Sunday, February 28, 2010

30-day Joy Practice: Join Me!

 

Earlier this month, I was blessed by an impromptu yoga class with a favorite teacher: Shiva Rea. I hadn't studied with her for about 2 years, but in her Venice Beach class I reconnected with what draws me to her teaching - she's the real deal, a true prophetess and mystic, and a great synthesizer of how to bring more joy into our daily lives.

I also was blessed to be asked to teach a class for Up2Yoga. While preparing for my April 1 class on Stress Resilience, I happened to listen to Shiva's session that is downloadable from Up2Yoga's site on Living Yoga Sadhanas. This may not mean much to you, but perhaps it should. Shiva is onto something incredibly juicy and transformative: start with the next new moon cycle (uh, today) and commit to a 30-day practice based on your energy now.

 

I am planning to start my 30-day Bhakti Sadhana starting with the next new moon on March 15, 2010. Care to join me? If so, download her details right here. Or listen to her audio file right here. Prepare for more joy, my friends!

Here's a little help from Wikipedia on the etymology of bhakti:

The Sanskrit noun bhakti is derived from the verb root bhaj, whose meanings include "to share in", "to belong to", and "to worship". It also occurs in compounds where it means "being a part of" and "that which belongs to or is contained in anything else." Bhajan, or devotional singing to God, is also derived from the same root. "Devotion" as an English translation for bhakti doesn't fully convey two important aspects of bhakti—the sense of participation that is central to the relationship between the devotee and God, and the intense feeling that is more typically associated with the word "love". An advaitic interpretation of bhakti goes beyond "devotion" to the realization of union with the essential nature of reality as ananda, or divine bliss. Bhakti is sometimes used in the broader sense of reverence toward a deity or teacher.

Here's a little more detail from Wikipedia on "sadhana."

The term sadhana means spiritual exertion towards an intended goal. A person undertaking such a practice is known as a sadhu or a sadhaka. The goal of sadhana is to attain some level of spiritual realization, which can be either enlightenment, pure love of God (prema), liberation (moksha) from the cycle of birth and death (Samsara), or a particular goal such as the blessings of a deity as in the Bhakti Sadhana can involve meditation, chanting of mantra (sometimes with the help of a japa mala), puja to a deity. Traditionally in some Hindu and Buddhist traditions in order to embark on a specific path of sadhana, firstly a guru may be required to give the necessary instructions. This approach is typified by some Tantric traditions, in which initiation by a guru is sometimes identified as a specific stage of sadhana. On the other hand, individual renunciates may develop their own spiritual practice without participating in organized groups. traditions.

I'm looking at the next part of the moon cycle, from the full moon today until the next new moon on 3/15/10, as my preparation phase. More on that as it unfolds.

    Sunday, February 21, 2010

    The Big "C" - How to Prevent Aggressively

    I want to re-post this provocative blog from today's Huffington Post by David Servan-Schreiber, M.D., Ph.D., who is the author of Anticancer: A New Way Of Life. Great info on how lifestyle choices are behind 85% of the crazy epidemic of cancer we have in the Western World (the other 15% is genetics - smaller than you might think).

    Take away message for aggressive prevention:
    • cut out sugar (feeds cancer cells & causes inflammation)
    • crank up fresh organic fruits, veggies & anti-inflammatory herbs & spices (turmeric, garlic)
    • exercise regularly - at least 6 times per week for 30 min
    • manage stress better with a contemplative practice
    • go green in your home/workplace/anywhere else you spend time
    We Can All Fight Cancer Better
    by David Servan-Schreiber, M.D, Ph.D.

    At age 31, my life took a sudden turn. I was an ambitious physician and neuroscience researcher who reveled in discovery and glittering science projects. Then, slipping into a brain scanner one evening in place of a subject who hadn't shown up, I was suddenly stripped of my white-coat status and thrown into the gray world of patients: That evening, I discovered that I had brain cancer.

    Being a physician and scientist is no protection from getting cancer. But it allowed me to dig deeply into the medical and scientific literature to find out everything I could do to help my body resist the disease most efficiently and try to beat the median survival of a few years.

    The first thing I learned is that we all carry cancer cells in us. But I also learned we all have natural defenses that generally prevent these cells from turning into an aggressive disease. These include our immune system, the part of our biology that controls and reduces inflammation, and the foods that reduce the growth of new blood vessels needed by developing tumors.

    In the West, one out of three people will develop cancer. But two-thirds will not. For these people, their natural defenses will have kept cancer at bay. I understood it would be essential for me to learn how to strengthen these defenses.

    A Cancer Epidemic

    My own disease is just one case in a cancer epidemic plaguing western societies. Cancer rates have been climbing steadily in the US since 1940. This is not due simply to the increase use of screening tests or the aging of our population: cancer has been rising in children and adolescents at a rate of 1 to 1.5 percent per year in the past 25 years. [1] And cancers that have no screening test (lymphomas, pancreatic and testicular cancers for example) have been increasing as fast or faster than those that do (breast, colon, prostate). [2]

    Asian countries did not experience this rise until recently. [3] Yet, Asian immigrants in the US have the same rates of western cancers as Caucasian Americans after one or two generations [4 , 5]

    Not a Genetic Lottery

    Thus, cancer is not a genetic lottery. A new model has emerged from the last 10 years of research. It moves away from genetics and squarely into life-style factors that we can learn to control.

    A New England Journal of Medicine study conducted by the University of Copenhagen showed that people who were adopted at birth had the cancer risk of their adoptive parents rather than that of the parents who gave them their genes [6]. At most, genetic factors contribute 15 percent to our cancer risk. What matters for 85 percent of cancers is what we do -- or do not do enough of -- with our life [3].

    Life-style Choices Trump Genes

    Indeed, a new Cambridge University study has shown that people who follow simple healthy life-style rules reduce their chances of dying from cardiovascular disease or cancer by roughly a factor of four. [7]

    At Ohio State University, another team followed women with breast cancer (stage II) who all had surgery and conventional treatment. Some did not do any more than that, but others participated in an education group focused on better nutrition, more physical activity, and simple relaxations methods such as "progressive muscle relaxation", similar to yoga. Those who learned to change their life-style were 68 percent less likely to die from their cancer in the next 11 years. [8]

    Other recent studies -- from the University of San Francisco -- found that such simple life-style changes in men with prostate cancer, completely change the way genes behave, including the genes of cancer cells. This research shows that life-style choices play on our genes like a pianist's fingers play on a keyboard ... transforming the body's ability to resist cancer growth. [9-11]

    And in 2009 a stunning reversal of groupthink on the role of genes in breast cancer: Women with the ominous BRCA-1 or 2 genes (80 percent chance of developing breast cancer), reduce their risk by 73 percent if they eat a good variety of vegetables and fruits, showed University of Montreal researchers. [12] Are these really "breast cancer genes" then, as they've been touted to be all along? Or are they simply junk-food intolerance genes?

    Changing the "Terrain"

    When it comes to treating cancer, there is no alternative to conventional treatments: surgery, chemotherapy, radiotherapy, immunotherapy or, soon, molecular genetics.

    However, these treatments target the tumor much like an army wages war: focusing on destroying the cancerous cells. They do not help prevent the disease if we don't have it, and, if we do, they do not help the body build up it's natural resistance to make the treatments work better.

    For prevention or better disease management, it is important to change the environment --- the "terrain" -- that supports the growth of new cancer cells, even if treatment pounds them with targeted attacks.

    Modern research suggests that cancer cells grow much faster under three circumstances:

    1. When our immune system is weakened and less capable of detecting and destroying budding tumors.

    2. When low-grade chronic inflammation in our body supports the multiplication of cells and the invasion of neighboring tissue.

    3. When tumors are allowed to develop new blood vessels to expand to a larger size, much like a city expands when allowed to develop new roadways.

    When we strengthen our immune system, reduce inflammation and reduce the growth of new blood vessel, we help create an anticancer "terrain".

    Anticancer Choices

    For better prevention, or better treatment results, nothing can beat the combination of conventional medicine (early screenings, or chemotherapy, surgery, radiotherapy, etc.) with an anticancer way of life: A way of living through which we begin to nourish every aspect of health within our bodies:

    1. Cleaning up our diet: reducing sugar -- which feeds cancer growth and inflammation. Refined sugar is abundant in desserts, soft drinks (one can of Coke contains 12 coffee-size packs of sugar...), sauces (Ketchup, ready-made salad dressing, etc.), white flour which is equivalent to sugar as far as the body is concerned (white bread, bagels, muffins, etc.), and reducing pro-inflammatory omega-6 fatty acids (red meats, dairy, corn, sunflower, soybean and safflower oils, and trans-fats).

    2. Adding anti-cancer foods: including in our diet every day, three times a day, foods that help fight cancer. Such as anticancer herbs and spices (green tea, turmeric, ginger , thyme, rosemary, mint, basil, sage), omega-3 rich foods (salmon, sardines, mackerel, walnuts, green vegetables), cruciferous vegetables (broccoli, cauliflower, cabbage), garlic, onions and leeks, red berries, plums, blueberries for dessert, dark chocolate (more than 70 percent cocoa), and even a little bit of red wine.

    3. Engaging in physical activity: it doesn't have to be marathon training, not even jogging. Just rapid walking 30 minutes six times a week already dramatically reduces the chances of a relapse after breast cancer treatment or the risk of advanced prostate cancer. And physical activity has been found to help survival with many different types of cancer. [13]

    4. Managing our response to stress: we can't avoid stress in our life, but we can learn to respond differently than with clenched teeth, stone-hard back muscles and pressure in our chest. Basic breathing techniques that have been around as part of oriental mental and physical hygiene techniques for thousands of years (Yoga, Chi Gong, mindfulness meditation) can transform our response to stress and strengthen our resistance to disease. And simply reaching out to one or two friends during hard times can even reduce the risk of dying from breast cancer by a factor of four. [14]

    5. Cleaning up our immediate environment: in-door pollutants, parabens and phthalates in cosmetics, scratched Teflon pans, percholorethylene of dry-cleaning, PVCs and bisphenol A from liquids in contact with hard plastics, radiomagnetic fields of prolonged cell phone exposures are the leading and most easily controlled causes.

    Conclusion

    As a physician with cancer, I've discovered that we can all create an anticancer biology for ourselves through the choices we make in our lives. They cannot replace the benefits of surgery, chemotherapy or radiotherapy, and do not have the same support from aqs many large controlled trials to back them up. However, the life-style changes discussed above are demonstrated to improve health and new scientific evidence suggests they slow down cancer too.

    Indeed, as strange as it may seem, I'm in better health and happier today than before I was ever ill. I feel more at peace, lighter, with more energy and drive and passion for life. A few years ago, my neuro-oncologist unwillingly reminded me of the odds against this happening when he told me "I don't if I should tell you this, but I'm always happy to see you at your follow-up visits, because you're one of the very rare patients I have who is doing well!"

    Most people who start on this health journey notice a difference within a few weeks. Recent studies suggest that such life-style changes start improving mood and well-being after two to four months, and can have an impact on cancer statistics within a year or two of follow-up. (Andersen et al. 2004, 2008; Blake-Mortimer et al. 1999; Fawzy et al. 1990, 1993; Monti et al. 2006, Spiegel et al. 1989)
    What I've learned in my own journey of 17 years with cancer is that the best way to go on living is to nourish life at all levels of my being: through my meals three times a day, through my walks in nature, through the meaning and purpose in my work, through the flow of love in my relationships, and through the protection of our environment. Science told me that this slows down cancer, but, perhaps even more importantly, it brings to my life, every day, a new light and a new purpose.

    References

    1. Steliarova-Foucher, E., et al., Geographical patterns and time trends of cancer incidence and survival among children and adolescents in Europe since the 1970s (the ACCIS project): an epidemiological study. The Lancet, 2004. 364(9451): p. 2097-2105.

    2. Parkin, D., et al., Cancer Incidence in Five Continents, Volumes I to VIII., in IARC CancerBase No. 7. 2005, World Health Organization: Lyon, France.

    3. Stewart, B.W. and P. Kleihues, eds. World Cancer Report. 2003, W.H.O IARC Press: Lyon, France.
    4. Yatani, R., et al., Trends in frequency of latent prostate carcinoma in Japan from 1965-1979 to 1982-1986. Journal of the National Cancer Institute, 1988. 80(9): p. 683-7.

    5. Sasco, A.J., [Migration and cancer]. Revue de Medecine Interne, 1989. 10(4): p. 341-8.

    6. Sorensen, T.I.A., et al., Genetic and environmental influences on premature death in adult adoptees. New England Journal of Medicine, 1988. 318: p. 727-32.

    7. Khaw, K.-T., et al., Combined Impact of Health Behaviours and Mortality in Men and Women: The EPIC-Norfolk Prospective Population Study. PLoS Medicine, 2008. 5(1): p. e12.

    8. Andersen, B.L., et al., Psychologic Intervention Improves Survival for Breast Cancer Patients: A Randomized Clinical Trial. Cancer, 2008. 113: p. 3450-3458.

    9. Ornish, D., et al., Increased telomerase activity and comprehensive lifestyle changes: a pilot study. The Lancet Oncology, 2008: p. doi:10.1016/S1470-2045(08)70234-1.

    10. Ornish, D., et al., Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proceedings of the National Academy of Sciences, 2008. 105: p. 8369-8374.

    11. Ornish, D., et al., Intensive lifestyle changes may affect the progression of prostate cancer. Journal of Urology, 2005. 174(3): p. 1065-9; discussion 1069-70.

    12. Ghadirian, P., et al., Breast cancer risk in relation to the joint effect of BRCA mutations and diet diversity. Breast Cancer Research & Treatment, 2009. 117: p. 417-422.

    13. World_Cancer_Research_Fund, Food, Nutrition and the Prevention of Cancer: A Global Perspective, W.C.R.F.a.A.I.f.R.o. Cancer, Editor. 2007, World Cancer Research Fund and American Institute for Research on Cancer: London, UK.

    14. Kroenke, C.H., et al., Social networks, social support, and survival after breast cancer diagnosis. Journal of Clinical Oncology, 2006. 24(7): p. 1105-11.

    Thursday, February 18, 2010

    Patch That Leaky Gut



    Wanted to post some info on Leaky Gut Syndrome. Here's a start - an informative post by Dr. Leo Galland, MD.

    It's a little techy, so thought I'd also post some help understanding the matter from Dr. Andy Weil, MD's website:

    Leaky gut syndrome is not generally recognized by conventional physicians, but evidence is accumulating that it is a real condition that affects the lining of the intestines. The theory is that leaky gut syndrome (also called increased intestinal permeability), is the result of damage to the intestinal lining, making it less able to protect the internal environment as well as to filter needed nutrients and other biological substances. As a consequence, some bacteria and their toxins, incompletely digested proteins and fats, and waste not normally absorbed may "leak" out of the intestines into the blood stream. This triggers an autoimmune reaction, which can lead to gastrointestinal problems such as abdominal bloating, excessive gas and cramps, fatigue, food sensitivities, joint pain, skin rashes, and autoimmunity. The cause of this syndrome may be chronic inflammation, food sensitivity, damage from taking large amounts of nonsteroidal anti-inflammatory drugs (NSAIDS), cytotoxic drugs and radiation or certain antibiotics, excessive alcohol consumption, or compromised immunity.
    My colleague, pediatrician Sandy Newmark, M.D., who deals with leaky gut syndrome in children, tells me that it isn't clear how many people have this disorder or exactly what problems can be attributed to it. Dr. Newmark says that it has been established that a significant percentage of children with autism have increased intestinal permeability, but it isn't known whether this is a cause or an effect of food sensitivities and an underlying metabolic problem.

    Thursday, February 11, 2010

    Psychiatric Medications - Effects on Breastfeeding

    Fantastic compilation of what psych drugs can do to our babies and how much gets in our breastmilk by Dr. Richard Oliva at UCSF.



    Summary of Data published on LactMed (http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?LACT) as of 02/01/10
    Drug
    Into Breastmilk?
    Effect on Infant/Safety/ Summary
    Fluoxetine
    The average amount of drug in breastmilk is higher with fluoxetine than with most other SSRIs and the long-acting, active metabolite, norfluoxetine, is detectable in the serum of most breastfed infants during the first 2 months postpartum and in a few thereafter.
    Adverse effects such as colic, fussiness, and drowsiness have been reported in some breastfed infants. Decreased infant weight gain was found in one study, but not in others. No adverse effects on development have been found in a few infants followed for up to a year. If fluoxetine is required by the mother, it is not a reason to discontinue breastfeeding. If the mother was taking fluoxetine during pregnancy or if other antidepressants have been ineffective, most experts recommend against changing medications during breastfeeding.
    Paroxetine
    Because of the low levels of paroxetine in breastmilk, amounts ingested by the infant are small and paroxetine has not been detected in the serum of most infants tested.
    Occasional mild side effects (alertness, constipation, sleepiness and irritability) have been reported, especially in the infants of mothers who took paroxetine during the third trimester of pregnancy, but the contribution of the drug in breastmilk is not clear. Most authoritative reviewers consider paroxetine one of the preferred antidepressants during breastfeeding.
    Sertraline
    Because of the low levels of sertraline in breastmilk, amounts ingested by the infant are small and is usually not detected in the serum of the infant, although the weakly active metabolite desmethylsertraline is often detectable in low levels in infant serum.
    Most authoritative reviewers consider sertraline one of the preferred antidepressants during breastfeeding.
    Citalopram
    Infants receive citalopram in breastmilk and it is detectable in low levels in the serum of some. The dosage that the infant receives and serum level achieved are probably related to the genetic metabolic capacity of the mother and infant.
    A few cases of minor behavioral side effects such as drowsiness or fussiness have been reported, but no adverse effects on development have been found in infants followed for up to a year. If citalopram is required by the mother, it is not a reason to discontinue breastfeeding. If the mother was taking citalopram during pregnancy or if other antidepressants have been ineffective, most experts recommend against changing medications during breastfeeding.
    Escitalopram
    Limited information indicates that maternal doses of escitalopram up to 20 mg daily produce low levels in milk and would not be expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months.
    Based on limited data, escitalopram appears to be preferable to racemic citalopram during breastfeeding because of the lower dosage and milk levels and general lack of adverse reactions in breastfed infants. Monitor the infant for drowsiness, especially in younger, exclusively breastfed infants and when using combinations of psychotropic drugs.
    Bupropion
    Limited information indicates that maternal bupropion doses of up to 300 mg daily produce low levels in breastmilk and would not be expected to cause any adverse effects in breastfed infants.
    There is little reported use in breastfed newborn infants and one case report of a possible seizure in a partially breastfed 6-month-old. If bupropion is required by a nursing mother, it is not a reason to discontinue breastfeeding. However, another drug may be preferred, especially while nursing a newborn or preterm infant. Exclusively breastfed infants should be monitored if this drug is used during lactation, possibly including measurement of serum levels to rule out toxicity if there is a concern.
    Duloxetine
    No published information is available on the use of duloxetine during breastfeeding; however, the dose in milk is low.
    An alternate drug that has been better studied may be preferred, especially while nursing a newborn or preterm infant. If duloxetine is required by the mother, it is not a reason to discontinue breastfeeding. Monitor the infant for drowsiness, adequate weight gain, and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of psychotropic drugs.
    Venlafaxine
    Infants receive venlafaxine and its active metabolite in breastmilk, and the metabolite of the drug can be found in the plasma of most breastfed infants, but no proven drug-related side effects have been reported.
    Breastfed infants, especially newborn or preterm infants, should be monitored for excessive sedation and adequate weight gain if this drug is used during lactation, possibly including measurement of serum levels of desvenlafaxine [O-desmethylvenlafaxine], to rule out toxicity if there is a concern. However, newborn infants of mothers who took the drug during pregnancy may experience poor neonatal adaptation syndrome as seen with other antidepressants such as SSRIs or SNRIs. Use of venlafaxine during breastfeeding has been proposed as a method of mitigating infant venlafaxine withdrawal symptoms,[1] but only one apparently successful case of this use has been reported.
    Desvenlafaxine
    Although no data are available for the use of desvenlafaxine during breastfeeding, it is the active metabolite of venlafaxine. Venlafaxine study data indicate that relatively large amounts of desvenlafaxine are likely to be excreted into breastmilk.
    Other agents may be preferred, especially while nursing a newborn or preterm infant. Breastfed infants should be monitored for excessive sedation and adequate weight gain if this drug is used during lactation, possibly including measurement of serum levels of desvenlafaxine to rule out toxicity if there is a concern. Because desvenlafaxine is available only as a sustained-release product, timing of nursing with respect to doses would not be useful.
    Lithium
    Random milk levels have been reported to range from 0.12 to 0.7 mEq/L and appear to be rather consistent at about 40 to 45% of the simultaneous maternal serum level.
    Limited data suggest that lithium in milk can adversely affect the infant when its elimination is impaired, as in dehydration or in newborn or premature infants. Neonates may also have transplacentally acquired serum lithium levels. The long-term effects of lithium on infants are not known, but limited data indicate no obvious problems in growth and development. Although lithium appears on many lists of drugs contraindicated during breastfeeding, other sources do not consider it a contraindication, especially in infants over 2 months of age and during lithium monotherapy. Lithium may be used in mothers of full-term infants who are willing and able to monitor their infants. Some investigators recommend monitoring infant serum lithium, serum creatinine, BUN, and TSH every 4 to 12 weeks during breastfeeding and maternal lithium therapy.[2][3] Breastfeeding should be discontinued immediately if the infant appears restless or looks ill.
    Valproic Acid
    Because of the low levels of valproic acid in breastmilk and infant serum, no unquestionable adverse reactions to valproic acid during breastfeeding have been reported.
    Theoretically, breastfed infants are at risk for valproic acid-induced hepatotoxicity, so infants should be monitored for jaundice and other signs of liver damage during maternal therapy. A questionable case of thrombocytopenia has been reported, so monitor the infant for unusual bruising or bleeding. One author recommends monitoring infant serum valproate levels, platelets and liver enzymes during therapy. Combination therapy with sedating anticonvulsants or psychotropics may result in infant sedation or withdrawal reactions.
    Carbamazepine
    Carbamazepine has relatively high levels in breastmilk and breastfed infants have serum levels that are measurable, but usually below the anticonvulsant therapeutic range.
    Most infants have had no adverse reactions, but sedation, poor sucking, withdrawal reactions and 3 cases of hepatic dysfunction have been reported. These have all been complicated because of intrauterine exposure and, in some cases, concurrent drug therapy. If carbamazepine is required by the mother, it is not a reason to discontinue breastfeeding. Monitor the infant for jaundice, drowsiness, adequate weight gain, and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of anticonvulsant or psychotropic drugs.
    Oxcarbazepine
    The relationship of the maternal dosage to the concentration in breastmilk can be quite variable, making calculation of the weight-adjusted percentage of maternal dosage less meaningful than usual.
    Limited information indicates that oxcarbazepine would not be expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months. Monitor the infant for drowsiness, adequate weight gain, and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of anticonvulsants.
    Lamotrigine
    Breastfed infants whose mothers are taking lamotrigine have relatively high plasma lamotrigine levels, averaging 30 to 35% of maternal serum levels; infant plasma levels up to 50% of maternal levels have been reported. Neonates are particularly at risk for high plasma levels because their ability to metabolize the drug by glucuronidation is limited and maternal plasma and milk levels can rise dramatically in the immediate postpartum period if the dosage is not reduced to the prepregnancy dosage.
    Additionally, lamotrigine can cause rare, but potentially fatal skin reactions. If lamotrigine is required by the mother, it is not necessarily a reason to discontinue breastfeeding, because many infants have been breastfed without adverse reactions. However, breastfed infants should be carefully monitored for side effects such as rash, drowsiness or poor sucking, including measurement of serum levels to rule out toxicity if there is a concern. If an infant rash occurs, breastfeeding should be discontinued until the cause can be established.
    Gabapentin
    Limited information indicates that maternal doses of gabapentin up to 2.1 grams daily produce relatively low levels in infant serum.
    Monitor the infant for drowsiness, adequate weight gain, and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of anticonvulsant or psychotropic drugs.
    Haloperidol
    Limited information indicates that maternal doses of haloperidol up to 10 mg daily produce low levels in milk and do not affect the breastfed infant.
    Very limited long-term follow-up data indicate no adverse developmental effects when haloperidol is used alone. However, combinations of antipsychotic agents can negatively affect development. Monitor the infant for developmental milestones, especially if other antipsychotics are used concurrently. In a small prospective study on the long-term effects of antipsychotics in breastfed infants, a decline in developmental scores was found at 12 to 18 months of age in 2 of the 4 the infants of mothers taking both chlorpromazine and haloperidol. The other 2 infants and all infants exposed to either drug alone developed normally.
    Risperidone
    Limited information indicates that maternal risperidone doses of up to 6 mg daily produce low levels in milk.
    Because there is little published experience with risperidone during breastfeeding and few long-term follow-up data, other agents may be preferred, especially while nursing a newborn or preterm infant.
    Olanzapine
    Limited information indicates that maternal doses of olanzapine up to 20 mg daily produce low levels in milk and undetectectable levels in the serum of breastfed infants.
    In most cases, short-term side effects have not been reported, but sedation has occurred. Very limited long-term follow-up of infants exposed to olanzapine indicates that infants generally developed normally, but combinations of antipsychotic agents can negatively affect development. Monitor the infant for drowsiness and developmental milestones, especially if other antipsychotics are used concurrently.
    Quetiapine
    Limited information indicates that maternal quetiapine oral doses of up to 400 mg daily produce low levels in milk. A 3-month-old infant who was breastfed 6 to 7 times daily during maternal use of 400 mg daily of quetiapine had a plasma quetiapine level of 1.4 mcg/L. This level was 6% of the mother's quetiapine plasma level at the same time.
    Because there is little published experience with quetiapine during breastfeeding and little long-term follow-up data, other agents may be preferred, especially while nursing a newborn or preterm infant.
    Clozapine
    A woman taking oral clozapine 50 mg daily had a milk clozapine level of 63.5 mcg/L one day postpartum. At 3 days postpartum her dose was increased to 100 mg daily, and at 7 days postpartum clozapine in milk was 115.6 mcg/L. Her infant was not breastfed and timing of the samples with respect to the doses was not stated.
    Because there is little published experience with clozapine during breastfeeding, and sedation and adverse hematologic effects have been reported in breastfed infants, other agents are preferred. If breastfeeding is undertaken by a mother who is taking clozapine, close monitoring of the infant for excessive sedation and periodic monitoring of the infant's white blood cell count is advisable.
    Aripirazole
    A women who was 6 months postpartum was taking aripiprazole 15 mg by mouth daily. Milk levels after 11 and 12 days of therapy (times not stated) at that dose were 13 and 14 mcg/L.
    Because there is little published experience with aripiprazole during breastfeeding, other antipsychotic agents are preferred.
    Ziprazidone
    Relevant published information was not found as of the revision date.
    Because there is no published experience with ziprasidone during breastfeeding, other antipsychotic agents are preferred.
    Clonazepam
    A mother taking clonazepam 2 mg twice daily had several milk level measurements on days 2 to 4 postpartum. The highest milk level was 10.7 mcg/L 4 hours after a dose. The authors calculated that an exclusively breastfed infant would receive a maximum of 2.5% of the maternal weight-adjusted dosage of clonazepam.
    Only a small number of cases of breastfeeding with clonazepam have been reported. If clonazepam is required by the mother, it is not a reason to discontinue breastfeeding. Monitor the infant for drowsiness, adequate weight gain, and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of psychotropic drugs. Monitoring of the infant's serum concentration may be indicated if excessive sedation occurs.
    Diazepam
    Diazepam is excreted into breastmilk and it and its active metabolite, nordiazepam, accumulate in the serum of breastfed infants with repeated doses. Because the half-life of diazepam and nordiazepam are long, timing breastfeeding with respect to the dose is of little or no benefit in reducing infant exposure.
    Other agents are preferred, especially while nursing a newborn or preterm infant. After a single dose of diazepam, as for sedation before a procedure, there is usually no need to wait to resume breastfeeding, although with a newborn or preterm infant, a cautious approach would be to wait a period of 6 to 8 hours before resuming nursing.
    Alprazolam
    The authors calculated that an exclusively breastfed infant whose mother was taking alprazolam in the normal dosage range would receive a dose of 0.5 to 5 mcg/kg/day or about 3% of the maternal weight-adjusted dosage.
    Because of reports of effects in infants, including sedation, alprazolam is probably not the best benzodiazepine for repeated use during nursing, especially with a neonate or premature infant. A shorter-acting benzodiazepine without active metabolites is preferred. After a single dose of alprazolam, there is usually no need to wait to resume breastfeeding.
    Lorazepam
    Lorazepam has low levels in breastmilk, a short half-life relative to many other benzodiazepines, and is administered directly to infants.
    Lorazepam would not be expected to cause any adverse effects in breastfed infants with usual maternal dosages. No special precautions are required.
    Trazodone
    Trazodone levels in milk are low
    Limited information indicates that trazodone levels in milk are low and would not be expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months or when doses of 100 mg or less are used at bedtime for sleep.
    Clonidine
    Using the average milk level data from this study, an exclusively breastfed infant would receive an estimated 4.1 to 8.4% of the maternal weight-adjusted dosage.
    Because of the high serum levels found in breastfed infants and the possible negative effects on lactation, other agents may be preferred, especially while nursing a newborn or preterm infant. Clonidine has complex, dose-related actions on both oxytocin and prolactin secretion. The net effect of the drug on nursing mothers has not been well studied. A case of hyperprolactinemia and gynecomastia occurred in a 6-year-old boy taking clonidine for hyperactivity and valproic acid for a seizure disorder. Galactorrhea ceased within 3 weeks of discontinuing clonidine. A case of clonidine-induced postpartum galactorrhea has also been reported.
    Prazosin
    Relevant published information was not found as of the revision date.
    Because no information is available on the use of prazosin during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant.
    Hydroxyzine
    Relevant published information was not found as of the revision date.
    Small occasional doses of hydroxyzine would not be expected to cause any adverse effects in breastfed infants. Larger doses or more prolonged use may cause drowsiness and other effects in the infant or decrease the milk supply, particularly in combination with a sympathomimetic or before lactation is well established. Single bedtime doses after the last feeding of the day may be adequate for many women and will minimize any effects of the drug. The nonsedating antihistamines are preferred alternatives.
    Imipramine
    Milk levels of imipramine and its metabolite are low and have been detected in only small quantities in the serum of breastfed infants.
    Immediate side effects have not been reported and a limited amount of follow-up has found no adverse effects on infant growth and development. Imipramine use during breastfeeding would usually not be expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months. Other agents may be preferred when large doses are required or while nursing a newborn or preterm infant.
    Clomipramine
    Using the average of the above concentrations, a fully breastfed infant would receive about 2.2% of the maternal weight-adjusted dosage of clomipramine in breastmilk.
    Limited evidence indicates that use of clomipramine during breastfeeding is acceptable. For use as an antidepressant, clomipramine may be less desirable than other tricyclic antidepressants that have been studied more thoroughly.
    Nortriptyline
    Because of the low levels of nortriptyline in breastmilk, amounts ingested by the infant are small and usually not been detected in the serum of the infant, although the less active metabolites are often detectable in low levels in infant serum.
    Immediate side effects have not been reported and a limited amount of follow-up has found no adverse effects on infant growth and development. Most authoritative reviewers consider nortriptyline one of the preferred antidepressants during breastfeeding.

    Wednesday, February 10, 2010

    Fantastic Interview with Tias Little

    Tias Little truly inspired me earlier this month when I took an all-day intensive on "Unwinding the Spine." I'm especially interested in his ideas about the habitual strain patterns we collect in our bodies, and how they show up as tightness, bracing, collapsing. Tias is an expert on yoga, structure and integration, and he is the founder of Prajna Yoga in Santa Fe, New Mexico. Check out his comments about how our hormones affect our bodies and habitual patterns - an area of great interest to me. -- SG

    The Emotional Body: An Interview with Tias Little

    by Lori Gaspar
    Tias Little, expert on yoga, Eastern philosophy, bodywork, and anatomy, has become one of the yoga teachers I study with regularly—attending his workshops whenever he is in my hometown of Chicago, as well as his teacher training at his home base in Santa Fe, New Mexico. Over the past few years, Tias has presented intensives in Naples , Florida , at Studio 41, a wonderful yoga studio that I drop into when I am in town visiting my husband’s parents. This year I scheduled my annual winter trip to Naples to coincide with the weekend Tias would be there. I caught up with him at the home of Studio 41’s founder Lisa Anderson, and had the chance to meet his wife, Surya, and their delightful 5-month old son, Eno.
    For the interview, Tias and I ventured onto Lisa’s front porch beneath a floral cascade of lavender-blue trumpet vines. Joining us were two wild ducks, Lisa’s gray and white cat, and an assortment of birds chirping away in the surrounding treetops. Sipping tea and warmed by the sun, I had to admit that interviewing Tias on a January afternoon in south Florida sure beat the last time I saw him–in Chicago during the dreary, overcast days of November.
    My questions were a follow-up to some of the ideas that Tias presented in his training concerning the link between our habitual physical patterns and the emotional body.
    Lori Gaspar: On the yogic path, there are five koshas, or sheaths, that move progressively inward toward the Self. The third sheath is the manamayakosha, or the emotional body. How do we access this layer? What do we do that is any different than accessing the first two layers: the physical body (annamayakosha) and the energetic body (pranamayakosha)?
    Tias Little: Well, I think most students begin by working in the annamayakosha, the physical sheath, and working through the muscular/skeletal system—first, by opening up the connective tissue of the body, and then working progressively more subtle over time. Anna literally means “food,” so it is the food sheath, or the gross sheath, which is not to be neglected. A lot of yoga students end up somewhat fasting themselves and not eating sufficiently, especially yoga teachers, running from class to class.
    LG: You mean not eating enough calories to get them through the day?
    TL: Yes, right. The annamayakosha is so important to maintain. But I would say that the pranamayakosha is this energetic sheath just underneath it, which, I think, includes the emotional body as well. It is convenient to separate out the sheaths for the sake of understanding, but, of course, there is such a connected link between all of the sheaths—they inter-penetrate.
    LG: What are some ways we tend to hold emotions in our bodies and some common armoring patterns that you see as a yoga teacher?
    TL: In the muscular body, it is so common for there to be patterns of holding. In my teaching over the years, I have seen different types of tension—tension due to fatigue or exhaustion or tension that comes from athleticism, or tension that comes from a kind of fear, or different emotional states that get embedded in the tissues.
    I think that the adrenal system is responsible for emotional response. It governs the fight-or-flight response. Really, the entire hormonal system impacts our emotional body. Yoga enables us to have some effect on our endocrine system, and a great goal to have in the practice is to be able to affect our hormonal firings. The adrenal system does govern this instinctual response of fight or flight—and I would add to that, collapse.
    LG: In your anatomy training at Moksha Yoga Center last November, you mentioned this—that the body typically responds to emotional triggers in three ways: fight, flight, and collapse. Can you explain further?
    TL: Collapse is not typically thought to be one of the adrenal responses—a going dead, or deflating or collapsing pattern. Peter Levine, in his book, Waking the Tiger, talks a lot about when animals are captured by their prey, they often play dead and freeze. This response happens in humans, as well, with all kinds of degrees of intensity. So the collapsing pattern can show up, say, as really flaccid tissue, lack of muscular tone, or a really unresponsive muscular connection.
    LG: Like people that can’t activate specific muscles?
    TL: Yes, what Thomas Hanna [author of the book, Somatics] calls “sensory motor amnesia.” It is the result of a kind of freezing, or locking, or collapsing. Collapsing is not the most common adrenal response. The fight-or-flight tendency, which I see a lot of, shows up as bracing—especially in the back body—feet, calves, hamstrings, buttocks, lower back, behind the heart, back of the neck. The back body is a real receptacle for this kind of bracing.
    LG: Why do you think that is? Why the back of the body?
    TL: Well, I guess we have to carry on. We have to stay present. So the back body ends up holding, like a buttress, in order for someone to stay in a situation—so that a fight or flight response can show up as bracing or gripping or really tight hamstrings. From a really young age, people are subject to threats of various kinds—physical, emotional, psychological, and the body tissues respond on an unconscious level. The threat goes right into the cellular structure as freezing or hardening or dehydrating.
    LG: Dehydrating . . . meaning no liquidity, no flow?
    TL: Yes, lack of blood flow, a tightening or hardening, a lack of sensory motor connection—what Thomas Hanna called sensory motor amnesia. I have always loved that expression.
    LG: So fight, flight, and collapse . . . fight would be the bracing, the holding-on kind of a thing, and flight would be . . . ?
    TL: The runners. Nonconfrontational people looking for the first escape possible. It is a type of withdrawal. Compared to the collapsing pattern, which can lead to real flaccid tissue, this running-flight response can lead to a lot of tightness, especially in the legs, hamstrings, and buttocks. So really, it is first chakra issues, survival issues. The adrenals are so connected to our sense of survival and instinct. And I think responses to threats at such an early age get set in our structure. Then we come to yoga at the age of 35 saying, “Oh, this looks good,” and we hit all this muscular skeletal tension. It is not something we readily think may be due to old patterns of holding.
    LG: When do these habitual holding patterns begin?
    TL: Some can begin as early as infancy as part of the startle response, but more often, I think, in grade school. Due to peer pressure and, of course, parental pressure and pressure from coaches . . . there can be a kind of armoring set up in response to a world that is challenging and complex and, at times, threatening. So I think the patterns can get set up really early, whether preverbal or preteen—which makes them even harder to move through in yoga practice. They can become such a part of our structure, and we completely identify with this structure. This is who I am. This is how I feel about myself. So that deep sense of self-identity is shaped by our environment, and I think that the straining patterns will show up in different ways. I mean tightness in the feet can really reflect issues of stability or lack of stability . . . lack of support in the family dynamic. Also, if one was in a family dynamic having to hold everything together, the shoulders, the upper trapezius, the midback end up really tight. So various parts of the body will be affected in differing ways, depending upon the source of stress.
    There has never been anything comprehensive written about this. I think, “Wow, if someone is really tight in their hips—why is that?” Well, it could be their structure; it could be partly to do with their genetic makeup or cultural background; and it could be due to habitual holding patterns due to the fight, flight, or collapse response. And then, if a person is really tight in their shoulders? Yes, it could be due to one’s reaction to the environment, the kind of pressures upon them.
    LG: In your [teacher] training [classes], you mentioned how, at puberty, young girls will slump their shoulders forward to hide their breasts. . . .
    TL: And girls who grow really quickly. You know, usually girls grow faster than boys. And, so, especially if they are tall at an early age, it is very common for teen girls to slouch.
    LG: In the training, you also mentioned that we hold our karma in our legs. What did you mean by that?
    TL: Well, because we are always on our feet. Our legs are so much about our deep sense of self-identity—because they hold us up. These patterns of fight, flight, or collapse . . . they show up a lot in the legs. They show up in the arms, too, because the arms are so much about receiving, nurturance, and being held by the mother. But the legs are so much about holding us up and our foundation. The knees and feet relate to the foundational chakras . . . so karma-wise, I think patterns of holding get set up in the legs, which, of course, is why we do standing poses—triangle pose, flank pose, the warrior sequence—to unlock the potential of the legs. The feet tend to be the receptacles for a lot of strain—ankles and arches, the big toe—suffering, compression, collapsing. And there is that connection of the periphery to the core—that is, the hands and feet are periphery, and they really link back into the psoas and back into the core body.
    LG: How do they link?
    TL: Well, through dog pose, for instance, the hands and the feet, fingers, toes, wrists, and ankles—they help conduct the flow of energy up into the limbs and into the core. It is very common for people to hold tension in their extremities, especially due to fear, like crimping the wrists, scrunching the toes, sweaty palms, sweaty feet. You know, energy is not really flowing in and out of the body. It is getting restricted in the extremities.
    LG: How do we know if an energetic block is caused by an emotional issue, a physical trauma, or an anatomical limitation?
    TL: Oftentimes, they are so enmeshed that it is hard to parse out. Well, this is due to an emotional issue, this is due to trauma, because oftentimes they all sort of go together. You know, if you had a bad fall, it will be compounded by [your] emotional reaction.
    I think through my own experience of many, many years of doing asana and really watching my breath patterns and observing my own rhythmic cycles, I can feel the difference. For me, fatigue tension is very different than, say, anxiety tension, which is different than tension that comes from skiing real hard.
    And I think that emotional tension is harder to get to in the body because we are so good at covering [it up].
    LG: Like masquerading or tiptoeing around it, you know . . . avoiding the issue?
    TL: Yeah…we have to in order to continue on with our peers and our parents and everything else. So we become very skillful at burying, or hiding, tension. And it is a Pandora’s box . . . it is frightening to start to really open that. It is very powerful to do psychotherapy work combined with yoga therapy, that is, to not only have a deep understanding of our emotional holding, but to know where it may reside in our bodies and to know how to work with it in the asanas.
    LG: What types of asanas are more effective for releasing emotional blocks? Or what about the length of time one holds postures—is it better to hold poses longer?
    TL: It depends upon the severity of the emotional blocks. For example, when working with someone who is a victim of child abuse or emotional or sexual abuse, it may be better to do passive, supported poses like bridge pose on the bolster or supta baddha konasana [supine bound-angle pose] . . . this kind of thing. If there is an issue related to a certain chronic, systemic strain pattern, but if it is not at an acute phase, then you could do really dynamic standing poses. Standing poses can be really valuable.
    However, if a student has some real holding in the body—that is, a lot of clenching and bracing, then holding poses too long could end up sort of driving the strain deeper in, as if [the student is] just hanging on for dear life. . . .
    LG: You mean people just start to grip again?
    TL: Yes. And, of course, our nervous systems are so good at doing that anyway—this forming an armor around armor around armor.
    LG: Just creating another pattern for yourself to break through?
    TL: Yeah . . . and, of course, the mentality of so many yoga classes is that the harder we push and the harder the pose is, the more one will advance. So bigger is not always better.
    One last thought. . . . The last kosha is the anandamayakosha, the sheath of bliss. The emotion of joy and deep harmony is ultimately what the practice strives for. That joy, of course, is the sweetest emotion. Yet, along the way, it is worth acknowledging some of the more restrictive emotions before getting to that body of bliss. Acknowledging and, of course, working with them.
    LG: You probably can’t really get the bliss if you are skipping over your issues, because, ultimately, they will hold you back. . . .
    TL: Yes, that’s true.
    Tias Little has practiced yoga since 1985. Today he is one of the foremost yoga teachers in the United States . His training is steeped in the classical yoga tradition, whereas his insightful and contemplative approach offers a contemporary perspective. His teaching reflects his expertise in yoga and anatomy, as well as his training in Iyengar and Ashtanga Vinyasa Yoga, Vipassana, Dzogchen, and Zen Buddhism. He presents yoga and anatomy trainings and intensives nationally and internationally. With a bachelor’s degree in English and a master’s degree in Eastern philosophy, Tias is a master of language—playfully interconnecting Eastern philosophies with our Western ideas, as well as revealing the relationship of the gross body with the subtle body. Tias is a frequent contributor to Yoga Journal and Yoga International magazines and has co-written the book sthiram sukham asanam (which means a position in which one can remain steady, calm, and comfortable) with his wife, Surya Little. Tias and Surya co-direct the studio YogaSource in Santa Fe .
    Lori Gaspar teaches yoga in Chicago . She is an instructor in the Moksha Yoga Center Teacher Training Program, and she apprentices with Iyengar Yoga teacher Gabriel Halpern at the Yoga Circle , Chicago . You may reach her at lorigaspar@comcast.net or 630.702.8908.
    This interview was also printed in the March/April, 2005, issue of YogaChicago.

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