manufacturing much estrogen and the treatment E2 is entering the breast more than desired amounts. Use cream rather than oral preparations, thus avoiding an increase in clotting factors and c-reactive protein. Also, cream dose is easier to adjust.
  • Increase 2/16 E ratio by encouraging patients to eat more vegetables and fruits, and less animal fat. Give Indole 3 Carbinol to patients with a high risk of breast cancer.
  • Avoid Provera. Use only natural bioidentical progesterone.
  • In pre-menopausal women with PMS, check E2 and progesterone levels on day 21 of cycle. If there is E2 dominance or Progesterone deficiency, give progesterone from day 14-28 of cycle. You will relieve PMS and very likely reduce the risk of breast cancer.
  • In women with DHEA or T deficiency use DHEA or T cream and monitor levels not to exceed 60th percentile of the reference range.
  • Treat insulin resistance rather than waiting for frank diabetes to develop (nutrition, exercise, chromium, DHEA, metformin, etc.)
  • Increase oxytocin levels (breastfeeding, breast and nipple stimulation, alcohol reduction).
  • Pay attention to free T3 in patients with symptoms of hypothyroidism. Use Armour thyroid rather than Synthroid when needed.
  • Don’t be afraid to use HGH for fear of cancer, when clear indications for HGH exist.


  1. Mady EA, Ramadan EE, Ossman AA. Sex steroid hormones in se

Can Couples Counselling Help?

Can Couples Counselling Help?

By Melissa Bienvenu

Reviewed by Brunilda Nazario, MD

You know to see a doctor for an ache or cough that won’t go away. But where can you turn if your relationship needs a shot in the arm?

For some couples, professional counselling is the answer.

“Studies show that, in the hands of a good counsellor, marriage counselling is successful 70- 80% of the time,” says William Doherty, PhD, LCSW. Doherty is a professor of family social science at the University of Minnesota.

“We don’t see our relationships and ourselves objectively,” he says. “Most people are far more aware of how their partner is contributing to the problems in the relationship than they are. When we can’t ‘fix’ ourselves, sometimes we need a third party’s perspective.”

When to See a Counsellor

The main complaints couples bring to therapy are “losing connection and high levels of conflict,” Doherty says. “My research shows that ‘growing apart’ is the single biggest reason people give for divorce. Or maybe there is a lot of conflict that is depleting your marriage and you just can’t resolve it on your own.”

Major life changes or high levels of stress can put pressure on a relationship, too.

Whatever the cause, it’s best to treat relationship problems sooner rather than later — just as you would an illness, says Michael McNulty, PhD, LCSW. He’s a psychotherapist who trains couples counsellors for The Gottman Institute.

McNulty says on average, couples wait 6 years after problems develop to seek counselling. And he says that’s unfortunate, because the sooner you get help, the better your chances of success.

How Counselling Works

The goal of therapy is to give couples problem-solving tools. Studies show that most newlyweds expect to agree with their spouse far more often than they actually will.

“We aren’t taught how to be in relationships or deal with the conflicts that come up,” McNulty says. “There are very basic things people can learn about friendship and conflict that make total sense, are easy to do, and can really help. And that is where counselling helps.”

Over the first few sessions, expect the therapist to interview both of you — together and sometimes separately. After that, the therapist should give you feedback and a plan for treatment.

The average length of counselling is 12 sessions, but it can be different for each couple.

After four or five sessions, you should be able to tell if the therapy is working. By this time, you and your partner should feel you’re communicating with each other in a more positive and effective manner, McNulty says. “[You] should look for small changes week in and week out.”

“You can tell that couples counselling is working,” Doherty says, “when you feel that there is some learning going on about the other partner. Maybe you are feeling more hope or seeing changes at home. If you were distant, maybe you feel closer. Maybe there is less conflict, or arguments are not so bad when you have them.”

Finding the Right Counsellor

“I encourage people to see someone who specializes in marriage counselling — at least 30% of their practice,” Doherty says. “They have seen it all, and they will roll up their sleeves and help you.”

Ask your friends, doctors, or clergy for names of counsellors they know and recommend. Some hospitals and social service organizations have referral services. Local chapters of the American Association of Marriage and Family Therapy, the National Association of Social Workers, or the American Psychological Association may be able to help, too.

Look for someone who has a background in couples therapy and advanced certification in couples work. Licensed marriage and family therapists (LMFTs) are likely to have more training as well.

Also look for a therapist who is caring and compassionate to both of you and doesn’t take sides. A therapist should keep control of sessions and not allow you to interrupt each other, talk over each other, speak for each other, or have heated exchanges.

McNulty says a good therapist will encourage couples to decide early on whether he or she is a good fit for them, and will offer a referral if not.

Couples counselling is not always covered by health insurance, although it may be if one partner is being treated for a mental health condition such as depression.

If Your Partner Won’t Go

If you want to try counselling and your partner doesn’t, experts say don’t give up.

“Tell them you are worried for the relationship, that you love them and want their help in making it succeed,” Doherty says. “You don’t have the conversation once. You have it over and over, and you don’t take no for an answer.”

If all else fails, try therapy alone, McNulty says. The counsellor may have ideas about how to change your partner’s mind.

Tips for Developing Mindful Attitudes

11 Tips for Developing Mindful Attitudes

By Patrizia Collard from Mindfulness-Based Cognitive Therapy For Dummies

Mindfulness can sometimes appear relatively simple (as in ‘just be’), but in fact it’s not so easy. Creating a mindful practice that leads to a mindful life requires you to change certain attitudes and behaviour patterns that otherwise get in the way of you living mindfully.

To help, here are 11 tips to make you aware of these necessary mindful mindsets and to help support you in acquiring them.

Tiny baby-steps are better than leaping forwards and then straining yourself to the extent that you may give up mindfulness altogether.

Mindfulness: Being non-judgemental

From the word go people are judged and evaluated: good boy, good girl, and so on are the responses adults utter when children manage a new skill. Judging is deeply engrained into your psyche and so you may find that letting go of judgement does not come naturally at first.

Equally you may become aware, when you look out for it, that like most people you have likes and dislikes and that these preferences are almost etched onto your subconscious.

The good news is that your brain has the capacity to expand and create new neuro pathways as you start to think and experience things differently.

The initial step is to pay attention fully when your mind is judging something. You may be surprised how often you judge something as pleasant or unpleasant throughout the day. Your mind is so overactive judging everything that it can make you dizzy when you become really aware of it. Every sense checks and labels experiences: seeing, hearing, tasting, smelling, touching and thinking. What an exhausting effort!

Use a mindfulness diary and write down all the judging, evaluating, appraising and so on that goes on in your mind during the course of half an hour. Don’t be shocked if you find hundreds of judgements going on. Afterwards, note down your any patterns in your likes or dislikes. For example, do you mainly judge yourself, other people, life, the government or activities you engage with, or just everything?

Judgement can and will happen while you’re practising meditation. You may have thoughts along the lines of: ‘Is this ever going to end?’ or ‘How can this stupid watching of my breath help my marriage?’ Simply notice that all thoughts of this nature are fruitless judgements and evaluations. Just observe them for what they are and, as best as you can, let them pass by before returning to your practice. If you don’t feed these thoughts, they’re most likely to reduce over time.

Plus, don’t think that you need certain conditions to be right so that you can practise successfully. Just accept, without judgement, however an exercise turns out. Even if you have to bring your attention back hundreds of times, congratulate yourself for noticing it and don’t hold on to judgements about good or bad meditations.

Having patience in your mindfulness

Patience is a gift that some people are bestowed with, but most people have to develop it slowly. And today’s quick-fix society doesn’t help, with takeaway meals, movies on demand, one-hour home deliveries. This convenience is all very well, but it doesn’t help you to develop patience.

The attitude to aim for is to allow mindful awareness to unfold moment by moment. Give yourself time and be assured that practising mindfulness in itself is practising kindness and patience. It’s a wonderful tool to have when you’re frightened, unwell or down in the dumps. In these difficult times, patience whispers into your ear that ‘this too will pass’.

Plus, if you develop patience and allow life to present itself to you as it is, you start to observe the little miracles that life presents: a flower growing out of a small crack in the wall, a smile from an unknown passerby, a beautiful scent in the air, the wind gently caressing your face and many, many more.

Mindfully cultivating childlike curiosity

Consider choosing an afternoon at the weekend and noticing all the little wonders and surprises occurring, as if you’re a child. If you have a child in your family, spend time with them and let them remind you: the miraculous taste of ice-cream or cake, the fun of blowing a dandelion and seeing all the tiny grey ‘umbrellas’ set off on their own, the joy of splashing yourself with water or licking out the chocolate residue from a bowl (using your fingers, of course!).

Think about what else makes you intensely curious. Perhaps try to listen to your favourite songs and see whether you notice something new about them: an instrument, a word you never noticed before, a change in rhythm.

Listen to Sir David Attenborough. Whenever he talks about an animal, he sounds as if he’s the first person who’s ever seen it. He’s an excellent example of living with childlike curiosity.

This attitude of curiosity is essential when you practise the formal mindfulness meditations. An open (beginner’s) mind helps you to notice that each meditation differs, that each moment is unique, and it helps to imprint this awareness onto your everyday thinking, too.

Trusting yourself and the science of mindfulness

‘There’s no right or wrong way of practising mindfulness, there’s only your way.’ This saying doesn’t mean that you don’t need good guidance and continuing development in mindfulness-based cognitive therapy (MBCT), but it does mean that ultimately you know best when to practise and how to arrange your practice room, for example. You intuitively feel when you need more time to engage with formal meditation or when you want a free-flowing day where you’re mindful from dawn to dusk. In particular, trust in yourself that sooner or later you’ll start noticing the benefits that MBCT brings to your life.

Respect what your body tells you, because this communication is ultimately of utmost importance when it comes to choosing the right posture of sitting or kneeling, for example. Don’t be a martyr to your pain. Experiment with postures, mindful movement, time of the day, and so on, and see what serves you best.

The other aspect of trust refers to the teachings of mindfulness itself. Modern-day scientific research proves that mindfulness works, revealing how it changes your brain structurally and alters your biochemistry. Therefore, you can read scientific evidence to support your mindfulness journey. At its roots, however, is an ancient wisdom that has continued over several thousand years, teaching awareness, kindness and compassion to help you feel more truly alive.

Working on personal growth and non-striving

Since childhood you may well have learned to strive, to become educated and, if at all possible, be successful. Success is usually seen in monetary rewards or status. While you strive and think that this success is what’s expected of you, you’re also told to be better than others. Schools and universities offer scholarships to the best students, not to the ones who may need or deserve them most.

Now, within the context of mindful living and practice, let go of these goals and to not strive. Mindfulness promotes the idea of non-doing (of just being). Isn’t that doing something? These requests can all seem rather confusing if not contradictory.

The most important aspect of non-striving is the awareness that you’re already perfect and that some areas of your life just need a little polishing, that’s all. Think of yourself as a diamond. Before it’s polished it looks like ordinary stone, but afterwards it radiates in all the colours of the rainbow and is beautiful.

Accepting things just as they are

Acceptance indicates that you’re prepared to do a reality check. Acknowledging that, for example, you drink too much, sleep too little, feel down in the dumps or bad about choices you’ve made, or are frightened by the noise of the wind, isn’t an easy step to take. You can feel that if you accept things as they are, at least for now, you may never be able to change them, but as the song says, this ‘ain’t necessarily so’. In fact, the exact opposite may be the outcome when you’ve faced your demons.

If you look the pain, fear, sadness, disease or whatever directly in the eye, you may be able to find or see a way through it. You need to know what you’re trying to cure or change before you can go about altering it. Sometimes, of course, acceptance means that a situation ‘is what it is’ and that you need to find out how to live around it, instead of letting it wear away the quality of your life completely.

Think about how much time you invest regularly in resisting what you don’t like, at least mentally. It takes up a great deal of strength to continue to resist or experience aversion towards things that are what they are. You can use up all your energy in resistance, leaving nothing left to produce change.

Thus, accepting your situation just as it is (for now) can be the starting point for living your life truly and engaging in it with a sense of adventure.

Letting go of negative thoughts

When you start engaging with regular meditation you soon find that a number of thoughts keep coming back, and a number of discomforts arise.

As best as you can, simply take each moment as it comes, neither attaching to it too strongly nor pushing it away. You can always say to yourself: ‘It’s okay; I want to feel it, just as it is, knowing all the while that soon everything passes.’

Think of letting go as being like closing your mind when you’re ready to fall asleep. You trust that you’re going to wake up in the morning, that the world will still exist and that you can experience another day. To find peace and sleep, you need to let go of worries and ruminations; the same is true for meditation.

Committing to commitment and self-discipline

In some ways, developing mindfulness skills is like learning any other ability. Unless you practise regularly you won’t achieve your goals or, for example, you won’t have access to the emergency breathing space meditation when you really need it.

So, do mindfulness exercises and meditations, rain or shine; put a date and time for your practice in your diary. Perhaps practise with a buddy and join a group nearby, if at all possible. Explore all the other activities that you can reduce to give you time and space for MBCT.


Mindfulness: Maintaining compassion

You need deep compassion for your mindfulness experience ? first of all for others, who’re most probably still doing their own thing even though you’re becoming more astutely aware of flaws and selfish actions. If you notice other people being in a ‘me, me, me’ state, remember that they may not know any better.

You also require self-compassion, which means observing your own flaws and suffering. The more mindful you become, the more delicate your sensors are in picking up when hurt is in the air. Sometimes this pain is caused by your own self-critical attitude, and if you do something wrong or lose your temper, only the attitude of self-compassion can give you the humility to own the mistake and say sorry.

Try not to have double standards and be stricter with yourself than you are with a friend. All humans make mistakes.

Being in the now with your mindfulness

Every practice, formal meditation or everyday mindfulness experience reminds you over and over to connect to one thing: the present moment. Now, at this moment, your life is happening.

The past is no longer accessible by you and the future isn’t here yet. Unless you focus on the here and now, you may miss out the miracle of life.

Observing a wider perspective

You’re important and so is everybody else, including all beings and the planet. Mindfulness invites you to see that you’re part of this bigger picture.

Mindful living in its larger perspective means bringing awareness to each moment and all that this moment encompasses: so if you see somebody who’s hungry in this moment, you may respond to hunger (maybe buy a sandwich); if you see somebody hurt, you may call the ambulance; if you see an elderly or frail person on the bus or train, you may mindfully offer your seat.

Mindful living changes your life, and the lives of the people around you as well.