Friday, November 6, 2009

Depression-Obesity Connection


Dr. Annie Sawyer


Medical doctors, healthcare professionals and obesity suffers are aware of the devastating impact of obesity on afflicted individuals has on the modern Western society. This complex medical condition can contribute directly to a number of other life-threatening diseases, including diabetes, cardiovascular disease, hypertension, stroke, Alzheimer disease, gout, kidney failure and even cancer. About one-third of U.S. adults and 16% of children and teens are currently obese, according to the National Centers for Disease Control and Prevention (CDC) and while it’s known that obesity increases risk of heart disease, Type 2 diabetes, stroke and even cancer, what is still not entirely known is what the exact metabolic syndrome cause is (CDC, 2008).
After experiencing modern scientific and technological civilization, it has become clear that existence of life on this planet may be endangered by rapid acute and chronic degeneration of human health, and that allopathic science, including its modern, materialistic approach, have been inadequate to preserve human health and well-being from such a decline. Not only internal treatments or external surgical applications, but also techniques of modern diagnosis such as blood tests and x rays are not only belated, but frequently harmful to human health (Kushi, 2006). Being overweight, alongside diabetes, elevated cholesterol levels, and an increased blood pressure, constitute the foundation of metabolic syndrome modern pandemic. Obesity increases chances of developing all of the co-morbid conditions that constitute the “deadly quartet” of the metabolic syndrome: Type 2 diabetes, high blood pressure, and high cholesterol (Wilborn et al., 2005). The World Health Organization (WHO, 2009) believes that we are on the edge of a global metabolic epidemic, and that by the year 2020 obesity will be the single biggest killer on the planet.
The connection between hormones and obesity, depression-weight gain is not contemporary news anymore. The explanation of the mechanism behind this is that depression, elevated chronic stress and anxiety, can cause significant release of cortisone from the adrenal glands. Cortisone is a hormone that can cause insulin resistance at a cellular level, making the delivery of glucose into the cells difficult if not impossible. This in turn causes vicious circle of a consequent hunger and weight gain. A new study done by a team (Kivimäki et al., 2009),published in BMJ analyzed data from four medical screenings of over 4,300 British civil servants aged 35 to 55, including screenings that assessed mental health and measurement of height and weight. Prospective association between obesity and depression: evidence from the Alameda County Study is published in the International Journal of Obesity and Related Metabolic Disorders (Roberts et al., 2003). As theory and research suggest, obesity and depression may be causally linked. A team of authors (Markowitz, Michael, Friedman, & Arent, 2008) proposed a bidirectional theoretical model identifying all the mechanisms behind the pathway “obesity-depression” and vice versa. Another research has shown that more than 50 percent of Americans increase their food intake when feeling stressed out. Comparatively with past times- people would lose their appetite, subsequently their weight in stressful situation. Nowadays with the increasing stress due to the downturn of the economy, massive lay off, decreasing our lifestyle standards, and mainly fear of the unknown are causing people to put on weight instead to shed pounds.
Cortisol, known in the literature as the “age accelerating “hormone, concomitantly increases its production from the suprarenal glands in times of stress. It promotes the aging process in general through memory loss, decreased cognitive function, interrupted sleep problems (insomnia), nervous system damage, decreased immune function, increased pro-inflammatory signaling factors (eicosanoids and interleukins), body fluid retention, elevated triglycerides, high total cholesterol, low good to bad cholesterol ratios, increased hypoglycemia (higher sugar cravings) due to increased insulin levels, insulin resistance, skin problems: wrinkles, adult acne, psoriasis, seborrhea, alopecia (hair loss) and many others. Data from a community-based study in 867 persons aged 65 years and over showed that depression combined with high levels of 24-hour urinary cortisol may increase probability of the metabolic syndrome by about 20%, and can be used for predicting the syndrome (In Chianti study, 2007). The study finally concluded that people with depression and high levels of urinary cortisol (> 111 µg) had an 84% increased probability of the metabolic syndrome compared to non-depressed people with normal cortisol levels (Vogelzangs et al., 2007).
Björntorp (2001) believes that a hyperactive hypothalamic-pituitary-adrenal (HPA) axis can cause significant fat accumulation- known as the whole mark of the syndrome. The author describes cortisol binding to the glucocorticoid receptors, which are multiple in visceral fat activating the enzyme lipoprotein lipase, and inhibiting lipid mobilization, which leads to rapid accumulation of triglycerides in the visceral area. Results from the Health ABC study are suggesting that the above effects are more pronounced when combined with low levels of sex steroid hormones, which have also been associated with depression (Morsink et al., 2007). A recent trial draws the conclusion that depression is an important co-morbidity with metabolic syndrome in a general population (Dunbar et al., 2008). Ghrelin is another peptide hormone, secreted from the stomach that binds to receptors on somatotrophs and potently stimulates secretion of growth hormone. Studies on ghrelin and its role in metabolic syndrome pathogenesis are still ongoing.
The human body seems well-designed to handle temporary spikes of physical and emotional stress, but how much, in which degree and in what way stress affects human health varies from person to person. Chronic emotional stress can dramatically increase risk of heart attack, stroke, and even cancer, as when people are stressed, their cardiovascular, nervous, hormonal and endocrine systems work in partnership to cope, provoking quick narrowing of vessels, increasing the rate of blood coagulation, causing irregular heartbeats, and building up arterial plaque. As proved in two separate studies, under stress, adrenal hormones induce the release of fat and sugar into the blood to be used for immediate energy supply (Bjorntorp, 2001; Bjorntorp & Rosmond, 2000).
Stress disrupts normal hormonal levels, influencing immune system strength and eating habits (Innes, Vincent & Taylor, 2007). People who are not able to handle stress show high blood sugar and decreased release of insulin from the pancreas (Viner, Mc Grath & Trudinger, 1996). Extreme emotional stress (grief, anger, worry, fear) can cause in individuals with vulnerably low stress resistant levels the so called “broken heart syndrome “(BHS), also known under the term “Stress Cardiomyopathy”. It is a condition in which intense emotional or physical stress can cause rapid and severe heart muscle weakness. This condition can occur following a variety of elevated emotional stressors such as grief (e.g. death of a loved one), fear of being laid off, extreme anger, and even unexpected pleasant surprise. It can also occur following numerous physical stressors to the body such as stroke, seizure, difficulty breathing (such as a flare of asthma or emphysema), or significant bleeding (John Hopkins Medicine). The pattern behind the link between stress and weight gain is not just the tendency to overeat when stressed, but the fact that your body produces cortisol in response to stress, and increased cortisol causes your body to store fat. So, even if you are watching your diet, or exercise daily, stress can cause you to gain weight, passively.
Depression and metabolic syndrome connection is researched by (Dunbar et al., 2008). Clots may easily block an artery already narrowed by plaque, resulting in a heart attack, stroke, aneurysm, or aortic dissection. People who practice meditation and yoga are able to control and manage stress better than those who do not practice. It is noted that people who change their total lifestyle strategy and who use stress management relaxing techniques are able to control metabolic syndrome much better than those who only change their diets. Stress management techniques can improve long-term glycemic control in Type 2 diabetes (Surwit et al., 2002). As explained in the HERS (2002) study, the low circulating level of hormones (HGH and testosterone in particular) promotes an increase in adipose tissue bulk. This leads to free fatty acids release, which are immediately transported to the liver, consequently stimulating the production of Apo-B, containing very low density lipoproteins (VLDL).
Insulin resistance leads to overproduction of triglyceride-rich lipoproteins and there is also a reduced activity of peripheral lipoprotein lipase which in turn supports the accumulation of triglyceride-rich lipoproteins in the circulation. Hlatky et al. (2002) teach that via the action of cholesterol ester transfer protein, triglycerides are transferred from these lipoproteins to high density lipoproteins in exchange for cholesterol esters. The enrichment of the triglyceride-rich remnant particles with cholesterol ester leads to formation of small dense LDL, known as VLDL. Moreover, because of this exchange, the level of high density lipoprotein (HDL) cholesterol falls.
People with a common mental health disorder, such as anxiety or depression, are twice as likely to be obese at the final screening compared with those who had no mental health disorder symptoms. Further, the risk of weight gain and obesity was the greatest for those who had more incidences of a common mental health disorder. Above all as greater the stress, the greater the weight gain is. In this latter case, your weight gain may have nothing to do with the foods you eat or the type and amount of exercise you do, but rather with your emotional health. In fact, the more anxious people get, the more they tend to turn to sugar, fat and salt to boost their mood, albeit temporarily. This explains why boredom, lots of free time or financial stress are three major factors that drive people to overeat.Pathologic and chronic overeating, due to constant overexcitement of the Hypothalamus/ Adrenal axis, aside can cause one to gain weight in and of by itself.
The Study of Women's Health Across the Nation (SWAN, 2003) involved more than 2,000 women from their 40s through menopause, and they questioned them about the unhappy events in their life over the past year. It was found that the more “negative features” the women reported, the more weight they gained. The above process was strictly “peri-or pre-menopausaly” connected. Thus, getting into a positive state of mind and having proper relaxation are two of the most important keys to good health. They can help lower cortisol levels, effectively help you reduce stress and also contribute to weight loss at the same time.
The Best Way to Fight the "Obesity-Depression" Vicious Circle is by:
1. “Self Commitment” – towalk, weight lift, exercise, meditate, do Yoga, Tai chi or Tai bo, or workout on a daily basis for at least 60-90 minutes.
2. “Self-Perseverance”: Establishing the belief that if you will commit you will succeed, especially if you will show strong perseverance.
3. “Self-Control”: Behavioral techniques as learning to read labels, listening to your inner voice, learning to cope with stress, using portion control techniques, learning to forgive and manage anger will teach you the mathematical equation of proper “self control”. One must recognize that he/she is the only responsible for everything they do and the way how they look is their proper business.
References:
Kivimäki, M.,, Lawlor, D. A., Manoux, A. S., Batty, D. G, Ferrie, J. E., Shipley, M. J., et al. (2009). Common mental disorder and obesity: insight from four repeat measures over 19 years: prospective Whitehall II cohort study. BMJ, 339, 3765
Hlatky, A.M., Boothroyd, D., Vittinghoff, E., Sharp, P., & Wooley, A. (2002). Quality of life and depressive symptoms in postmenopausal women after receiving hormone therapy: Results from the heart and estrogen/progestin replacement STUDY (HERS Trial). The Journal of the American Medical Association, 287, 591 -597.
Kushi, L. H. (2006). Epidemiologic research on the obesity epidemic- cocio-environmental perspective. Epidemiology, 17, 131-133.
Roberts, R, E., Deleger, S., Strawbridge, W. J., Kaplan, G. A. (2003). Prospective association between obesity and depression: evidence from the Alameda County Study. International Journal of Obesity,27,514–521.
Markowitz, S.,Michael, A.,Friedman, M. A., & Arent, S. M. (2008). Understanding the Relation Between Morsink, L. F.,
Vogelzangs, N., Nicklas, B. J., Beekman, A. T., Satterfield, S., & Rubin, S. M. (2007). Associations between sex steroid hormone levels and depressive symptoms in elderly men and women: results from the Health ABC Study. Psychoneuroendocrinology, 32, 874-883. Obesity and Depression: Causal Mechanisms and Implications for Treatment. Clinical Psychology, 15, 1-20
Vogelzangs, N., Suthers, K., Ferrucci, L., Simonsick, E. M., Ble, A., & Schrager, M. (2007). Hypercortisolemia depression is associated with the metabolic syndrome in late-life. Psychoneuroendocrinology, 32, 151-519.
Bjorntorp, P. (2001). Do stress reactions cause abdominal obesity and co morbidities? Obesity Review, 2, 73-86
Bjorntorp, P., & Rosmond, R. (2000). The metabolic syndrome--a neuroendocrine disorder? The British Journal of Nutrition, 83, 49-57.
Innes, K. E., Vincent, H. K., & Taylor, A. G. (2007). Chronic Stress and Insulin Resistance-related Indices of Cardiovascular Disease Sisk, part 2: Potential role for Mind-Body Therapies Alternative Therapies in Health and Medicine, 13, 44-51.
Viner. R., Mc Grath, M., & Trudinger, P. (1996). Family stress and metabolic control in diabetes. Archives of Disease in Childhood, 74, 418-421
Surwit, S. R., Van Tilburg, A. L. M., Zucker, N., Mc Caskill, C. C., Parekh, P., Feinglos, N. M., et al. (2002). Stress management improves long-term glycemic control in type 2 diabetes. Diabetes Care, 25, 30-34.
Dunbar, J. A., Reddy, P., Davis-Lameloise, N., Philpot, B., Laatikainen, T., Kilkkinen, A., et al., (2008) Depression: an important comorbidity with metabolic syndrome in a general population. Diabetes Care 31, 2368-73.

If you would like to learn more on the above topic, please call and require a personal consultation: (715) 392-7591; (218) 213-6167; or (218) 213-7087
These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.

Free Testosterone- the main Culrprit Behind Obesity in Menopausal Women


Dr. Annie Sawyer

Visceral fat (VF), also known as an independent predictor of metabolic syndrome, type 2 diabetes, and cardiovascular disease (CVD), is significantly increasing with the transition to menopause. As it is already known, visceral fat (VF), that is surrounding the internal organs around the waistline, is metabolically different type of fat from the subcutaneous one, located beneath the skin. Many researchers have shown the well known fact that visceral fat is a source of inflammation that contributes to premature atherosclerosis and risk of acute coronary syndrome.
At the same time, there is very little known on the exact mechanism of how and which exactly hormonal changes during the period of menopause are closely related to the increase in visceral fat. An amazing new discovery published in Obesity (2009) as a longitudinal, community-based study done at Rush University Medical Center (Chicago, Illinois), discovered the little known and almost unrecognized relationship between high bioavailable testosterone and visceral fat in middle aged women in various menopausal stages of transition. This study, also known as the Study of Women's Health Across the Nation (SWAN) examines the cross-sectional relationship between free (bioavailable) testosterone and computed tomography (CT) assessed visceral fat in women in different age of their menopausal transition. The researchers selected randomly 359 women (47, 2% black) aged between 42-60 years from a complete community census in which a 72% participation rate was achieved. In several multivariate models, bioavailable testosterone was associated with VF independent of age, race, percent total body fat, and other cardiovascular risk factors.
The research proved that the culprit behind the VF accumulation is likely not the advanced age (as it was commonly believed), but the change in hormone balance that occurs during the menopause transition. As a final conclusion of SWAN-the elevated free and bioavailable testosterone in women was proved as stronger predictor than estradiol decline and was interchangeable in its strength of association with sex hormone-binding globulin (SHBG). As bioavailable testosterone was associated with VF even after adjusting the available insulin resistance, this suggests that free testosterone plays an important and maybe a main role in regional fat distribution. Janssen stated: “For many years, it was thought that estrogen protected premenopausal women against cardiovascular disease and that the increased cardiovascular risk after menopause was related only to the loss of estrogen’s protective effect. But our studies suggest that in women, it is the change in the hormonal balance – specifically, the increase in active testosterone – that is predominantly responsible for visceral fat, and for the increased risk of cardiovascular disease”.
Findings from the new SWAM study may have direct implications in explaining the effect of menopause-related testosterone predominance on VF accumulation and subsequent cardiovascular risk (Janssen, I., Powell, L., Kazlauskaite, R., et al., 2009). In Janssen proper words: “Of all the factors we analyzed that could possibly account for the increase in visceral fat during this period in a woman’s lifetime, levels of active testosterone proved to be the one most closely linked with abdominal fat.” The study’s findings are extending proceeding of an earlier research conducted by the same authors on testosterone’s link with what is called the metabolic syndrome during menopause, published in the Archives of Internal Medicine in 2008. That study, examining women six years before and six years after their final menstrual period, found that the rise in metabolic syndrome – a collection of risk factors for heart disease – corresponded with the rise in testosterone activity.
References:
1. Janssen I, Powell LH, Kazlauskaite R, et al. Testosterone and visceral fat in midlife women: The study of Women's Health Across the Nation (SWAN) Fat Patterning Study. Obesity (Silver Spring) 2009;
2. Increase in visceral fat during menopause linked with testosterone. Rush news release. August 20, 2009. Retrieved from: http://www.rush.edu/webapps/MEDREL/servlet/NewsRelease?id=1263
If you would like to learn more on the above topic, please call and require a personal consultation: (715) 392-7591; (218) 213-6167; or (218) 213-7087
These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.

Aging & Hormones


Dr. Annie Sawyer



There are multiple factors and symptoms or syndromes of aging that negatively affect our quality of life, such as increased body fat, loss of lean muscle tissue, lower energy levels due to low mitochondrial supply, decreased sexual function, common depressive symptoms, and weakened immune function or decreased skin turgor (Scuteri et al., 2005 & Gause-Nilson et al., 2006). The increasing prevalence of the metabolic syndrome among U.S. adults is proved to be a major aging factor as well (Ford et al., 2004). Not known as metabolic syndrome at first, this constellation of abnormalities is recognized as placing individuals at dramatically increased risk for cardiovascular disease.
A study published in 2004 in the Journal of the American Medical Association (JAMA) followed more than 1,200 men for 11 years. Some researchers (Lakka et al., 2002), found that men with metabolic syndrome were 160-320% more likely to die from coronary heart disease than those without metabolic syndrome. Besides the increased prevalence of metabolic syndrome and, in general, the worse cardiovascular risk profile and clinical outcomes, people with a lower social position have often to face a worse medical assistance, which can increase the rate of missing diagnoses of cardiovascular risk factors and target organ damage (Perel at al., 2006).
The “neuroendocrine theory of aging” explains the intimate connection between hormones and degenerative diseases as postulated by Dilman Dean (1960). The metabolic pattern of aging is explained as a combination of: a) reduced receptor sensitivity to insulin (insulin resistance); b) obesity; c) altered lipid profile (elevated VLDL, LDL, triglycerides, and total cholesterol; d) hypercortisolemia (elevated cortisol and decreased DHEA); e) decreased androgen output in men; f) increased gonadotropins (LH and FSH); g) decreased immunity and increased incidence of autoimmune antibodies; h) elevated blood pressure, and i) functional hypothyroidism. The entire aging cascade causes hormonal and metabolic shifts that can lead to aging, degenerative diseases and future mortality. Although it may seem strange, abdominal fat could affect the human brain, and be responsible for dementia in advanced age (Earl et al., 2002).
As seen from the HERS (2002) study, the low circulating level of hormones (HGH and testosterone in particular) promotes an increase in adipose tissue bulk. This leads to free fatty acids release, which are immediately transported to the liver, stimulating the production of Apo-B containing very low density lipoproteins (VLDL). Insulin resistance leads to overproduction of triglyceride-rich lipoproteins and there is also a reduced activity of peripheral lipoprotein lipase which in turn supports the accumulation of triglyceride-rich lipoproteins in the circulation. Hlatky and co-authors (2002) explain that via the action of cholesterol ester transfer protein, triglycerides are transferred from these lipoproteins to high density lipoproteins in exchange for cholesterol esters. The enrichment of the triglyceride-rich remnant particles with cholesterol ester leads to formation of small dense LDL. Moreover, because of this exchange, the level of high density lipoprotein cholesterol falls (Hlatky et al., 2002).
According to Giampapa (2004), as people age the body’s ability to metabolize glucose, a factor also referred to as “glucose tolerance” progressively diminishes. In his proper words: “The aging body simply does not respond to the action of insulin, resulting in elevated levels of glucose in the bloodstream. This is referred to as ‘glucose intolerance,’, and its causes as well as main consequences include being overweight, due to continual wear and tear on the pancreas from years of eating and a decrease in the overall amount of insulin and other important hormone production. Another cause is that the human cells are not able to absorb glucose like they did when younger.” As the author states, glucose intolerance renders glucose less available for use by muscle tissue, leading to higher insulin levels (hyperinsulinemia) and higher blood sugar levels (hyperglycemia). The hypothalamus senses this condition and sends signals to the pituitary gland to inhibit secondarily the secretion of human growth hormone (HGH). HGH stimulates the process of fat burning. At the same time, the pancreas is stimulated to release insulin, secondarily diminishing HGH production. Thus the elevation in blood sugar not only creates insulin resistance, obesity, type 2 diabetes and cardiovascular disease, but can also decrease the secretion of HGH (the main hormone of youth) leading to premature aging. In another study it is proved that complementary human growth hormone replacement can improve body composition in healthy older men, without changes in functional ability (Papadakis et al., 1996). In conclusion, HGH production is a complex process and requires the normal function of other organs and hormones to work.
The effect of Human Growth Hormone (HGH) in metabolic syndrome healing can be easily explained: it has important effects on protein, lipid and carbohydrate metabolism. A validated age report and correlation with HGH in centenarian prevalence are discussed in a study by Perls et al. (1999). In some cases a direct effect of growth hormone has been clearly demonstrated, in others IGF-I has been postulated to be the critical mediator, and in some cases it appears that both (direct and indirect) effects are at play (Giampapa et al., 2004 & Papadakis et al., 1996):
a) Protein metabolism: In general, growth hormone stimulates protein anabolism in many tissues. This effect reflects increased amino acid uptake, increased protein synthesis and decreased oxidation of proteins.
b) Fat metabolism: Growth hormone enhances the utilization of fat by stimulating triglyceride breakdown and oxidation in adipocytes.
c) Carbohydrate metabolism: Growth hormone is one of a battery of hormones that serves to maintain blood glucose within a normal range. HGH is often said to have anti-insulin activity, because it suppresses the abilities of insulin to stimulate uptake of glucose in peripheral tissues and enhance glucose synthesis in the liver. Somewhat paradoxically, administration of growth hormone stimulates insulin secretion, leading to hyperinsulinemia.
Another hormone, called Cortisol, concomitantly increases its production from the suprarenal glands. Cortisol is known as the “age accelerating” or the hormone of "aging" as it is also produced in times of elevated stress. Generally it promotes the aging process through memory loss, decreased cognitive function, interrupted sleep problems (insomnia), nervous system damage, decreased immune function, increased pro-inflammatory signaling factors (eicosanoids and interleukins), body fluid retention, elevated triglycerides, high total cholesterol, low HDL, high LDL. and low good to bad cholesterol ratios, increased sugar cravings due to increased insulin levels, insulin resistance, skin problems (wrinkles, adult acne, psoriasis, seborrhea, alopecia (hair loss) and many others. Data from In Chianti study (a community-based study in 867 persons aged 65 and over), showed that depression combined with high levels of 24-hour urinary cortisol increases probability of the metabolic syndrome by about 20%, and can be used for predicting the syndrome (Vogelzangs et al., 2007). The study concluded that people with depression and high levels of urinary cortisol (> 111 µg) had an 84% increased probability of the metabolic syndrome compared to non-depressed persons with normal cortisol levels.
A study by Björntorp (2001) suggests that a hyperactive hypothalamic-pituitary-adrenal HPA) axis can cause significant abdominal fat accumulation- representing the whole mark of the syndrome. The author describes cortisol binding to the glucocorticoids receptors, which are multiple in the visceral fat, activating the enzyme lipoprotein lipase, and inhibiting lipid mobilization, which leads to rapid accumulation of triglycerides in the visceral area. Results from the Health ABC study are suggesting that the above effects are more pronounced when combined with low levels of sex steroid hormones, which have also been associated with depression (Morsink et al. 2007). As a conclusion from the above and multiple other studies, a recent trial draws the conclusion that depression is an important co-morbidity with metabolic syndrome in a general population (Dunbar et al., 2008).
Ghrelin is a peptide hormone secreted from the stomach that binds to receptors on somatotrophs and potently stimulates secretion of growth hormone.
HGH secretion requires the following:
a) Pituitary/hypothalamus stimulation;
b) Pancreatic regulation for optimum production of insulin and blood sugar in the blood, glucagon, leptin and cortisol levels;
c) Correct hepatic (liver) nourishment and functioning for the conversion of HGH to insulin growth factor 1 (IGF-1) according to Rudman’s HGH theory, published in The Journal of American Geriatrics Society(1985).
If you would like to learn more on the above topic, please call and require a personal consultation: (715) 392-7591; (218) 213-6167; or (218) 213-7087
These statements have not been evaluated by the Food and Drug Administration. The material in this newsletter is provided for informational purposes only. Thus our intentions are not to diagnose, cure, mitigate, treat or prevent any disease. If you use the information in this newsletter without the approval of your health professional, the authors of this letter do not assume any responsibility. Copyright @ 2009, Natural Health-Wellness LLC. All rights reserved.