Category Archives: Nutrition

Will Soy Prevent or Reverse Disease?



Will Eating and/or Drinking Soy Prevent or Reverse Dis-ease or So-called Disease?

Cancer is a group of dis-eases characterized by the uncontrolled fermentation and degeneration of body cells. Over 10 million Americans today are cancer survivors, and about 1.4 million Americans are expected to be diagnosed each year.1

“Diet plays an important role in the prevention and treatment of ALL cancerous conditions, and soy protein is one of the leading anti-acid or alkalizing and therefore anti-carcinogenic foods being studied,” stated Dr. Robert O. Young, Director of Research at the pH Miracle Living Center.

SOY FOODS & CANCER

There has been much focus during the past 15 years on the anticancer effects of soy foods.2There are several presumed chemopreventive agents in the soy bean,6 but the isoflavones have received the most attention.3 A particular interest lies in the role of soy foods and isoflavones in reducing the risk of breast and prostate cancer.2

SOY & BREAST CANCER

Data modestly supports the hypothesis that soy food intake may reduce the incidence of breast cancer. A recently published analysis found the relative risk for breast cancer was 95 percent when comparing high- vs. low-soy consumers.5 However, many of the case-control and prospective studies included in this analysis were of poor quality.6

Rodent studies have generally shown that isoflavones, or soy protein, inhibit chemically induced mammary tumors when given prior to tumor initiation7-9, although there are a number of exceptions.10-12 Interestingly, the chemopreventive effects of isoflavones appear to be affected by the background dietary choices.

When the isoflavone genistein was added to the semi-purified diet, chemically induced rodent mammary tumors were not inhibited, but when added to the regular chow diet, tumor development was suppressed by approximately 50 percent.13 This suggests that animal research, which most commonly uses semi-purified diets, may actually underestimate the potential anticarcinogenic effects of soy and other foods.

Soy & Markers of Breast Cancer

In contrast to the animal and epidemiologic data, there is little clinical evidence that soy or isoflavones favorably affect markers of breast cancer risk including breast tissue density,14, 15serum estrogen levels,16, 17 and breast cell proliferation.18 There is limited evidence that estrogen metabolism is favorably affected19 and that menstrual cycle length is increased (which decreases cancer risk).16

Nevertheless, there remains considerable enthusiasm for the possibility that soy food intake contributes to the low breast cancer rate in Japan.

Early Intake of Soy May Reduce Breast Risk

There is both epidemiologic 20-22 and animal 23, 24 data in support of the hypothesis that early soy intake reduces later risk of developing breast cancer. This hypothesis is consistent with mounting evidence that early life influences — parity, lactation, age at menses, birth weight, etc. — impact risk of developing breast cancer.25-36 Studies of migrants suggest that the first 20 years of life have an especially profound impact on risk.36-38 The epidemiologic data suggest just one to two servings of soy foods is protective.

Breaking News – Soy Breast Cancer Study

Soy Breast Cancer Study Holds Promise, But Calls for Further Research

For more than 15 years, soy foods have been actively investigated for their possible role in reducing breast cancer risk. Initial enthusiasm about this hypothesis was based on several observations. These include the low breast cancer rates in Japan, early animal research indicating that soy beans in rodent diets reduced mammary tumor development and evidence suggesting that the isoflavones (phytoestrogens) in soy foods may exert anti-estrogenic effects.

However, establishing a relationship between cancer risk and diet – especially specific foods – is much more difficult than establishing such links in the case of other chronic diseases such as coronary heart disease. This is because there are few well-established non-invasive indicators of cancer risk, and studies are very rarely conducted for long enough to measure actual differences in tumor incidence. Consequently, it is difficult to claim with confidence whether a particular intervention increases or decreases the chances of developing cancer.

Epidemiologic research is a useful mode of investigation for exploring a relationship between diet and cancer. Epidemiology is the study of the patterns, causes, and control of disease in groups of people. There are two primary types of epidemiologic studies, case-control and prospective studies. In case-control studies, scientists compare people with cancer to those without in hopes of identifying characteristics such as lifestyle or diet that are more common to one group than the other. In prospective studies, scientists first evaluate the characteristics of a large group of healthy people, then follow those subjects for many years in hopes of identifying whether certain factors are more common to those who develop cancer than to those who don’t. Generally, prospective studies are considered more credible than case-control studies. It is important to recognize, however, that epidemiologic studies cannot establish cause and effect relationships. Only clinical trials can do that. But epidemiologic studies are often used as a basis for clinical research.

To evaluate the relationship between soy intake and breast cancer risk, Bruce Trock and colleagues from the Johns Hopkins School of Medicine and Georgetown University conducted a meta-analysis of epidemiologic studies. A meta-analysis is the statistical analysis of a large collection of results from individual studies for the purpose of integrating the findings. This particular analysis included 12 case-control studies and 6 prospective studies. The major finding of this analysis was that when all women (Asian and non-Asian, pre- and postmenopausal) were considered, soy intake was associated with a 14% reduction in breast cancer risk. That is, women consuming higher quantities of soy were 14% less likely to develop breast cancer than women who consumed relatively little soy. However, subgroup analysis revealed that soy was more protective against pre- compared to postmenopausal breast cancer, and was protective in studies involving non-Asian women but not Asian women.

The analysis by Trock and colleagues provides modest support for the notion that soy may protect against breast cancer. A 14% reduction is certainly noteworthy, but for several reasons the study results should be interpreted with caution.

First, in many studies, soy intake was not actually quantified. Rather, it was estimated based on the urinary excretion of isoflavones. Because urinary isoflavone excretion varies so much from person to person, it provides only a rough approximation of soy intake. Furthermore, although soy was found to be protective in studies involving non-Asian women, the intake of soy by the women in these studies was quite low. There is some doubt as to whether such low intakes are sufficient to exert biological effects. Since soy foods are still consumed by only a minority of people in non-Asian countries – and are often favored by especially health-conscious individuals – we must consider the possibility that the perceived cancer-protective effects of soy may result from an overall healthy lifestyle, rather than soy consumption per se. Although the researchers employed statistical techniques to try to separate the effects of soy from other factors common to people who eat soy, this is very difficult to do.

While some evidence, including the new analysis by Trock and colleagues, suggests soy foods may reduce breast cancer risk, no conclusions can be made at this time. Nevertheless, because soy foods provide excellent nutrition, they can play an important role in an overall healthy diet, regardless of their possible relationship to breast cancer protection.

SOY & PROSTATE CANCER

The soy bean isoflavone genistein inhibits the growth of both androgen-dependent39-42 and androgen-independent39, 42-45 prostate cancerous cells, depending on the level of soy doses administered. In addition, genistein inhibits the invasive capacity of prostate cancerous cells 42and enhances the ability of radiation to kill these cells.46 However, the concentration of genistein required to exert these effects is higher than the serum isoflavone levels of people who eat soy foods.47-49 Nevertheless, several observations suggest these effects are biologically relevant.39,44-49

Regional Diets Can Impact Prostate Cancer

In Japan, although many men have prostate cancer, few die of this dis-ease. This is because the small tumors often referred to as latent prostate cancer, not uncommon to Japanese men, rarely progress to the more advanced form of this disease.51, 52 Isoflavones in combination with tea extracts were shown to reduce tumor growth in mice more effectively than either agent alone.9

In Asia, and especially in Japan, where prostate cancer mortality rates are low, both soy foods and tea are important components of their diet. There are likely several factors that contribute to this clinical situation in Japanese men and according to the International Prostate Health Council, and isoflavone intake from soy foods may be one.53

There has been limited epidemiologic investigation of the relationship between soy intake and prostate cancer. These studies have produced mixed results but can be said to be consistent with the hypothesis that soy intake reduces prostate cancer risk.

A recent analysis of 10 epidemiologic studies found that soy intake was associated with a one-third reduction in prostate cancer risk.5 However, many of the epidemiologic studies involved a small number of cases54, 55 and/or did not comprehensively evaluate soy food intake. However, a recent comprehensive Japanese case-control study found that when comparing the highest with the lowest soy food intake cases, risk was reduced by nearly 50 percent.56

Soy May Help Treat Existing Prostate Cancer

Data suggests that soy foods may be useful in the treatment of existing prostate cancer, but this remains speculative. A study of 11 trials, three involving healthy subjects57-59 and eight involving prostate cancer patients,60-67 examined the effects of isoflavones on PSA levels. No benefits were noted in healthy subjects, but among the cancer patients one-half noted favorable effects.68Recent intervention data demonstrate that reducing prostate cancer risk is not dependent upon reductions in PSA levels.69

References

  1. American Cancer Society. Cancer Facts and Figures; 2005.
  2. Messina MJ, Persky V, Setchell KD, Barnes S. Soy intake and cancer risk: a review of thein vitro and in vivo data. Nutr Cancer 1994;21:113-131.
  3. Messina M, Barnes S. The role of soy products in reducing risk of cancer. J Natl Cancer Inst 1991;83:541-546.
  4. Sarkar FH, Li Y. Soy isoflavones and cancer prevention. Cancer Invest 2003;21:744-757.
  5. The health claim petition: soy protein and the reduced risk of certain cancers. 2004.(Accessed at http://www.fda.gov/ohrms/dockets/dockets/04q0151/04q0151.htm.)
  6. Yan L, Spitznagel E. A meta-analysis of soy foods and risk of breast cancer in women. Int J Cancer Prevention 2005;1:281-293.
  7. Messina MJ, Loprinzi CL. Soy for breast cancer survivors: a critical review of the literature.J Nutr 2001;131:3095S-3108S.
  8. Magee PJ, Rowland IR. Phyto-oestrogens, their mechanism of action: current evidence for a role in breast and prostate cancer. Br J Nutr 2004;91:513-531.
  9. Zhou JR, Yu L, Mai Z, Blackburn GL. Combined inhibition of estrogen-dependent human breast carcinoma by soy and tea bioactive components in mice. Int J Cancer 2004;108:8-14.
  10. Cohen LA, Zhao Z, Pittman B, Scimeca JA. Effect of intact and isoflavone-depleted soy protein on NMU-induced rat mammary tumorigenesis. Carcinogenesis 2000;21:929-935.
  11. Day JK, Besch-Williford C, McMann TR, Hufford MG, Lubahn DB, MacDonald RS. Dietary genistein increased DMBA-induced mammary adenocarcinoma in wild-type, but not ER alpha KO, mice. Nutr Cancer 2001;39:226-232.
  12. Thomsen AR, Mortensen A, Breinholt VM, Lindecrona RH, Penalvo JL, Sorensen IK. Influence of Prevastein(R), an Isoflavone-Rich Soy Product, on Mammary Gland Development and Tumorigenesis in Tg.NK (MMTV/c-neu) Mice. Nutr Cancer 2005;52:176-188.
  13. Kim H, Hall P, Smith M, Kirk M, Prasain JK, Barnes S, Grubbs C. Chemoprevention by grape seed extract and genistein in carcinogen-induced mammary cancer in rats is diet dependent. J Nutr 2004;134:3445S-3452S.
  14. Atkinson C, Warren RM, Sala E, Dowsett M, Dunning AM, Healey CS, Runswick S, Day NE, Bingham SA. Red-clover-derived isoflavones and mammographic breast density: a double-blind, randomized, placebo-controlled trial. Breast Cancer Res 2004;6:R170-179.
  15. Maskarinec G, Takata Y, Franke AA, Williams AE, Murphy SP. A 2-year soy intervention in premenopausal women does not change mammographic densities. J Nutr2004;134:3089-3094.
  16. Kurzer MS. Hormonal effects of soy in premenopausal women and men. J Nutr2002;132:570S-573S.
  17. Maskarinec G, Franke AA, Williams AE, Hebshi S, Oshiro C, Murphy S, Stanczyk FZ. Effects of a 2-year randomized soy intervention on sex hormone levels in premenopausal women. Cancer Epidemiol Biomarkers Prev 2004;13:1736-1744.
  18. Palomares MR, Hopper L, Goldstein L, Lehman CD, Storer BE, Gralow JR. Effect of soy isoflavones on breast proliferation in postmenopausal breast cancer survivors. Breast Cancer Res Treatment 2004;88 (Suppl 1):4002.
  19. Brown BD, Thomas W, Hutchins A, Martini MC, Slavin JL. Types of dietary fat and soy minimally affect hormones and biomarkers associated with breast cancer risk in premenopausal women. Nutr Cancer 2002;43:22-30.
  20. Shu XO, Jin F, Dai Q, Wen W, Potter JD, Kushi LH, Ruan Z, Gao YT, Zheng W. Soy food Intake during Adolescence and Subsequent Risk of Breast Cancer among Chinese Women.Cancer Epidemiol Biomarkers Prev 2001;10:483-488.
  21. Wu AH, Wan P, Hankin J, Tseng CC, Yu MC, Pike MC. Adolescent and adult soy intake and risk of breast cancer in Asian-Americans. Carcinogenesis 2002;23:1491-1496.
  22. Korde L, Fears T, Wu A, West D, Pike M, Hoover R, Ziegler R. Adolescent and childhood soy intake and breast cancer risk in Asian-American women. Breast Cancer Res Treat2005;88 (suppl 1):S149.
  23. Lamartiniere CA, Zhao YX, Fritz WA. Genistein: mammary cancer chemoprevention, in vivo mechanisms of action, potential for toxicity and bioavailability in rats. J Women’s Cancer 2000;2:11-19.
  24. Hilakivi-Clarke L, Onojafe I, Raygada M, Cho E, Skaar T, Russo I, Clarke R. Prepubertal exposure to zearalenone or genistein reduces mammary tumorigenesis. Br J Cancer1999;80:1682-1688.
  25. Russo J, Lareef H, Tahin Q, Russo IH. Pathways of carcinogenesis and prevention in the human breast. Eur J Cancer 2002;38 Suppl 6:S31-32.
  26. Hamilton AS, Mack TM. Puberty and genetic susceptibility to breast cancer in a case-control study in twins. N Engl J Med 2003;348:2313-2322.
  27. Elias SG, Peeters PH, Grobbee DE, van Noord PA. Breast cancer risk after caloric restriction during the 1944-1945 Dutch famine. J Natl Cancer Inst 2004;96:539-546.
  28. Michels KB, Ekbom A. Caloric restriction and incidence of breast cancer. JAMA2004;291:1226-1230.
  29. Lee SY, Kim MT, Kim SW, Song MS, Yoon SJ. Effect of lifetime lactation on breast cancer risk: a Korean women’s cohort study. Int J Cancer 2003;105:390-393.
  30. Leon DA, Carpenter LM, Broeders MJ, Gunnarskog J, Murphy MF. Breast cancer in Swedish women before age 50: evidence of a dual effect of completed pregnancy. Cancer Causes Control 1995;6:283-291.
  31. Zheng T, Duan L, Liu Y, Zhang B, Wang Y, Chen Y, Zhang Y, Owens PH. Lactation reduces breast cancer risk in Shandong Province, China. Am J Epidemiol 2000;152:1129-1135.
  32. Zheng T, Holford TR, Mayne ST, Owens PH, Zhang Y, Zhang B, Boyle P, Zahm SH. Lactation and breast cancer risk: a case-control study in Connecticut. Br J Cancer2001;84:1472-1476.
  33. Vatten L. Can prenatal factors influence future breast cancer risk? Lancet 1996;348:1531.
  34. Michels KB, Trichopoulos D, Robins JM, Rosner BA, Manson JE, Hunter DJ, Colditz GA, Hankinson SE, Speizer FE, Willett WC. Birthweight as a risk factor for breast cancer.Lancet 1996;348:1542-1546.
  35. Freudenheim JL, Marshall JR, Vena JE, Moysich KB, Muti P, Laughlin R, Nemoto T, Graham S. Lactation history and breast cancer risk. Am J Epidemiol 1997;146:932-938.
  36. Hemminki K, Li X. Cancer risks in second-generation immigrants to Sweden. Int J Cancer 2002;99:229-237.
  37. Shimizu H, Ross RK, Bernstein L, Yatani R, Henderson BE, Mack TM. Cancers of the prostate and breast among Japanese and white immigrants in Los Angeles County. Br J Cancer 1991;63:963-966.
  38. Hemminki K, Li X, Czene K. Cancer risks in first-generation immigrants to Sweden. Int J Cancer 2002;99:218-228.
  39. Peterson G, Barnes S. Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation.Prostate 1993;22:335-345.
  40. Onozawa M, Fukuda K, Ohtani M, Akaza H, Sugimura T, Wakabayashi K. Effects of soy bean isoflavones on cell growth and apoptosis of the human prostatic cancer cell line LNCaP. Jpn J Clin Oncol 1998;28:360-363.
  41. Shen JC, Klein RD, Wei Q, Guan Y, Contois JH, Wang TT, Chang S, Hursting SD. Low-dose genistein induces cyclin-dependent kinase inhibitors and G(1) cell-cycle arrest in human prostate cancer cells. Mol Carcinog 2000;29:92-102.
  42. Santibanez JF, Navarro A, Martinez J. Genistein inhibits proliferation and in vitro invasive potential of human prostatic cancer cell lines. Anticancer Res 1997;17:1199-1204.
  43. Naik HR, Lehr JE, Pienta KJ. An in vitro and in vivo study of antitumor effects of genistein on hormone refractory prostate cancer. Anticancer Res 1994;14:2617-2619.
  44. Kyle E, Neckers L, Takimoto C, Curt G, Bergan R. Genistein-induced apoptosis of prostate cancer cells is preceded by a specific decrease in focal adhesion kinase activity. Mol Pharmacol 1997;51:193-200.
  45. Bhatia N, Agarwal R. Detrimental effect of cancer preventive phytochemicals silymarin, genistein and epigallocatechin 3-gallate on epigenetic events in human prostate carcinoma DU145 cells. Prostate 2001;46:98-107.
  46. Hillman GG, Forman JD, Kucuk O, Yudelev M, Maughan RL, Rubio J, Layer A, Tekyi-Mensah S, Abrams J, Sarkar FH. Genistein potentiates the radiation effect on prostate carcinoma cells. Clin Cancer Res 2001;7:382-390.
  47. Doerge DR, Chang HC, Churchwell MI, Holder CL. Analysis of soy isoflavone conjugation in vitro and in human blood using liquid chromatography-mass spectrometry. Drug Metab Dispos 2000;28:298-307.
  48. Chang HC, Churchwell MI, Delclos KB, Newbold RR, Doerge DR. Mass spectrometric determination of Genistein tissue distribution in diet-exposed Sprague-Dawley rats. J Nutr2000;130:1963-1970.
  49. Dalu A, Haskell JF, Coward L, Lamartiniere CA. Genistein, a component of soy, inhibits the expression of the EGF and ErbB2/Neu receptors in the rat dorsolateral prostate. Prostate1998;37:36-43.
  50. Messina M. Emerging evidence on the role of soy in reducing prostate cancer risk. Nutr Rev 2003;61:117-131.
  51. Yatani R, Kusano I, Shiraishi T, Hayashi T, Stemmermann GN. Latent prostatic carcinoma: pathological and epidemiological aspects. Jpn J Clin Oncol 1989;19:319-326.
  52. Shibata A, Whittemore AS, Imai K, Kolonel LN, Wu AH, John EM, Stamey TA, Paffenbarger RS. Serum levels of prostate-specific antigen among Japanese-American and native Japanese men. J Natl Cancer Inst 1997;89:1716-1720.
  53. Griffiths K. Estrogens and prostatic disease. International Prostate Health Council Study Group. Prostate 2000;45:87-100.
  54. Jacobsen BK, Knutsen SF, Fraser GE. Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States) [see comments]. Cancer Causes Control 1998;9:553-557.
  55. Severson RK, Nomura AM, Grove JS, Stemmermann GN. A prospective study of demographics, diet, and prostate cancer among men of Japanese ancestry in Hawaii.Cancer Res 1989;49:1857-1860.
  56. Lee MM, Gomez SL, Chang JS, Wey M, Wang RT, Hsing AW. Soy and isoflavone consumption in relation to prostate cancer risk in China. Cancer Epidemiol Biomarkers Prev2003;12:665-668.
  57. Urban D, Irwin W, Kirk M, Markiewicz MA, Myers R, Smith M, Weiss H, Grizzle WE, Barnes S. The Effect of Isolated Soy Protein on Plasma Biomarkers in Elderly Men with Elevated Serum Prostate Specific Antigen. J Urol 2001;165:294-300.
  58. Adams KF, Chen C, Newton KM, Potter JD, Lampe JW. Soy isoflavones do not modulate prostate-specific antigen concentrations in older men in a randomized controlled trial.Cancer Epidemiol Biomarkers Prev 2004;13:644-648.
  59. Jenkins DJ, Kendall CW, D’Costa MA, Jackson CJ, Vidgen E, Singer W, Silverman JA, Koumbridis G, Honey J, Rao AV, Fleshner N, Klotz L. Soy consumption and phytoestrogens: effect on serum prostate specific antigen when blood lipids and oxidized low-density lipoprotein are reduced in hyperlipidemic men. J Urol 2003;169:507-511.
  60. Hussain M, Banerjee M, Sarkar FH, Djuric Z, Pollak MN, Doerge D, Fontana J, Chinni S, Davis J, Forman J, Wood DP, Kucuk O. Soy isoflavones in the treatment of prostate cancer. Nutr Cancer 2003;47:111-117.
  61. Fischer L, Mahoney C, Jeffcoat AR, Koch MA, Thomas BE, Valentine JL, Stinchcombe T, Boan J, Crowell JA, Zeisel SH. Clinical characteristics and pharmacokinetics of purified soy isoflavones: multiple-dose administration to men with prostate neoplasia. Nutr Cancer2004;48:160-170.
  62. deVere White RW, Hackman RM, Soares SE, Beckett LA, Li Y, Sun B. Effects of a genistein-rich extract on PSA levels in men with a history of prostate cancer. Urology2004;63:259-263.
  63. Spentzos D, Mantzoros C, Regan MM, Morrissey ME, Duggan S, Flickner-Garvey S, McCormick H, DeWolf W, Balk S, Bubley GJ. Minimal effect of a low-fat/high soy diet for asymptomatic, hormonally naive prostate cancer patients. Clin Cancer Res 2003;9:3282-3287.
  64. Jarred RA, Keikha M, Dowling C, McPherson SJ, Clare AM, Husband AJ, Pedersen JS, Frydenberg M, Risbridger GP. Induction of Apoptosis in Low to Moderate-Grade Human Prostate Carcinoma by Red Clover-derived Dietary Isoflavones. Cancer Epidemiol Biomarkers Prev 2002;11:1689-1696.
  65. Kumar NB, Cantor A, Allen K, Riccardi D, Besterman-Dahan K, Seigne J, Helal M, Salup R, Pow-Sang J. The specific role of isoflavones in reducing prostate cancer risk. Prostate2004;59:141-147.
  66. Dalais FS, Meliala A, Wattanapenpaiboon N, Frydenberg M, Suter DA, Thomson WK, Wahlqvist ML. Effects of a diet rich in phytoestrogens on prostate-specific antigen and sex hormones in men diagnosed with prostate cancer. Urology 2004;64:510-515.
  67. Kranse R, Dagnelie PC, van Kemenade MC, de Jong FH, Blom JH, Tijburg LB, Weststrate JA, Schroder FH. Dietary intervention in prostate cancer patients: PSA response in a randomized double-blind placebo-controlled study. Int J Cancer 2005;113:835-840.
  68. Messina M, Kucuk O, Lampe J. An overview of the health effects of isoflavones with an emphasis on prostate cancer risk and prostate specific antigen levels. JAOAC; (accepted).
  69. Meyer F, Galan P, Douville P, Bairati I, Kegle P, Bertrais S, Estaquio C, Hercberg S. Antioxidant vitamin and mineral supplementation and prostate cancer prevention in the SU.VI.MAX trial. Int J Cancer 2005;116:182-186.

What Causes the Elevation of Cholesterol Levels In the Blood?

After all, what causes the elevation of cholesterol levels in blood?

The following are some suggestions from the medical literature about factors, beyond the famous but wronged and simplistic idea that foods based on saturated fats cause the development of atherosclerosis (1, 22), suggesting that stress, high carbohydrate diets (sugar acid) and smoke may raise total cholesterol and low density lipoproteins levels:

1. Stress increases metabolic acids
a) Anxiety and cholesterol elevation (2, 3, 4, 5, 6, 7, 8, 9, 10, 11)
b) Hostility and cholesterol elevation (12, 13, 14)
c) Extreme physical exertion and cholesterol elevation (15)

2) High carbohydrate diets or the acid sugar and cholesterol elevation (16, 17, 18).

Continue reading What Causes the Elevation of Cholesterol Levels In the Blood?

The Dangers of Drinking Cow’s Milk!

10527262_10152224047863317_4714492967142919885_n-1
Due to the extreme processes that milk goes through and the high amounts of antibiotics, hormones, and genetically-modified substances that cows are continually exposed to, I believe there are real and eminent concerns associated with drinking milk from cows. All cows release toxins through their milk, as milk is a natural exit-portal for substances that the body cannot use.

“Ingredients” Added to Cow’s Milk

A Veritable Hormone Cocktail: including pituitary, steroid, hypothalamic, and thyroid hormones (remember most cows are extremely stressed)

Gastrointestinal Peptides: Nerve and epidermal growth factors, and the growth inhibitors MDGI and MAF rBGH (Recombinant Bovine Growth Hormone): a genetically engineered hormone directly linked to breast, colon and prostrate cancer. This is injected into cows to increase milk production[1]

Pus: National averages show at least 322 million cell-counts of pus per glass! [2] This is well-above the human limit for pus-intake, and has been directly linked to paratuberculosis bacteria, as well as Crohn’s disease. The pus comes from infected udders on the cows known as mastitis.

Blood Cells: The USDA allows up to 1.5 million white blood cells per milliliter of commonly-sold milk. [3] Yes, you are drinking cows blood in the milk and the USDA allows this!

Antibiotics: Currently, cows are in such a state of disease and mistreatment that they are continually being injected with antibiotic medicines, and rubbed down with chemical-laden ointments to deal with their chronic infections. Currently, regulating committees only test for 4 of the 85 drugs in dairy cows. This means that the other 81 drugs in cow’s milk are coming directly into your glasses and bodies.

Estimates show that 38% of milk in the U.S. is “contaminated with sulfa drugs or other antibiotics,” according to a study by the Centre for Science in the Public Interest and published in the Wall Street Journal on December 29, 1989. A study from the FDA data showed that over half of all milk was laden with traces of pharmaceuticals yet nothing has been done to control this.

How Does This Affect the Cows?

Not only are people drinking these toxins, they are also taking in the energetic effects of the life of the cow.

Studies show that many cows are infected with incredibly painful infections such as mastitis. [4] Due to over-milking, artificial hormones, bacteria and medications, cow’s udders can become chronically inflamed, thus altering the color and taste of the milk.

Over time, this bacterial invasion causes harm to the cow’s mammary gland, reeking havoc on the milk being produced. From parasitic worms to cancerous tumors, these diseases are often passed along to the next generation of cows, and more often, into the milk we drink.

Often times the conditions in which cows live, as well as the rigorous milking regimes, cause dairy cattle to live in a permanent state of sympathetic (stress) response, as well as adrenal over-load. When our adrenal glands are overworked for long periods of time, there is a overload of cortisol in the blood. When we drink this milk, we are then exposed to the millions of stress-response cells in the milk of cows. It is no wonder that we are a chronically stressed society!

Avoid Dangers Related to Cow’s Milk

Here are some ways to avoid the dangers associated with cow’s milk:

Replace cow’s milk with healthy natural substitutes: raw almond milk, raw hazel nut milk, raw coconut milk or my favorite – hemp milk.

If you do insist on drinking cow’s milk, make sure to buy only the non-genetically modified, range fed, organic raw versions. Even better, talk to your local organic farmer to make sure the cow’s are treated kindly.

Eliminate cheese because it is concentrated milk and always buy organic versions. Goat’s milk or cheese would be a better choice if you choose to continue to drink animal milk!

– Dr. Edward F. Group III, DC, ND, DACBN, DCBCN, DABFM

References:
The Cancer Prevention Coalition and Food & Water. New study Warns of Breast and Colon Cancer Risks from rBGH Milk. 1996 January 23.
PETA. Cows Used for Their Milk. The Dairy Industry.
Adkinson RW, Gough RH, Graham R, Yilmaz A. Implications of proposed changes in bulk tank somatic cell count regulations. J Dairy Sci. 2001 Feb;84(2):370-4
The Merck Veterinary Manual. Mastitis in Cattle. Merck Sharp & Dohme Corp.

!0 Billion Reasons to NOT EAT MEAT!

Photo

Meat Declared TOO Dangerous/ACIDIC for Human Consumption – Causes Cancer!

Processed Meats Declared too Dangerous/Acidic for Human Consumption

88_frankfurters
The World Cancer Research Fund recently completed a detailed review of 7,000 clinical studies covering links between diet and cancer. Upon conclusion it is evident that processed meats are dangerous for human consumption and consumers should stop buying and eating processed meats.
What are processed meats?Processed meats include bacon, sausage, hot dogs, sandwich meat, packaged ham, pepperoni, salami and nearly all meat found in prepared frozen meals. Processed meats are usually manufactured with a carcinogenic (linked to promote and cause cancer) ingredient known as sodium nitrate. Sodium nitrate is primarily used as a colour fixer by meat companies to make the packaged meats look bright red and fresh. Monosodium glutamate is also added on a regular basis to enhance the savoury flavour.
Sodium Nitrate has been strongly linked to the formation of cancer-causing nitrasamines in the human body, leading to a sharp increase in the risk of cancer for those consuming them. A 2005 Hawaii University study found that eating processed meats increased the risk of pancreatic cancer by 67%, whilst another study found that it increased the risk of colorectal cancer by 50%. These are scary numbers for those consuming processed meats on a regular basis.
Monosodium glutamate (MSG) is a second dangerous chemical found in virtually all processed meat products. MSG is a dangerous excitotoxin linked to neurological disorders such as migraine headaches, Alzheimer’s disease, loss of appetite control, obesity and many other serious health conditions. Manufacturers use MSG to add an addictive savory flavor to dead-tasting processed meat products.
Foods to NEVER eat:
  • Beef jerky
  • Bacon
  • Sausage
  • Pepperoni
  • Hot dogs
  • Sandwich meat
  • Deli slices
  • Ham/Pork
  • Frozen pizzas with meat
  • Canned soups containing meat
  • Frozen meals with meat
  • Ravioli and meat pasta foods
  • Turkey
  • Chicken
  • Beef
…and many more meat products
If its so dangerous to consume why are they allowed to sell it?
Unfortunately now days the food industry interests now dominate the actions of the government regulators. The USDA for example tried to ban sodium nitrate in the late 1970′s but were overridden by the meat industry insisting the chemical was ‘safe’. Today the food and agriculture corporations hold tremendous influence over the food industry and as a result  consumers have little protection from dangerous chemicals intentionally added to foods, medicines and personal care products.
To avoid the dangers of processed meats:
  • Always read ingredient labels
  • Don’t buy anything made with sodium nitrate or MSG
  • Avoid eating red meats served by restaurants, schools, hospitals, hotels or other institutions without asking for details
  • Eat more fresh green organic fruit and vegetables
  • Avoid processed meats always
  • Spread the word and tell others about the dangers of sodium nitrate and MSG and the acids in meat including nitric acid, sulphuric acid, phosphuric acid and uric acid, all poisons to the body.
Antioxidants naturally found in fresh organ fruits and vegetables have been shown to help prevent the formation of cancerous-causing nitrosamines, protecting you from the devastating health effects of animal proteins. The best defence of course is to avoid animal protein/flesh all together!

Why Eating Meat and Cheese Is Making Your Body Dangerously Over-Acid Leading To Sickness and Disease Including Diabetes and/or Cancer!

 

Twenty-Five Scientific Points In Understanding Dr. Young’s “New Biology” and Why Eating Meat and Cheese Is Making Your Body Dangerously Over-Acid Leading To Sickness and Disease Including Diabetes and Cancer!

The following scientific discourse are twenty-five important points to understand concerning the creation of sodium bicarbonate (NaHCO3) and hydrochloric acid (HCL) in the stomach lining, the ingestion of protein, cheese and sugar in any form and how acid/alkaline biochemistry, physiology, and anatomy relate to health, sickness, and disease.

Unfortunately, contemporary medical doctors and scientists as well as alternative health practitioners do not understand how acid/base are created in the body and the onset of latent tissue acidosis in the colloidal connective tissue or the “Schade”. Welcome to the 21st century and Dr. Young’s “New Biology.”

How is acid/base created in the body?

1) The parietal or cover cells of the stomach split the sodium chloride of the blood. The sodium is used to bind with water and carbon dioxide to form the alkaline salt, sodium bicarbonate or NaHCO3. The biochemistry is: H20 + CO2 + NaCl = NaHCO3 + HCL. This is why a call the stomach an alkalizing organ NOT an organ of digestion. The stomach DOES NOT digest the food or liquids you ingest it alkalizes the food and liquid you ingest.

2) For each molecule of sodium bicarbonate (NaHCO3) made, a molecule of hydrochloric acid (HCL) is made and secreted into the so-called digestive system – specifically, the stomach (the gastric pits in the stomach) – to be eliminated. Therefore HCL is an acidic waste product of sodium bicarbonate created by the stomach to alkalize the food and liquids ingested.

3) The chloride ion from the sodium chloride (salt) binds to an acid or proton forming HCL as a waste product of sodium bicarbonate production. HCL has a pH of 1 and is highly toxic to the body and the cause of indigestion, acid reflux, ulcers and cancer.

4) When large amounts of acids, including HCL, enter the stomach from a rich animal protein or dairy product meal, such as meat and cheese, acid is withdrawn from the acid-base household. The organism would die if the resulting alkalosis – or NaHCO3 (base flood) or base surplus – created by the stomach was not taken up by the alkalophile glands that need these quick bases in order to build up their strong sodium bicarbonate secretions. These glands and organs are the stomach, pancreas, Brunner’s glands (between the pylorus and the junctions of the bile and pancreatic ducts), Lieberkuhn’s glands in the liver and its bile with its strong acid binding capabilities which it has to release on the highly acidic meat and cheese to buffer its strong acids of nitric, sulphuric, phosphoric, uric and lactic acids.

5) When a rich animal protein and dairy product meal is ingested, the stomach begins to manufacture and secrete sodium bicarbonate (NHCO3) to alkalize the acids from the food ingested. This causes a loss in the alkaline reserves and an increase in acid and/or HCL found in the gastric pits of the stomach. These acids and/or HCL are taken up by the blood which lowers blood plasma pH. The blood eliminates this increase in gastrointestinal acid by throwing it off into the Pishinger’s spaces.

6) The space enclosed by these finer and finer fibers is called the Pishinger’s space, or the extracellular space that contains the fluids that bath and feed each and every cell while carrying away the acidic waste from those same cells. There is no mention of this organ in American physiology text books. There is mention of the extracellular space but not of any organ that stores acids from metabolism and diet, like the kidney. I call this organ the “pre-kidney” because it stores metabolic and gastrointestinal acids until they can be buffered and eliminated via the skin, urinary tract, or bowels.

7) After a rich animal protein or dairy product meal, the urine pH becomes alkaline. The ingestion of meat and cheese causes a reaction in acidic fashion in the organism by the production of sulfuric, phosporhoric, nitric, uric, lactic, acetylaldehyde and ethanol acids, respectively, but also through the formation and excretion of base in the urine. Therefore eating meat and cheese causes a double loss of bases leading to tissue acidosis and eventual disease, especially inflammation and degenerative diseases.

8) During heavy exercise, if the the resulting lactic acid was not adsorbed by the collagen fibers, the specific acid catchers of the body, the organism would die. The total collection of these fibers is the largest organ of the body called SCHADE, the colloidal connective tissue organ. NO liquid exchange occurs between the blood and the parenchyma cells, or in reverse, unless it passes through this connective tissue organ. This organ connects and holds everything in our bodies in place. This organ is composed of ligaments, tendons, sinew, and the finer fibers that become the scaffolding that holds every single cell in our bodies in place. When acids are stored in this organ, which includes the muscles, inflammation and pain develop. The production of lactic acid is increased with the ingestion of milk, cheese, yogurt, butter and especially ice cream.

That is why I have stated, “acid is pain and pain is acid.” You cannot have one without the other. This is the beginning of latent tissue acidosis leading to irritation, inflammation and degeneration of the cells, tissues and organs.

 

9) The more acidity created from eating meat, cheese, milk or ice cream the more gastrointestinal acids are adsorbed into the the collagen fibers to be neutralized and the less sodium bicarbonate or NaHCO3 that is taken up by the alkalophile glands. The larger the potential difference between the adsorbed acids and the amount of NaHCO3 generated with each meal, the more or less alkaline are the alkalophile glands like the pancreas, gallbladder, pylorus glands, blood, etc. The acid binding power of the connective tissue, the blood, and the alkalophile glands depends on its alkali reserve, which can be determined through blood, urine, and saliva pH, including live and dried blood analysis as taught by Dr. Robert O. Young. The saliva pH is an indication of alkali reserves in the alkalophile glands and the urine pH is an indication of the pH of the fluids that surround the cells or the Pishinger’s space.

10) The iso-structure of the blood maintains the pH of the blood by pushing off gastrointestinal or metabolic acids into the connective tissue or the Pishinger’s space. The blood gives to the urine the same amount of acid that it receives from the tissues and liver so it can retain its iso-form. A base deficiency is always related to the deterioration of the deposit ability of the connective tissues or the Pishinger’s space. As long as the iso-structure of the blood is maintained, the urine – which originates from the blood – remains a faithful reflected image of the acid-base regulation, not of the blood, but of the tissues. The urine therefore is an excretion product of the tissues, not the blood. So when you are testing the pH of the urine, you are testing the pH of the tissues.

11) A latent “acidosis” is the condition that exists when there are not enough bases in the alkalophile glands because they have been used up in the process of neutralizing the acids adsorbed to the collagen fibers. This leads to compensated “acidosis.” This means the blood pH has not changed but other body systems have changed. This can then lead to decompensated “acidosis” where the alkaline reserves of the blood are used up and the pH of the blood is altered. Decompensated “acidosis” can be determined by testing the blood pH, urine pH and the saliva pH. The decrease in the alkaline reserves in the body occurs because of hyper-proteinization, (eating Meat and Cheese!)or too much protein, and hyper-carbonization, or too much sugar. This is why 80 to 90 year old folks are all shrunk up and look like prunes. They have very little or no alkaline reserves in their alkalophile glands. When all the alkaline minerals are gone, so are you and your battery runs down. The charge of your cellular battery can be measured by testing the ORP or the oxidative reduction potential of the blood, urine or saliva using an ORP meter. As you become more acidic this energy potential or ORP increases.

12) If there is not enough base left over after meat and cheese or surgary meal, or enough base to neutralize and clear the acids stored in the connective tissues, a relative base deficiency develops which leads to latent tissue acidosis. When this happens the liver and pancreas are deficient of adequate alkaline juices to ensure proper alkalization of the food in your stomach and small intestine.

13) Digestion or alkalization cannot proceed without enough of these alkaline juices for the liver and pancreas, etc., and so the stomach has to produce more acid in order to make enough base, ad nauseam, and one can develop indigestion, nausea, acid reflux, GERD, ulcers, esophageal cancer and stomach cancer. All of these symptoms are not the result of too much acid or HCL in the stomach. On the contrary, it is the result of too little base in the form of sodium bicarbonate!

14) Therefore the stomach is NOT an organ of digestion as currently taught in ALL biology and medical texts, BUT an organ of contribution or deposit. It’s function is to deposit alkaline juices to the stomach to alkalize the food and to the blood to carry to the alklophile glands!!!!

15) There is a daily rhythm to this acid base ebb and flow of the fluids of the body. The stored acids are mobilized from the connective tissues and Pishinger’s spaces while we sleep.
These acids reach their maximum (base tide) concentration in this fluid, and thereby the urine (around 2 a.m. is the most acidic). The acid content of the urine directly reflects the acid content of the fluid in the Pishinger’s spaces, the extracellular fluid compartments of the body. On the other hand, the Pishinger’s spaces become most alkaline around 2 p.m. (the base flood) as then the most sodium bicarbonate (NaHCO3) is being generated by the cover cells of the stomach to alkalize the food and drink we have ingested.

16) If your urine is not alkaline by 2 p.m. you are definitely in an ACIDIC condition and lacking in alkaline reserves. The pH of the urine should run between 6.8 and 8.4 but ideally 7.2 or greater.

17) After a high protein meal or meat or cheese, the free acids formed such as sulfuric, phosphoric, uric, and nitric acids stick to the collagen fibers to remove them from the blood and protect the delicate pH of the blood at 7.365. The H+ or proton ions from these acids are neutralized by the next base flood, the sodium bicarbonate produced after the meal. The H+ or proton ion combines with the carbonate or HCO3, converts to carbonic acid, H2CO3, which converts to CO2 and H2O. The sulfuric and other acids from proteins are neutralized as follows where the HR represents any acid with the R as its acid radical (SO4, PO4, or NO3) HR + NaHCO3 H2O + NaR (Ca, Mg, K)+ CO2.

18) Medical doctors and savants are not taught in medical school and therefore do not understand or recognize latent tissue acidosis. They understand and recognize compensated acidosis and decompensated acidosis. In compensated acidosis, breathing increases in order to blow off more carbonic acid which decreases PCO2 because of the lowered carbonate or HCO3. When the breathing rate can no longer get any faster and when the kidneys can no longer increase its’ function to keep up with the acid load, then the blood pH starts to change from a pH of 7.365 to 7.3 then to 7.2. At a blood pH of 6.95 the heart relaxes and the client goes into a coma or dies.

19) Metabolism of a normal adult diet results in the generation of 50 to 100 meq of H+ or proton per day, which must be excreted if the urine acid-base balance is to be maintained. A meq is a milliequivalent which is an expression of concentration of substance per liter of solution, calculated by dividing the concentration in milligrams per 100 milliliters by the molecular weight. This process involves two basis steps; 1) the reabsorption of the filtered sodium bicarbonate or NaHCO3 and, 2) excretion of the 50 to 100 meq of H+ or proton produced each day by the formation of titratable acidity and NH4+ or ammonium. Both steps involve H+ or proton secretion from the cells of the kidney into the urine.

20) Sodium bicarbonate (NaHCO3) must be reabsorbed into the blood stream, since the loss of NaHCO3 will increase the net acid load and lower the plasma NaHCO3 concentration. The loss of NaHCO3 in the urine is equivalent to the addition of H+ to the body since both are derived from the dissociation of H2CO3 or carbonic acid.

21) The biochemistry is: CO2 + H2O = H2CO3 = HCO3 + H+. The normal subject must reabsorb 4300 meq of NaHCO3 each day! The secreted H+ or proton ions are generated within the kidney cells from the dissociation of H2O or water. This process also results in the equimolar production OH- or hydroxyl ions. The OH- ions bind to the active zinc-containing site of the intracellular carbonic anhydrase; they then combine with CO2 to form HCO3- ions which are released back into the kidney cells and returned to the systemic circulation. Second, the dietary acid load is excreted by the secretion of H+ or proton ions from the kidney cells into the urine. These H+ or proton ions can do one of two things: the H+ or proton ions can be combined with the urinary buffers, particularly HPO4, in a process called titratable acidity (The biochemistry is: H+ + HPO4 = H2PO4), or the phosphate buffering system or the H+ or proton ions can combine with ammonia (NH3) to form ammonium as follows: NH3 + H+ = NH4.

22) This ammonia is trapped and concentrated in the kidney as ammonium which is then excreted in the urine.

23) In response to acid load, 36% of the H+ or proton goes intracellular in exchange for the release of Na+ (sodium) into the blood stream. 15% of the acid goes intracellular in exchange for K+ (potassium) – common in diabetics. 6% of the H+ or proton or acid goes directly into the cell to be buffered by intracellular processes. 43% is buffered extracellularly as NaHCO3- or sodium bicarbonate combining with H+ or proton to form H2CO3 or carbonic acid which breaks down to CO2 or carbon dioxide to be released by the lungs. 10% of CO2 or carbon dioxide is excreted through the lungs and 90% is used by the body to reabsorb alkaline minerals and make sodium bicarbonate for buffering gastrointestinal and metabolic acids.

The biochemistry is: CO2 + H2O = H2CO3 = HCO3 + H+.24) Of all the ways the body can buffer metabolic and dietary acids, the excretion of protein (the eating of meat and cheese) generated acid residues is the only process that does not add sodium bicarbonate back into blood circulation. This creates a loss of bases which is the forerunner of all sickness and disease. In the long run, the only way to replace these lost bases is by eating more alkaline electron-rich green foods and long-chain polyunsaturated fats. Eating meat and cheese is definitely hazardous to your health. That is why I say, “a cucumber a day keeps the doctor away while eating meat, cheese and even an apple creates more excess acid in the colloidal connective tissues, leading to latent tissue acidosis.

25) With over 30 years of research and testing over 500,000 samples of blood and over 1,000,000 samples of urine and saliva I have come to the conclusion that the Human Body is an acid producing organism by function – yet, it is an alkaline organism by design. Eating animal protein, especially meat and cheese and sugar from any source are deadly acidic choices – unless you interested in becoming sick, tired and fat over time.

Bottom line – the pH Miracle Lifestyle and Diet is a program that focuses on the foundational principal that the body is alkaline by design and yet acidic by function. This make this program the ultimate program for preventing and reversing aging and the onset of sickness and dis-ease. I would say that the pH Miracle Lifestyle and Diet is the diet for a longer healthier life.

Please remember this very important truth, hydrochloric acid is not the cause of digestion but the result of digestion. Start alkalizing today and begin improving the quality and quantity of your life today.

To learn more about the pH Miracle Lifestyle and Diet go to:
http://www.phmiracleliving.com and http://www.articlesofhealth.blogspot.com