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Jun 27, 2016

Wearable Fitness Trackers: They’re Popular, But Are they Accurate?

By Leandro Pucci, Contributing Writer

Wearable fitness trackers are everywhere these days.
Consumers are using these devices to monitor exercise, sleep, and a host of other related health parameters. Health care researchers are also using the devices in the context of clinical studies. The choice of brands, features, and styles of wearable trackers is also expanding rapidly. 
Wearable TrackerBut are these devices reliable? Can we trust the numbers they give us? How accurate are they when it comes to gauging levels of energy expenditure, sleep cycles or other physiological measurements?
There is actually some medical literature on the accuracy of fitness trackers. The consensus seems to be that  consumer-level monitors show a good degree of accuracy for the measurement of steps, duration of activity, and sleep quality, but only moderate accuracy for quantifying total daily energy expenditure or energy output during physical activity (Ferguson T, et al. Int J Behav Nutr Phys Act. 2015 Mar 27;12:42)
Accelerometers vs Heart Rate Monitors
Fitness trackers come in two basic types: accelerometer-based monitors that use predictive equations applied to a user’s acceleration in different directions to estimate energy expenditure; and heart rate devices, that use equations based on age, height, gender, physical-activity level, and resting heart rate to estimate caloric expenditure.
Of the two, the first is more widespread in the consumer market. Popular devices such as the Fitbit, Jawbone, Nike Fuelband, and Polar Loop all fit under the accelerometer category.
A closer look at the different models shows that the mode of exercise being measured can play a huge role in accuracy of these monitors.
Dr. Gregory Welk, Director of the Nutrition and Wellness Research Center at Iowa State University heads a team of researchers that have been studying the accuracy of consumer-level activity monitors compared with the types of monitors used for scientific research.
His team has conducted research for twenty years on various types of accelerometers. Now that the consumer market is being literally flooded with these devices, and multiple manufacturers have released their devices largely without any documented evidence of accuracy, Welk thinks that the research community has a responsibility to help evaluate them, so consumers can make more informed, intelligent choices.
To verify if consumer-centric trackers give accurate readings on calories burned, Dr. Welk’s team recruited 56 men and women aged 18-65, who used the two types of monitors in the context of semi-structured periods of low activity, aerobic exercise, and resistance exercise.
The participants had an average Body Mass Index (BMI) of 24 kg/m2, with body fat compositions averaging 21.2%. They were asked to simultaneously wear five consumer monitors and two research monitors while doing 20 minutes of sedentary activities of their choice, 25 minutes of aerobic exercise, and 25 minutes of resistance training with five-minute rests between the different activity periods.
They tested the Fitbit Flex, Jawbone UP 24, Misfit Shine, Nike FuelBand SE and Polar Loop devices representing the consumer products category. The professional research products were Actigraph GT3X-plus and BodyMedia Core.
The investigators used the Oxycon Mobile, a portable metabolic monitor that measures breathing, heart rate, and fat burned as a reference standard against which all the wearable monitors were compared
The average Energy Expenditure (total calories) measured by the Oxicon Mobile was just under 319 Kcal during the exercise periods. Measurements obtained from the consumer-level activity monitors varied from 275 Kcal to 396 Kcal. The research monitors had the most accurate total calories estimations.
Large Margin of Error
According to the researchers the Jawbone UP 24, Nike Fuelband SE and Fitbit Flex, in general, gave “reasonable accurate” estimations (Bai Y, et al. Med Sci Sport Exerc. 2015; 151-158)
In terms of measuring calorie expenditure during resistance exercise, all the trackers had no less than 25% margin of error in their results—a fairly large margin, according to the Iowa researchers.
For sedentary activity, the results also varied. The Misfit Shine, Nike Fuelband SE, and one research monitor had error rates of less than 20%. For the aerobic part of the test, one consumer tracker and one research tracker had error rates under 20%.
The overall margins of error in all devices were similar to results from earlier evaluations of consumer trackers by the University of Iowa team (Lee JM, et al. Med Sci Sports Exerc. 2014; 46(9): 1840-8).
What it comes down to is that in general, fitness trackers are more accurate or effective for activities such as walking or running on a level ground. When activities move away from this scenario the readings become less accurate.
Indeed, the devices have large margins of error for accurately estimating calories burned. But from the viewpoint of working practically with patients, they can still be great tools for promoting behavior change, so long as one does not focus too much on specific numbers.
The main value of tech tools like this is that they can promote accountability, and provide context for communication between practitioners and their patients. At the end of the day, the value of exercise trackers is that they really can help some people to get some exercise every day and to stay motivated.
Dr. Welk says there is an urgent need is for greater standardization with regard to the outputs and indicators used in wearable tracking devices. Consumer products will always vary in precision to some degree. But the emergence of some type of “Seal of Evidence” or an endorsement by a national regulatory group could go a long way in pushing companies to document, report, and ultimately improve the accuracy of their products.
Leandro M, Pucci is Candidate for a Master of Science degree in Nutrition and Integrative Health from Maryland University of Integrative Health (MUIH). He is currently working towards becoming a Certified Nutrition Specialist. He holds a Personal Trainer Certification by the American College of Sports Medicine, and is working on becoming Certified Strength and Conditioning Specialists by the National Strength and Conditioning Association.Leandro has a special interest in the health concerns related to metabolic syndrome, nutrition and exercise as medicine.

Prostate Assessment Tool

If you score a 7 or higher, it is strongly advised to schedule a prostate examination. Men 55 and over should have a yearly prostate examination as well.
Dr. Wiancek, N.D.
970-926-7606



Jun 24, 2016

EAT RIGHT TO STAY HEALTHY


From Dr.Wiancek's book "The Natural Healing Companion":

      The way to stay healthy is to keep your immune system strong and proper nutrition is the number one way to keep it in good working order. Food is the best medicine of all, provided you eat the right balance of nutrients, proteins, fats, and carbohydrates. Study after study links dietary deficiency to disease.
What constitutes a healthy diet? Specific requirements vary from one person to another, but the following general guidelines will get you off to a good start.
Eat at least five servings of fruits and five servings of vegetables a day, the best way to do this is to eat a salad with five different vegetables in it—the more colorful the salad, the greater the variety of nutrients you are getting. For fruits, eat a fruit salad or several fruit snacks during the day, or sprinkle a variety of fruits on your morning cereal
Eating fruits and vegetables increases the amount of fiber in your diet and helps you get your required daily quota of vitamins and minerals. The benefits include a reduced risk of disease, lower cholesterol and blood pressure, and help in losing weight. More than 200 studies have shown that eating fruits and vegetables helps protect you from various forms of cancer. Other studies indicate similar protection against cardiovascular disease, diabetes, stroke, diverticulosis, and cataracts.
One piece of fruit or 1/2 cup of a vegetable constitutes a single serving. Because cooking destroys valuable nutrients, try to eat fruits and vegetables raw, or steam vegetables lightly before eating. Precooked, frozen, and canned fruits and vegetables are lower in nutrients and higher in sodium, sugar, and preservatives.
Eat five servings of whole grains a day, Avoid white bread, white rice, and ocher heavily processed grains. Even if they are "enriched" or "fortified, they are still lacking essential nutrients. Instead, look for foods made from 100 percent whole grains, without added refined sugars (check the ingredients list on labels. A "whole grain" consists of 1) the bran, which contains fiber, B vitamins, fats, minerals, and protein; 2) the germ, a source of protein, fats, and vitamins A, Bs and E; and 3) the endosperm, which contains complex carbohydrates. Most of the vitamins and minerals in grains are found in their outer layers (the bran and germ) and processing removes both the layers and the nutrients.
A slice of bread or a cup of cooked grain or pasta constitutes one serving. Eat more complex carbohydrates. In the same vein, you should increase your intake of complex carbohydrates and reduce your intake of simple carbohydrates. Complex carbohydrates are found in unprocessed, unrefined vegetables; in dried beans and peas; in whole wheat products; and in grains including rye, barley, quinoa, millet, brown rice, buckwheat, corn, kamut, and oats. (Remember that white breads, white rice, and many pastas and breakfast cereals have been stripped of most of their complex carbohydrates during processing).
Simple carbohydrates are mainly in sugars: white and brown sugar, corn syrup, soft drinks, candy, dried fruit, jellies and jams, canned or frozen fruits, ice cream, and pudding. Simple carbohydrates contribute nothing to your diet except calories, and they can upset the way in which the body metabolizes sugar, leading to high blood sugar and adult-onset diabetes. Instead, use unrefined sweeteners such as 100 percent natural maple syrup, honey, and fruit juices. Avoid artificial sweeteners, as research shows they can aggravate diabetes and may cause cancer.
Eat at Least 25 grams of fiber daily. Dietary fiber comes from plant cell walls, which our bodies cannot digest, there are two types: insoluble (wheat bran is one example) and soluble, which can be found in oat bran, apples, cherries, and dandelion root, among other foods. A combination of both is recommended to help prevent breast cancer and intestinal diseases such as appendicitis, diverticulosis, and colon cancer.
Eat fish, but curb your intake of other animal products. Red meat, including beef and pork, is associated with increased risk of heart attacks, several forms of cancer, prostate disease, high blood pressure, and a host of other diseases. No more than one serving of red meat per week is recommended.
Chicken and turkey are better for you than red meat, but studies show that ocean fish are far preferable and offer protection against heart disease, multiple sclerosis, cancer, high blood pressure, inflammatory conditions including rheumatoid arthritis, and other diseases. Salmon, mackerel, cod, albacore tuna, halibut, anchovies, and herring are particularly good for you. In general, ocean-caught fish are more healthful than farm-raised fish.

Jun 20, 2016

INTENSIVE LIFESTYLE CHANGES MAY AFFECT THE PROGRESSION OF PROSTATE CANCER





Purpose: Men with prostate cancer are often advised to make changes in diet and lifestyle, although the impact of these changes has not been well documented. Therefore, we evaluated the effects of comprehensive lifestyle changes on prostate specific antigen (PSA), treatment trends and serum stimulated LNCaP cell growth in men with early, biopsy proven prostate cancer after 1 year. 

Materials and Methods: Patient recruitment was limited to men who had chosen not to undergo any conventional treatment, which provided an unusual opportunity to have a nonintervention randomized control group to avoid the confounding effects of interventions such as radiation, surgery or androgen deprivation therapy. A total of 93 volunteers with serum PSA 4 to 10 ng/ml and cancer Gleason scores less than 7 were randomly assigned to an experimental group that was asked to make comprehensive lifestyle changes or to a usual care control group.

Results: None of the experimental group patients but 6 control patients underwent conventional treatment due to an increase in PSA and/or progression of disease on magnetic resonance imaging. PSA decreased 4% in the experimental group but increased 6% in the control group (p  0.016). The growth of LNCaP prostate cancer cells (American Type Culture Collection, Manassas, Virginia) was inhibited almost 8 times more by serum from the experimental than from the control group (70% vs 9%, p 0.001). Changes in serum PSA and also in LNCaP cell growth were significantly associated with the degree of change in diet and lifestyle.

Conclusions: Intensive lifestyle changes may affect the progression of early, low grade prostate cancer in men. Further studies and longer term followup are warranted. Although this decision was made for reasons unrelated to this study, the choice to perform watchful waiting was clinically reasonable in these men. This subgroup of patients provided an unusual opportunity to have a nonintervention randomized control group to avoid the confounding effects of interventions such as radiation, surgery or androgen deprivation therapy. MATERIALS AND METHODS Patients in this study had biopsy documented prostate cancer with Gleason less than 7, serum PSA 4 to 10 ng/ml, and stages T1 and T2 disease. They had elected not to undergo conventional treatment. Patients were excluded if they had active prostatitis, had already made comprehensive lifestyle changes, had other life threatening comorbidities or major psychiatric disturbances, or were abusing alcohol, nicotine or other drugs. The University of California-San Francisco Committee on Human Research institutional review board approved this study and all patients provided proper consent. A randomized consent design was chosen to decrease the likelihood that control group patients might make diet and lifestyle changes comparable to those of the experimental group that could dilute between group differences and increase the likelihood of a type 2 error by decreasing the amount of information about the lifestyle intervention available to the control group. 

8 Of the 181 patients who were eligible for the study 93 enrolled, including 44 in the experimental group and 49 in the control group. Reasons for refusal to participate were unwillingness to make or not make comprehensive lifestyle changes and/or refusal to undergo periodic testing. An additional 15 patients with Gleason scores of 7 or greater were excluded because it is a unique prognostic category with biologically distinct and more aggressive neoplasms. Three experimental group patients withdrew soon after beginning the intervention because they said it was too difficult to follow and they refused further testing. No other patients were lost to followup. 

Experimental group patients were prescribed an intensive lifestyle program that included a vegan diet supplemented with soy (1 daily serving of tofu plus 58 gm of a fortified soy protein powdered beverage), fish oil (3 gm daily), vitamin E (400 IU daily), selenium (200 mcg daily) and vitamin C (2 gm daily), moderate aerobic exercise (walking 30 minutes 6 days weekly), stress management techniques (gentle yoga based stretching, breathing, meditation, imagery and progressive relaxation for a total of 60 minutes daily) and participation in a 1-hour support group once weekly to enhance adherence to the intervention. 
The diet was predominantly fruits, vegetables, whole grains (complex carbohydrates), legumes and soy products, low in simple carbohydrates and with approximately 10% of calories from fat. The diet is intensive but palatable and practical. In earlier studies most patients were able to adhere to this diet for at least 5 years.

A registered dietitian was available for nutrition education and counseling. A nurse case manager contacted patients by telephone once weekly for the first 3 months and once monthly thereafter. Control group patients were asked to follow the advice of their physicians regarding lifestyle changes. All therapeutic decisions, including whether to undergo conventional treatment during the study course, were deferred to the personal physician of each patient. Serum PSA was measured twice at baseline and at 1 year. 

Patients were counseled to avoid activities that might affect PSA for 3 days prior to testing, including sexual activity, exercise and digital rectal examination. Serum PSA was measured at Memorial Sloan-Kettering Cancer Center prospectively by a heterogeneous sandwich magnetic separation assay with the Immuno 1™ System. Testosterone was measured by a competitive immunoassay with an Immulite® automated analyzer. 

LNCaP cells were grown in 75 cm2 flasks in RPMI-1640 medium without phenol red, as previously described in detail.12 Cells were collected using 0.25% Trypsin-ethylenediaminetetraacetic acid (Sigma Chemical Co., St. Louis, Missouri) and then experiments were performed in duplicate (5 103 cells per well in 96-well plates). After 24 hours fresh medium composed of 10% fetal bovine serum (FBS) or 10% human serum was replaced and the cells were incubated (37C, 5% CO2) for 48 hours. FBS served as a control for each assay and results are expressed as percent FBS. Cell growth was assessed by MTS Assay (Promega, Madison, Wisconsin). For apoptosis cells were plated at a density of 1 104 cells per well in 96-well culture plates and incubated as described for the growth assay. After 48 hours apoptosis was detected by Cell Death Detection ELISAPLUS (Roche Applied Science, Indianapolis, Indiana). CRP determinations were done in duplicate by ultrasensitive enzyme-linked immunosorbent assay with 1.6 ng/ml sensitivity, and with intra-assay and interassay coefficients of variation of 3.9% and 5.1%, respectively. 

Dietary intake assessing the percent of calories from fat and mg cholesterol was measured with a semiquantitative food frequency questionnaire. Nutrient assessment was calculated elsewhere using United States Department of Agriculture food composition tables and other sources. The frequency and duration of exercise and of stress management techniques were assessed by self-reporting questionnaires. Attendance at group support sessions was recorded. The level of adherence to the recommended lifestyle change was based on a formula validated in previous studies.

A total score of 1 indicated 100% adherence to the program and 0 indicated no adherence. Eligible patients were randomly assigned to the control or the intervention group. Assessment of outcome measures were done while blinded to group assignment. Baseline equivalence of the 2 groups were analyzed using the independent sample t test in the case of continuous variables and the chi-square test of association in the case of categorical variables. 

Between group differences in baseline to 12-month changes in clinical and behavioral outcomes were compared using ANCOVA with baseline values as covariates. Although control patients were not asked to make changes in diet and lifestyle, some did so in varying degrees, that is 18% to 137% (experimental group 58% to 316%). As a secondary analysis, we correlated the degree of lifestyle change with changes in serum PSA, LNCaP cell growth, LNCaP apoptosis, serum testosterone and CRP across the 2 groups regardless of group assignment with baseline values as a covariate. Natural log transformation achieved normality (ln-CRP). 

All reported significance levels are 2-sided and p 0.05 was considered the required value for concluding tAt baseline there were no significant differences between the groups in demographic or clinical measures (table 1). Subject age, PSA and Gleason scores in those who were randomized into the study but refused to participate were not significantly different from values in those who participated. After 1 year adherence to the intervention was 95% in the experimental group and 45% in the control group. There were no adverse events attributable to the lifestyle intervention. Diet, exercise, stress management techniques and group support improved significantly more in the experimental group than in the control group (table 2). 
Six control group patients withdrew before 12 months and underwent conventional treatment, including radical prostatectomy in 3, and androgen deprivation, external beam radiation and brachytherapy in 1 each. Four of these patients underwent conventional treatment due to an increase in PSA during the study and 2 underwent it due to progression of prostate cancer, as assessed by magnetic resonance imaging compared with earlier studies. 

In contrast, no experimental group patients underwent conventional treatment during the study. Changes in serum PSA and LNCaP cell growth from baseline to 12 months were significantly different between the groups, showing more favorable changes in the experimental group. 
Specifically serum PSA decreased an average of 0.25 ng/ml or 4% of the baseline average in the experimental group but it showed an average increase of 0.38 ng/ml or 6% of the baseline average in the control group (F  5.6, p  0.016, fig. 1). Serum from experimental group patients inhibited LNCaP cell growth by 70%, whereas serum from control group patients inhibited growth by only 9% (p 0.001, fig. 2). CRP decreased more in the experimental group (p  0.07). There were no significant differences between the groups in serum testosterone or in apoptosis (table 3). Pearson correlations between changes in serum PSA, LNCaP, apoptosis, testosterone and CRP, and following recommended lifestyle changes in the entire sample indicated that the extent to which participants made changes in diet and lifestyle was significantly related to decreases in PSA (r  0.23, p  0.035, fig. 3) and to LNCaP cell growth (r 0.37, p 0.001, fig. 4).

Key words: prostate, prostatic neoplasms, prostate-specific antigen, life style, nutrition Increasing evidence from epidemiological and laboratory studies suggests that diet and lifestyle may have a role in the development of prostate cancer.1–5 The intake of total and specific vegetables, tomato products (lycopene), vitamin E, selenium, vitamin C and soy products has been inversely associated with prostate cancer risk. In addition, epidemiological evidence and migrant studies indicate that the incidence of clinically significant prostate cancer is much lower in parts of the world where people eat a predominantly low fat, plant based diet.6 There is considerable interest in the role of diet and lifestyle changes as complementary therapy in those with prostate cancer, especially because no consensus exists regarding the relative benefits and risks of conventional treatments in many patients. Many men are making changes in diet and lifestyle in the hope of preventing or slowing the progression of prostate cancer without the benefit of data from randomized, controlled trials to help guide these decisions. We examined if comprehensive changes in diet and lifestyle may affect the progression of prostate cancer, as measured by serial prostate specific antigen (PSA), treatment trends and serum stimulated LNCaP cell growth, in men with early, biopsy proven prostate cancer. To assess possible mechanisms mediating the relationship between changes in lifestyle and these measures we also evaluated changes in testosterone and C-reactive protein (CRP). Patient recruitment was limited to men who had chosen not to undergo any conventional treatment and who had low risk prostate cancer, as defined by baseline serum PSA and Gleason score. Submitted for publication September 9, 2004. Study received University of California-San Francisco Committee on Human Research institutional review board approval. Supported by Department of Defense Uniformed Services University Grant MDA905–99 –1– 0003 via the Henry M. Jackson Foundation Grant 600 – 06971000 –236, The Prostate Cancer Foundation, National Institutes of Health 5P50CA089520 – 02 University of California-San Francisco Prostate Cancer Specialized Program of Research Excellence, Bucksbaum Family Foundation, Ellison Foundation, Fisher Foundation, Gallin Foundation, Highmark, Inc., Koch Foundation, Resnick Foundation, Safeway Foundation, Wachner Foundation, Walton Family Foundation and Wynn Foundation. Foundation, Walton Family Foundation and Wynn Foundation. No supporting agencies were involved in the design or conduct of the study, in the collection, analysis or interpretation of the data, or in the preparation, review or approval of the manuscript. *
Correspondence: Preventive Medicine Research Institute, University of California-San Francisco, 900 Bridgeway, Sausalito, California 94965 (e-mail: d.ornish@pmri.org). † Financial interest and/or other relationship with Random House and Harper-Collins. ‡ Financial interest and/or other relationship with TAP Pharmaceutical Products, AstraZeneca, Pfizer and National Institutes of Health. 0022-5347/05/1743-1065/0 Vol. 174, 1065–1070, September 2005 THE JOURNAL OF UROLOGY® Printed in U.S.A. Copyright © 2005 by AMERICAN UROLOGICAL ASSOCIATION DOI: 10.1097/01.ju.0000169487.49018.73 1065
DEAN ORNISH, GERDI WEIDNER, WILLIAM R. FAIR, RUTH MARLIN, ELAINE B. PETTENGILL, CAREN J. RAISIN, STACEY DUNN-EMKE, LILA CRUTCHFIELD, F. NICHOLAS JACOBS, R. JAMES BARNARD, WILLIAM J. ARONSON, PATRICIA MCCORMAC, DAMIEN J. MCKNIGHT, JORDAN D. FEIN, ANN M. DNISTRIAN, JEANMAIRE WEINSTEIN, TUNG H. NGO, NANCY R. MENDELL AND PETER R. CARROLL‡ From the Departments of Urology (PRC) and Medicine (DO) and Preventive Medicine Research Institute (DO, RM, EBP, CJR, SDE, LC, PM, DJM, JDF, JW, GW), University of California-San Francisco, San Francisco and Departments of Physiological Science (RJB, THN) and Urology (WJA), University of California-Los Angeles, Los Angeles, California, Department of Urologic Oncology, Memorial SloanKettering Cancer Center (WRF and AMD), New York and Department of Statistics, State University of New York at Stony Brook (NRM), Stony Brook, New York, and Windber Research Institute (FNJ), Johnstown, Pennsylvania ABSTRACT 

THE CRANIOSACRAL TREATMENT

THE CRANIOSACRAL SYSTEM
You are probably aware of the many systems that the body is made up of including the respiratory system, digestive system, the cardiovascular system, etc. The body also has a very subtle system unrecognized by science until fairly recently which is known as the craniosacral system. The craniosacral (CS) system consists of the membranes that form the meninges of the brain and spinal cord (down to the sacrum), the bones of the skull to which the membranes attach, other structures related to the meninges, the cerebrospinal fluid, and the structures that produce, contain and reassorb the cerebrospinal fluid. The cornerstone of the CS system is the finding that the bones of the skull are able to move as the cerebrospinal fluid moves through the membranes.

 Cerebrospinal fluid is made in the brain and travels through the CS system. It is then reassorbed into the blood via the venous system.  Production of this fluid (CSF) is halted when a certain pressure level is reached. As the pressure then drops, the CSF production begins again. This ebb and flow of fluid through the meninges of the brain causes there to be a CS rhythm unique to that system.

Since the membranes through which the CSF flows are attached to the skull bones, they move in response to the increase and decrease in pressure. The movement of these bones forms the basis of the CS diagnosis and treatment. The diagnosis of physiological problems is based on the clinician’s ability to assess the rate, amplitude and symmetry of the CS rhythm. The rate of CS rhythm will go up and the amplitude will go down when the meningeal membranes are restricted somewhere. Lack of symmetry helps the clinician assess where a loss of physiological motion is occurring. This could be from injuries, inflammation, scars, etc.

There is a connective tissue sheath that surrounds all body parts. This sheath is known as fascia, and is connected to the CS system and is thus kept in motion. There will be a rocking motion of the sacrum and a widening and narrowing of the head during the CS pulse. A skilled clinician will also be able to feel this rhythm on other parts of the body as the fascia moves with the CS rhythm. The clinician will correct the rhythm with gentle, subtle movements of the skull, the sacrum and other areas where fascia is restricted. The following pages describe this treatment further.


WHAT CS IS USED FOR?
Because the CS system is connected to the rest of the body by its connection to the fascia, restriction can affect many other systems, most notably the nervous system, musculoskeletal system, vascular system, endocrine system, etc. Because of these relationships, CS therapy is used to treat many different conditions. In our clinical setting, we have found them to be helpful for headaches, sinus problems, concussions, anxiety, stress in general , endocrine problems, muscular fatigue or stress, depression, TMJ problems and pain.

WHAT TO EXPECT
Your clinician will have you lie on a table on your back. You may wish to be covered with a sheet or blanket. Even though you will remain fully clothed, the relaxing nature of the treatment may make you feel a little cold. The clinician will then palpate (i.e. examine the CS rhythm by touch) by placing her/his hands on your head then your sacrum. You may be asked to shift your body slightly from time to time, but there is no other way that you need to be involved except to relax and enjoy the treatment. An attempt will be made to keep the room quiet and darkened to enhance the relaxing atmosphere. The clinician will use a very gentle light touch. She/he may move your head from time to time as she/he applies her/his hands to the different bones of the skull, but these movements will be gentle. The clinician will apply very light pressure as she/he attempts to release the restrictions she/he has felt.

The clinician will also use her/his hands on your abdomen and chest to release restrictions of the fascia at these points. She/he may also return to the sacrum from gentle release of restrictions there. More advanced clinicians may feel the CS rhythm in the body fascia by lightly holding your feet, your knees or your shoulders or by very lightly stretching your neck upwards. For facial bones that are more easily accessible through the mouth, the clinician may place a gloved finger into your mouth and very gently move these bones. This technique would be explained in detail to you before it is done. There are no surprises and should be no discomfort. If discomfort is experienced, you should let the clinician know at once so she/he may adjust the pressure or location of her/his hands.
You may feel yourself drifting off into a sort of sleep or you may drift off into a sound sleep. This is normal and you should allow yourself this level of relaxation. The treatment can take anywhere from 45 to 60 minutes depending on how extensive it needs to be. Your clinician can explain to you afterwards what she/he felt and what releases were obtained if you wish to know. You may feel a little “spacey” afterwards. You will probably be very relaxed and may wish to sit in the waiting area before going on to your next activity.

If you have never had a craniosacral treatment it is a great treatment especially for headaches, pain, misalignment, stress, concussions, anxiety, insomnia, muscle pain and depression. To make an appointment please call our office at 970-926-7606.

Jun 13, 2016

Healthy Granola

Ingredients 

  • 4 cups organic oats
  • ½ cup slice almonds
  • ½ cup brown sugar
  • ½ tsp of sea salt
  • 1 tsp of ground cinnamon
  • ¼ cup safflower or peanut oil
  • ¼ cup honey
  • 1 tbsp of vanilla
  • ½ cup of raisins or dried cranberries
  • ½ cup flax seeds

Directions
  • Preheat oven to 300 degrees. In a bowl, mix the oats, almonds, brown sugar, salt and cinnamon. 
  • In a saucepan warm the oil and honey. Stir in vanilla. 
  • Pour liquid over oat mixture, stir.
  • Spread granola in a baking pan. Bake 40 minutes or until lightly brown, stirring every 10 minutes.
  • Let cool completely.
  • Stir in ground flax seeds and raisins/cranberries.
  • Seal granola in air tight container and store at room temperature or freeze for 3 months.
Makes 9 cups (24 servings)
Nutritional facts: 186 calories, 1 g of saturated fat, 3 g of fiber and 4 g of protein.
This recipe is a great way to lower cholesterol, increase fiber intake and get your protein!

Jun 3, 2016

NSAIDs and your health

NSAIDs (non-steroidal anti-inflammatory drugs) include ibuprofen, naproxen, diclofenac and celecoxib. The uses of these over-the-counter drugs range from menstrual cramps to sports injury. Although it is stated on the drug facts label of these OTC drugs, many people fail to recognize that these drugs increase ones risk for stroke and heart attacks. An increase can occur in the first weeks of use. It is alarming that these drugs are FDA approved and still being sold over the counter! Meanwhile, the FDA is strengthening there warnings that NSAIDs "can cause heart attacks and strokes," why not just pull them off the shelves?
Here are some facts pulled straight from the FDA's website:

"Based on our review and the advisory committees’ recommendations, the prescription NSAID labels will be revised to reflect the following information:
  • The risk of heart attack or stroke can occur as early as the first weeks of using an NSAID. The risk may increase with longer use of the NSAID.
  • The risk appears greater at higher doses.
  • It was previously thought that all NSAIDs may have a similar risk. Newer information makes it less clear that the risk for heart attack or stroke is similar for all NSAIDs; however, this newer information is not sufficient for us to determine that the risk of any particular NSAID is definitely higher or lower than that of any other particular NSAID.
  • NSAIDs can increase the risk of heart attack or stroke in patients with or without heart disease or risk factors for heart disease. A large number of studies support this finding, with varying estimates of how much the risk is increased, depending on the drugs and the doses studied.
  • In general, patients with heart disease or risk factors for it have a greater likelihood of heart attack or stroke following NSAID use than patients without these risk factors because they have a higher risk at baseline.
  • Patients treated with NSAIDs following a first heart attack were more likely to die in the first year after the heart attack compared to patients who were not treated with NSAIDs after their first heart attack.
  • There is an increased risk of heart failure with NSAID use.

There are other options when dealing with headaches, cramps, inflammation,etc. Temporarily treating one ailment with the risk of creating another is not medicine.