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http://www.drmcdougall.com/misc/2010nl/nov/parkinsons.htm
Parkinson’s Disease and Other Diet-induced Tremors
James Parkinson originally described a condition of “shaking palsy” in 1817, which subsequently became known as Parkinson’s disease (PD). This condition has become the second most common neurodegenerative disease (after Alzheimer's disease), affecting approximately 1% of the population of the US over 65 years of age. People severely affected with PD characteristically have a tremor seen in their hands and head at rest, stiffness, weakness, slow movements, and postural instability. They take small steps when walking and have speech and swallowing disturbances. With time, disease progression often results in loss of mental function (dementia).
PD results from damage to an area of the brain called the substantia nigra (named because of its dark color). The substantia nigra produces large amounts of the neurotransmitter dopamine. Dopamine deficiency is the hallmark feature in PD. Insufficient production of this neurotransmitter substance negatively affects the nerves and muscles controlling movement and coordination, resulting in the major symptoms characteristic of PD.
Famous people alive today with this disabling condition include actor Michael J. Fox and prize-fighter Mohammad Ali. Mr. Fox’s condition began at age 29 and has lasted for 19 years. He is an exception since most patients do not show signs of PD until after the age of 50.
Mr. Fox has raised $214M for his foundation for PD. Even though he has been reported to have an interest in vegetarian diets, his foundation has focused on stem cell research, which has been, and will likely continue to be, a dead-end path. Instead, as with most other chronic diseases, his focus should be on the highly likely dietary causes of PD. Correcting the cause will at the very least lead to avenues for prevention.
The Western Diet Causes Parkinson’s Disease
The strongest contact we have with our environment is our food. Therefore, observing variations in incidence of diseases across populations should immediately lead researchers to focus their attention on the foods people eat. The incidence of PD is relatively high throughout Europe and North America.1 In contrast, rural Africans, Chinese, and Japanese, whose diets tend to be vegan or quasi-vegan, have substantially lower rates.1 The observation that incidence of PD is similar in African-Americans and in whites, all of whom eat the Western diet, further indicates that environmental factors, not race or genetics, are responsible for PD.2
Specific foods have been targeted. For example, the consumption of milk in midlife was found to be associated with subsequent development of PD.3 Men who consume more than two glasses of milk have twice the incidence of PD as men who do not drink cow’s milk. The American Cancer Society's Cancer Prevention Study II Nutrition Cohort study has found almost twice the incidence of PD in the highest consumers of milk.4
Three Possible Mechanisms for Diet-caused Brain Damage
After accepting the possibility that PD is due, at least in part, to what we eat, then the next logical question is: how is this damage mediated? There are three common ways our diet could kill the dopamine-producing cells of the substantia nigra:
1) Autoimmune Reactions
One probable mechanism begins with the destruction of the blood brain barrier by dietary components, especially the fats. Once this barrier becomes ineffective (permeable) then immune cells (antibodies) produced outside of the nervous system can enter the cerebrospinal fluid and attack the brain’s cells. Dairy proteins are notorious for causing this kind of reaction, known as molecular mimicry. In susceptible people, cow’s milk protein may enter the bloodstream from the intestine.5,6 The body recognizes this as a foreign protein, like a virus or bacteria, and makes antibodies against it. Unfortunately, these antibodies are not specific only to the cow’s milk protein; they find similar proteins in the nervous system.
2) Vascular Disease
The compromise of the blood supply to the brain caused by vascular closures leads to the death of brain tissues. The mechanisms are the same as those that lead to heart attacks and common strokes. One proposed link between PD and atherosclerosis is iron, a nutrient associated with meat consumption.7
3) Environmental Chemicals
Most pesticides work by interfering with the nervous system of insects, so findings of brain damage in people exposed to pesticides and other environmental chemicals should be no surprise.8-10 Convincing examples of this toxicity to the brain are seen in people who work with toxic chemicals; for example, sheep farmers who were exposed to organophosphate pesticides (in the course of dipping sheep to rid them of infestations) performed significantly worse than non-exposed farmers in tests to assess sustained attention and speed of information processing.11
Studies show that exposure to pesticides and insecticides causes Parkinson's disease in humans by damaging the brain’s cells of genetically susceptible people.12-15 An insecticide, dieldrin, is among the most likely culprits.16 Patients with PD have a reduced capacity for detoxification of these toxic compounds. Enzyme systems that metabolize these brain-damaging chemicals are a result of genetic traits. The concentrations of deldrin compounds in the substantia nigra were significantly higher in PD tissues.14
Pesticides Bio-accumulate in Animals
The highest levels of pesticides are found in foods high on the food chain—meaning animal foods. Estimates are that 89% to 99% of the chemical intake into our body is from our food, and most of this is from foods high on the food chain: meat, poultry, eggs, fish, and dairy products.18,19 Fish and other marine life are especially important sources of brain-damaging chemicals like polychlorinated biphenyls (PCBs) and methylmercury (MeHg).20
The scenario looks like this: Low concentrations of environmental chemicals are present in sea vegetables and in seawater. Fish consume these poisons; concentrate them in their own body fat; cows eat fishmeal, and concentrate these noxious wastes even more into their fat; then chickens eat dead cow remnants and the toxins become packed further into their flesh. Finally people get the strongest doses, as they are at the top end of the food chain. Even worse are the consequences for little people—the greatest concentrations of tissues damaging contaminates are delivered to babies nursing from pollutant-overloaded mothers. Understand that this accumulation is lifelong, and therefore, what you do as a child may come to haunt you as an adult in the form of birth defects for your children, cancer, and brain damage. Fortunately, eating a clean diet prevents exposure and helps these chemicals to leave the body.
A Starch-based Diet Helps People with Parkinson's Disease
Prevention of further progression of this form of neurologic deterioration would be expected from removal of the dietary causes.21 However, once the brain tissue is lost it should not be expected to regenerate. Prevention is key.
Dopamine production in the brain is reduced by poor food choices and enhanced when the diet is high in carbohydrates (starches) and low in animal proteins. Carbohydrate increases dopamine production in the brain by allowing easier passage of the dopamine precursor, tyrosine, through the blood-brain barrier into the fluids surrounding the nervous system (the cerebrospinal fluids).22,23 Meats, poultry, eggs, and dairy foods are high in heavy neutral amino acids that block the entry of the dopamine precursor, tyrosine, into the brain.
One case report has suggested a low-animal-food diet is beneficial for people who have already developed PD.24 A 75-year-old man with PD for eight years changed to a quasi-vegan diet for two years. During this time his PD did not appear to have advanced, his dosage of PD medications (levadopa) did not increase, and his quality of life was reported to have improved—an atypical course for this disease.
A healthy diet can also be expected to result in loss of excess body fat, which will allow for improved mobility. People with PD often suffer with constipation, which is relieved by dietary fiber found in plant foods and by removal of dairy proteins, which paralyze the bowels.25 Consider the total picture: Someone with PD needs to be as healthy as possible, and they especially need to avoid the problems, like obesity, type-2 diabetes, vascular insufficiency, arthritis, and bowel dysfunctions, known to be caused by the Western diet. You should not expect the brain tissues that have been lost to grow back; nor lost functions to return. Slowing or stopping progression of the PD is your realistic goal.
A Low-animal-protein, Starch-based Diet Improves the Effectiveness of Medication
Dopamine deficiency is the hallmark feature in PD. Unfortunately, dopamine in the brain cannot be replaced by taking a dopamine pill because this natural chemical does not cross the blood-brain barrier to replenish cerebrospinal fluid. The discovery in 1968 of an isomer of dopamine, levodopa (L-dopa), was a major revolution in the management of PD, which still lasts today. L-dopa readily crosses the blood-brain barrier and then is converted into dopamine once it enters the nervous system. The medication is so specific that a “levodopa challenge test” can confirm a diagnosis of Parkinson's disease. If a patient's symptoms improve, then they are likely to have Parkinson's, ruling out other neurological diseases.
L-dopa and dietary proteins use the same transportation system in the intestine and the blood-brain barrier, competing for access to the blood and cerebrospinal fluid.26 Therefore, a high protein diet, based on meats, dairy products, eggs, and fish results in a competition that reduces the effectiveness of the drug. Levodopa is often sold in combination with another medication, carbidopa, which slows the breakdown of levodopa. Examples include Sinemet, Parcopa, Atamet, and Stalevo. The effectiveness of L-dopa tends to decrease after four to five years of usage.
Patients are often advised to avoid protein (meat, poultry, fish and eggs) during the day and limit these foods to the evening meal in order to improve the effectiveness of their medication. However, eating these animal foods at the evening meal means the patient cannot move all night long— being able to turn over in bed, get up to use the bathroom, or adjust their bedclothes. The incorrect belief that animal foods are the only reliable source of “good” protein leads to this kind of mismanagement of people with PD. The truth is a starch-based diet (low in competing heavy neutral amino acids) provides all necessary proteins and amino acids and should be the diet of people with (and without) PD throughout each day and night.
Essential Tremors from Meat-Eating
Essential tremor (ET), a type of involuntary shaking with no known cause, is among the most prevalent neurological diseases, affecting 4.0% of individuals aged 40 years and older, and 6.3% of individuals 60 years and older. The tremor is most commonly in the hands, but may affect the head, eyelids, vocal cords, and any other muscles. Harmane is a potent, tremor-producing beta-carboline alkaloid found in high concentrations in muscle foods (beef, chicken and pork); cooking of these meats leads to further increases in concentrations.27 Thus the amount of harmane in cooked meat is a function of cooking temperature and time. Pan-frying and grill/barbequing produce the highest concentrations. Elevated harmane in the blood is also due in part to a hereditarily reduced capacity to metabolize it into inactive substances.27 You should not expect the brain tissues that have been lost to grow back; nor lost functions to return. Slowing or stopping progression of the tremors is your realistic goal.
Medications, such as beta-blockers (propranolol), tranquilizers (clonazepam) and antiseizure drugs (primidone), are recommended for treatment, but are of little benefit with significant side effects.
Detoxifying the Body with Starches
Eliminate foods high on the food chain (meats and dairy products) from your diet and replace them with foods low on the food chain (starches, vegetables, and fruits—preferably organically grown) in order to clean your body. The human body has detoxification systems that have evolved over 300 million years to protect animals from the natural toxins found in plants. These same systems will also rid your body of synthetic pollutants. These natural detoxifying compounds are found in plants, and they are also potent inhibitors of chemically induced cancer.28-31 In addition, the energy required for the detoxifying processes is most effectively provided by clean-burning carbohydrates found in plants (meat, fish, poultry and vegetable oils have no carbohydrate and cheese has only miniscule amounts). Not surprisingly, malnutrition from under- and over-nutrition (such as when people eat the American diet) almost invariably leads to a reduced capacity to deactivate these pollutants and therefore increases their toxicity.31
Losing weight on any “diet” releases stored pollutants as the body fat is dissolved.32-34 This is good, especially when the diet you are using to cause the weight loss is low in pollutants and full of detoxifying substances. In no time at all consuming a healthy diet will clean your body of brain-damaging chemicals and restore the tissues in order to prevent PD and systemic damage.
References:
1) Zhang Z. X., Roman G. C. Worldwide occurrence of Parkinson’s disease: an updated review.Neuroepidemiology. 1993; 12: 195-208.
2) Schoenberg B. S., Osuntokun B. O., Adeuja A. O. et al. Comparison of the prevalence of Parkinson’s disease in black populations in the rural United States and in rural Nigeria: door-to-door community studies.Neurology. 1988; 38: 645-646.
3) Park M, Ross GW, Petrovitch H, et al. Consumption of milk and calcium in midlife and the future risk of Parkinson disease. Neurology. 2005;64:1047-1051.
4) Chen H, O'Reilly E, McCullough ML, Rodriguez C, Schwarzschild MA, Calle EE, Thun MJ, Ascherio A. Consumption of dairy products and risk of Parkinson's disease. Am J Epidemiol. 2007 May 1;165(9):998-1006.
5) Winer S. T cells of multiple sclerosis patients target a common environmental peptide that causes encephalitis in mice. J Immunol. 2001 Apr 1;166(7):4751-6.
6) Lauer K. Diet and multiple sclerosis. Neurology. 1997 Aug;49(2 Suppl 2):S55-61.
7) Altamura S, Muckenthaler MU. Iron toxicity in diseases of aging: Alzheimer's disease, Parkinson's disease and atherosclerosis. J Alzheimers Dis. 2009;16(4):879-95.
8) Schantz SL, Widholm JJ, Rice DC. Effects of PCB exposure on neuropsychological function in children.Environ Health Perspect. 2003 Mar;111(3):357-576.
9) Patandin S, Lanting CI, Mulder PG, Boersma ER, Sauer PJ, Weisglas-Kuperus N. Effects of environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42 months of age. J Pediatr. 1999 Jan;134(1):33-41.
10) Paolini M, Sapone A, Gonzalez FJ. Parkinson's disease, pesticides and individual vulnerability. Trends Pharmacol Sci. 2004 Mar;25(3):124-9.
11) Stephens R, Spurgeon A, Calvert IA, Beach J, Levy LS, Berry H, Harrington JM. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Lancet. 1995 May 6;345(8958):1135-9.
12) Elbaz A, Levecque C, Clavel J, Vidal JS, Richard F, Amouyel P, Alperovitch A, Chartier-Harlin MC, Tzourio C. CYP2D6 polymorphism, pesticide exposure, and Parkinson's disease. Ann Neurol. 2004 Mar;55(3):430-4.
13) Menegon A, Board PG, Blackburn AC, Mellick GD, Le Couteur DG. Parkinson's disease, pesticides, and glutathione transferase polymorphisms. Lancet. 1998 Oct 24;352(9137):1344-6.
14) Corrigan FM, Wienburg CL, Shore RF, Daniel SE, Mann D. J Organochlorine insecticides in substantia nigra in Parkinson's disease. Toxicol Environ Health. 2000 Feb 25;59(4):229-34.
15) Petersen MS, Halling J, Bech S, Wermuth L, Weihe P, Nielsen F, Jrgensen PJ, Budtz-Jrgensen E, Grandjean P. Impact of dietary exposure to food contaminants on the risk of Parkinson's disease.Neurotoxicology. 2008 Jul;29(4):584-90.
16) Weisskopf MG, Knekt P, O'Reilly EJ, Lyytinen J, Reunanen A, Laden F, Altshul L, Ascherio A. Persistent organochlorine pesticides in serum and risk of Parkinson disease. Neurology. 2010 Mar 30;74(13):1055-61.
17) Singh M, Khanna VK, Shukla R, Parmar D. Association of polymorphism in cytochrome P450 2D6 and N-acetyltransferase-2 with Parkinson's disease. Dis Markers. 2010;28(2):87-93.
18) Duarte-Davidson R. Polychlorinated biphenyls (PCBs) in the UK population: estimated intake, exposure and body burden. Sci Total Environ. 1994 Jul 11;151(2):131-52.
19) Liem AK. Exposure of populations to dioxins and related compounds. Food Addit Contam. 2000 Apr;17(4):241-59.
20) Petersen MS, Halling J, Bech S, Wermuth L, Weihe P, Nielsen F, Jørgensen PJ, Budtz-Jørgensen E, Grandjean P. Impact of dietary exposure to food contaminants on the risk of Parkinson's disease.Neurotoxicology. 2008 Jul;29(4):584-90.
21) McCarty MF. Does a vegan diet reduce risk for Parkinson's disease? Med Hypotheses. 2001 Sep;57(3):318-23.
22) Fernstrom JD, Wurtman RJ, Hammarstrom-Wiklund B, Rand WM, Munro HN, Davidson CS. Diurnal variations in plasma concentrations of tryptophan, tryosine, and other neutral amino acids: effect of dietary protein intake. Am J Clin Nutr. 1979 Sep;32(9):1912-22.
23) Wurtman RJ, Wurtman JJ, Regan MM, McDermott JM, Tsay RH, Breu JJ. Effects of normal meals rich in carbohydrates or proteins on plasma tryptophan and tyrosine ratios. Am J Clin Nutr. 2003 Jan;77(1):128-32.
24) Schwartz RH. Parkinson's disease and vegan diet. Med Hypotheses. 2004;63(1):178.
25) El-Hodhod MA, Younis NT, Zaitoun YA, Daoud SD. Cow's milk allergy related pediatric constipation: appropriate time of milk tolerance. Pediatr Allergy Immunol. 2010 Mar;21(2 Pt 2):e407-12.
26) Barichella M, Cereda E, Pezzoli G. Major nutritional issues in the management of Parkinson's disease.Mov Disord. 2009 Oct 15;24(13):1881-92.
27) Louis ED, Zheng W. Beta-carboline alkaloids and essential tremor: exploring the environmental determinants of one of the most prevalent neurological diseases. ScientificWorldJournal. 2010 Sep 1;10:1783-94.
28) Hanausek M, Walaszek Z, Slaga TJ. Detoxifying cancer causing agents to prevent cancer. Integr Cancer Ther. 2003 Jun;2(2):139-44.
29) Smith TJ, Yang CS. Effect of organosulfur compounds from garlic and cruciferous vegetables on drug metabolism enzymes. Drug Metabol Drug Interact. 2000;17(1-4):23-49.
30 Smith TJ. Mechanisms of carcinogenesis inhibition by isothiocyanates. Expert Opin Investig Drugs. 2001 Dec;10(12):2167-74.
31) Furst A. Can nutrition affect chemical toxicity? Int J Toxicol. 2002 Sep-Oct;21(5):419-24.
32) Pelletier C, Imbeault P, Tremblay A Energy balance and pollution by organochlorines and polychlorinated biphenyls. Obes Rev. 2003 Feb;4(1):17-24.
33) Imbeault P, Chevrier J, Dewailly E, Ayotte P, Despres JP, Mauriege P, Tremblay A. Increase in plasma pollutant levels in response to weight loss is associated with the reduction of fasting insulin levels in men but not in women. Metabolism. 2002 Apr;51(4):482-6.
34) Hue O, Marcotte J, Berrigan F, Simoneau M, Doré J, Marceau P, Marceau S, Tremblay A, Teasdale N. Increased plasma levels of toxic pollutants accompanying weight loss induced by hypocaloric diet or by bariatric surgery. Obes Surg. 2006 Sep;16(9):1145-54.
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Milk consumption tied to Parkinson's disease
-Drinking a glass or two of milk a day may raise the risk of Parkinson'sdisease in men, research suggests.
-The relationship between Parkinson's and milk consumption has been suspected for decades1 and was first reported by researchers a few
This is probably it:
Dairy food linked with Parkinson's disease in men
Amy Norton
Fri, Apr 20, 2007
Reuters
NEW YORK (Reuters Health) - A new study has confirmed a relationship between consuming large amounts of dairy products and an increase in the rate of Parkinson's disease in men, but the reason for this relationship remains a puzzle.
Researchers found that among more than 130,000 U.S. adults followed for 9 years, those who ate the largest amount of dairy foods had an increased risk of developing Parkinson's disease, a disorder in which movement-regulating cells in the brain die or become impaired.
There was a clear pattern seen among men, whose Parkinson's risk increased in tandem with consumption of diary, particularly milk. The results were more ambiguous among women, however.
The findings, which appear in the American Journal of Epidemiology, echo those of earlier studies that found a link between dairy consumption and Parkinson's in men, but not women.
For now, it's not clear what effect, if any, dairy foods might have on women's risk of the disease. Nor is it known why there is a relationship seen in men, lead study author Dr. Honglei Chen, a researcher at the National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, told Reuters Health.
Larger studies are needed to find out which dairy products might be responsible, and why, according to Chen.
The findings are based on detailed dietary and lifestyle information collected from 57,689 men and 73,175 women who took part in a cancer prevention study. Over 9 years, 250 men and 138 women were diagnosed with Parkinson's disease.
Men with the highest levels of dairy consumption were 60 percent more likely to develop the disease than those who consumed the least amounts of dairy, the study found. Men in the highest-intake group consumed an average of 815 grams of dairy per day, which is roughly equivalent to three to four glasses of milk; those in the lowest-intake group consumed 78 grams of dairy per day, on average.
Milk, rather than dairy products like yogurt and cheese, explained most of the association, according to Chen's team.
This study and previous ones indicate that calcium, vitamin D and fat are not responsible for the link between dairy foods and Parkinson's disease. One theory is that pesticides or other nerve-damaging toxins present in milk could contribute to Parkinson's disease over time. However, dairy foods would likely be only a small part of most people's exposure to these chemicals, according to Chen.
Furthermore, pesticide residues may also be present in other foods, but no other foods were related to Parkinson's disease risk in this study, the researcher noted.
For now, Chen said there is no reason to shun dairy because of the potential relationship to Parkinson's disease. "Given some of the potential health benefits of dairy foods, people can still enjoy their moderate amounts."
However, the researcher added, since the dairy-Parkinson's link has now been seen consistently in different studies, further research is needed to understand why.
SOURCE: American Journal of Epidemiology, May 1, 2007.
REUTERS http://www.nbcnews.com/id/18203093/
http://bacteriality.com/2009/04/04/milk/
In a recent prospective study appearing in Neurology, researchers at various scientific institutions including many in Korea set out to examine the relation between milk and calcium intake in midlife and the risk of Parkinson’s disease. The team analyzed data based on records of dietary intake observed from 1965 to 1968 in 7,504 men enrolled in a cohort called the Honolulu Heart Program. The men ranged from 45 to 68 years of age.Parkinson’s disease (PD) is a degenerative condition affecting movement and balance in more than one million Americans each year: its prevalence is expected to rise in aging populations.
The men were followed for three decades. At that point, 128 men had developed Parkinson’s. But… cue drum roll… the risk of Parkinson’s disease increased as the amount of milk consumed each day rose. Heavy milk drinkers, who drank more than 16 oz a day, were 2.3 times more likely to develop Parkinson’s disease than those men who didn’t drink any milk. Milk was related to PD whether it was whole or skim.
One may ask, “Why?” The beautiful person with the milk mustache in the latest magazine add told me milk was good for me!
Perhaps it’s the calcium? Nope. The team, under Dr. Park, used careful statistical analysis to rule out the possibility that calcium could have caused the increased disease incidence. “In addition, calcium intake from non-dietary sources was not related to PD, further suggesting that a role for calcium in altering PD risk is absent,” states the paper, which was published in the March issue of theJournal of Neurology.
Total fat and protein also had no relation with the risk of PD. Park and team suggest that neurotoxins such as organochlorine, tetrahydroisoquinoline, and heptachlor may be to blame, but even they would concede that this explanation is speculative at best. In fact, according to the study’s authors, “Unfortunately, there are no clear explanations for the relation between milk intake and the risk of PD.”
What the researchers fail to even consider is that since the 1930′s, milk suppliers have been fortifying milk with vitamin D. According to, A. W. Norman in the book, Vitamin D: The calcium homeostatic steroid hormone, “There developed in the 1940′s, and continues to the present, a large business of industrial production of vitamin D3 used for the supplementation of foods for human consumption: milk (both homogenized and evaporated), some margarine and breads. Since the 1960′s vitamin D3 has been used also for the supplementation of farm animal and poultry food. In 1973 in the United States some 290 trillion (290 x 1012) International Units of vitamin D3 was manufactured and sold for over 3 million dollars. This vitamin D3 is the equivalent of approximately 8 tons.”
This strongly suggests that the men in the Honolulu heart study were drinking vitamin D fortified milk. With this in mind, the powerful secosteroid incorrectly labelled “vitamin” D seems like an extremely logical culprit for the rise in PD amongst subjects drinking higher amounts of milk. As described in this recent paper, vitamin D’s steroidal properties allow it slow the innate immune response. While this allows for palliation and symptom reduction in the short-term, it causes chronic bacteria that very likely contribute to the progression of PD to proliferate more easily.
When writing previously about vitamin D, I’ve argued that, “One of the abiding weaknesses of studies on vitamin D is that researchers do not follow subjects consuming the secosteroid for a sufficient period of time. Instead they track subjects over the course of weeks, months, or one or two years, during the period of time when study participants are usually feeling the palliative effects of the secosteroid. Researchers will rarely, if ever, track subjects over the course of decades, the length of time needed to begin to note the negative changes that chronic bacteria cause later in life.”
So hooray for the authors of the Honolulu Heart Study who spent the time and money to monitor subjects for 30 years after their dietary intake was reported. Clearly, when it comes to vitamin D, patience is needed for the negative impact of consuming the secosteroid to be noted.
Another clue that vitamin D likely caused the increase in PD risk among men drinking more milk in the Honolulu study was that consumption of cheese and ice-cream did not affect PD risk. The explanation? Although these products are made from milk, they are generally made from milk before it has been fortified with vitamin D.
That Park and team did not even consider the vitamin D in milk as a possible cause for the increase PD among men consuming more of the substance speaks to the incredible strength of the current consensus that fails to recognize the immunosuppresive properties of vitamin D. This is bound to change, but in the meantime, vitamin D fortified milk should at least come with the message, “Immunosuppressive steroid included at no extra charge!!”
- Filed under: medical research, News Flash, vitamin d
44 Responses for "Milk consumption tied to Parkinson’s disease"
William B. Grant April 5th, 2009 at 10:12 am 1
It is incorrect to suggest that vitamin D is the component of milk that gave rise to Parkinson’s disease. Uric acid is protective against PD. Milk protein reduces serum uric acid. That is the link.
Uric acid in Parkinson’s disease. Schlesinger I, Schlesinger N. Mov Disord. 2008 Sep 15;23(12):1653-7.
Diet, urate, and Parkinson’s disease risk in men. Gao X, Chen H, Choi HK, Curhan G, Schwarzschild MA, Ascherio A. Am J Epidemiol. 2008 Apr 1;167(7):831-8.
Amy Proal April 5th, 2009 at 2:15 pm 2
Hi Dr. Grant,
As someone who advocates high levels of vitamin D supplementation I understand your interest in my article.
Thank you for your input on the subject, but after reading the first study you posted on uric acid and PD I am very confused. You state that increased uric acid production due to milk consumption would accelerate the development of Parkinson’s.
However the study you’ve posted states the opposite – that high levels of uric acid are actually protective against PD. The researchers contend that PD may result in part from oxidative stress, and that because it is an antioxidant, uric acid may reduce such stress and subsequently PD risk.
Right in the abstract the researchers state, “High levels of SU [serum urate, the salt derived from uric acid] may have a neuroprotective effect. High SU levels reduced the risk of developing PD and correlated with slower PD progression.”
The authors go on to reference the Honolulu Heart study directly, saying that of the men in the study, “Individuals who at baseline had SU levels above the median value had a 40% reductionin in PD risk.”
These data directly conflicts with your contention that milk protein, which according to you reduces uric acid, would exacerbate PD.
The authors of the Neurology study on which I originally wrote this piece presented a number of possible reasons why milk may exacerbate PD, but did not mention milk protein’s effect on uric acid. The study you mentioned offers a compelling reason for that omission.
Best,
Amy
Hi,
Let me try again.
Milk consumption is risk factor for Parkinson’s disease as you correctly noted; see, also, Chen et al. [2007].
Uric acid reduces the risk of Parkinson’s disease, as you also noted. See, also, Kutzing and Firestein [2008]. The study I mentioned [Schlesinger and Schlesinger, 2008] had this sentence: “Milk and meat consumption as well as exercise modify the risk of developing PD possibly through their influence on SU levels.” You may have inferred that milk increased serum uric acid, but it is different from meat, it reduces serum uric acid [Schlesinger, 2005].
Peroxynitrite is a risk factor for Parkinson’s disease [Pacher et al., 2007; Kutzing and Firestein, 2008].
Uric acid reduces concentrations of peroxynitrite [Kutzing and Firestein, 2008].
Those with Parkinson’s disease were found to have lower levels of serum 25-hydroxyvitamin D [Evatt et al., 2007].
Q.E.D.
References
Consumption of dairy products and risk of Parkinson’s disease. Chen H, O’Reilly E, McCullough ML, Rodriguez C, Schwarzschild MA, Calle EE, Thun MJ, Ascherio A. Am J Epidemiol. 2007 May 1;165(9):998-1006.
Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. Evatt ML, Delong MR, Khazai N, Rosen A, Triche S, Tangpricha V. Arch Neurol. 2008 Oct;65(10):1348-52.
Altered uric acid levels and disease states. Kutzing MK, Firestein BL. J Pharmacol Exp Ther. 2008 Jan;324(1):1-7.
Pacher P, Beckman JS, and Liaudet L (2007) Nitric oxide and peroxynitrite in health and disease. Physiol Rev 87: 315–424.
Dietary factors and hyperuricaemia. Schlesinger N. Curr Pharm Des. 2005;11(32):4133-8.
Uric acid in Parkinson’s disease. Schlesinger I, Schlesinger N. Mov Disord. 2008 Sep 15;23(12):1653-7.
H Dr. Grant,
Sorry, I misinterpreted your interpretation.
Well then, maybe milk could also cause Parkinson’s by reducing serum uric acid.
However I still believe the vitamin D hypothesis is valid. Hopefully future research will make the issue more clear.
In the Evatt study you cite in which patients with Parkinson’s disease were found to have lower levels of 25-D, have you considered that the low 25-D in such patients could be the result rather than the cause of the disease process?
Take a look at the following paper:
http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf
Best,
Amy
Ron April 6th, 2009 at 9:13 am 5
Hello Amy,
I would like to ask what is the explanation of the MP science about the maps at sunarc.org showing so clearly much higher cancer and MS rates in northern states than in southern states. Is there any explanation other than lack of Vit. D from the Sun? Thank you.
Paul Albert April 6th, 2009 at 11:36 am 6
Hi Ron,
My comment here addresses how observational studies are flawed.
If you are concerned about cancer, you should know that patients on the Marshall Protocol avoid consumption of vitamin D, and, when necessary, exposure to light. The Marshall Protocol cohort has 1,000+ patients, many of whom have been doing the MP for years. This is an extremely high risk population – multiple co-morbidities are the rule, rather than the exception.
Yet, the number of MP patients who have had metastasizing cancer totals zero.
Note that this data is anecdotal. In the next few years, I trust that we’ll be able to make this claim in the context of a peer-reviewed paper. Stay tuned.
Best,
Paul
Zen April 6th, 2009 at 4:20 pm 7
Interesting debate on the comments.
This begs the question: Vitamin C has been shown to lower Serum Uric Acid levels – does this mean the higher doses of Vitamin C might actually increase one’s risk of getting Parkinson’s?
Hi Zen,
There is no evidence that antioxidants such as vitamin C (or even substances which conserve antioxidants) reduce the incidence of disease. See the New Scientist article on the subject. The article is three years old, but the best evidence remains the same.
The last 20 years has seen one antioxidant after the next flame out when controlled studies have scrutinized their efficacy…. No doubt, the antioxidants du jour will prove equally ineffective. I’m looking at you, Acai berries!
Best,
Paul
Thanks for your input Paul…I do agree that the push for people to consume antioxidants is not necessarily backed up in the scientific literature. That’s another reason why I personally don’t believe Parkinson’s is caused by oxidative stress and could be ameliorated with an antioxidant. I believe that evidence points towards chronic bacteria as the cause for PD.
Zen, that still doesn’t answer your question as to whether taking more vitamin C would increase Parkinson’s risk. I sure haven’t seen any studies that associate vitamin C with higher PD risk. So good question!
Since I’m the one who thinks the vitamin D in milk is to blame for increased PD incidence I guess this question goes to Dr. Grant…….
Best,
Amy
Martin April 8th, 2009 at 7:59 pm 10
Dear Amy
You wrote:
In the Evatt study you cite in which patients with Parkinson’s disease were found to have lower levels of 25-D, have you considered that the low 25-D in such patients could be the cause rather than the result of the disease process?
didnt you mean “could be the result rather than the cause” ?….
Martin
Hi Martin,
Yes..you are absolutely right.
Let me try that again – the low levels of vitamin D in the PD patients could be the RESULT rather than the CAUSE of the disease process.
OK! Geez….my mind has really been elsewhere while I’ve been writing comments in this thread. Probably because my sister is getting married and I’m trying to run her wedding website at the same time but still no excuse.
Thanks so much for setting me straight!
Amy
Phil Schoner April 16th, 2009 at 10:14 am 12
I suppose that the study linking low 25-D to PD never bothered to analyze for the active metabolite, 1,25-D. Since 25-D is the precursor for 1,25-D, low 25-D levels could indicate high levels of the active form as it is converted.
Phil
Hi Phil,
I think you’re right. I certainly don’t see any data on the subjects’ 1,25-D levels in the paper. Frustrating indeed!
Amy
Dr. Venkata N Joshi April 17th, 2009 at 7:06 am 14
I believe in natural theory of cause and effect. If the cause is an error of fortifying natural milk with Vit.D3, so is the effect. No natural substance in its natural form becomes a cause for an imbalance. Provided natural substances are not used accordingly can be the cause for an imbalance, as too much of anything or inadequate both together with inappropriate is the cause of every imbalance.
Hi Dr. Joshi,
No natural substance in its natural form becomes a cause for an imbalance.
What about hemlock or any number of other “natural” substances that do a person no good?
With all due respect, yours is a philosophical argument. Instincts are useful, but absent real evidence, they can only take a scientist so far.
Best,
Paul
Kate Zephyrhawke May 5th, 2009 at 1:18 am 16
Here is a book written by an M.D. supporting the Parkinson’s-bacteria connection. http://tinyurl.com/cjebyu
Kate
Very interesting Kate. Thanks for sharing!
Best,
Amy
Joseph Campisi May 12th, 2009 at 3:05 pm 18
Very interesting article, and website in general.
I do wonder why there is no mention of a prevention regimen on your website (that I can find so far). Researching Lyme Disease the herbs samento and cumanda have been very effective against a broad range of pathogens. Elecampane root is 100% effective against MRSA. It seems to me avoiding vitamin D supplementation and anti-microbial herbal teas would both be a good prevention idea!
Hi, Paul Albert,
thank you for your response. Interestingly any substance which come in wrong contact/consumption would give adversity or illness, even an unseen abuse from mind is sufficient to cause damage psycho-somatically. coming to the hemlock, natural substances with above theory of moderation/tolerance can enhance/boost immune responses. for example honey bee stings to use of processed poisonous herbs/minerals in Ayurveda. processing techniques nullify toxicity and enhance tolerance other wise well tolerant sweet substances or cheese in excess may cause food poisoning.
Hi Joseph,
Thanks for your insight but I don’t agree that any of the techniques you suggest would stop L-form bacteria or other chronic bacteria from spreading. We actually recommend that herbal tea be drunk in only low levels because it has high levels of chlorogenic acid – a chemical that dysregulates the VDR nuclear receptor and subsequently slows the innate immune response. Patients on the MP are prohibited from using herbs or others supplements like the ones you mention.
The only way an herb would help protect against L-from bacteria is if it caused a rise in symptoms (an immunoopathological response) that we know signifies bacterial death. If the herb causes a feeling of wellness or does not increase inflammation, it most likely has immunosuppresive properties that actually allow L-form bacteria to spread more easily in the long run.
The best way to prevent the spread of L-form and other bacteria that cause chronic disease is to do the MP. Even a healthy person can benefit from Benicar activating their immune system. Then they can use antibiotics when necessary to enhance the effects of the Benicar in allowing them to target any bacteria they may have accumulated thus far. In fact, we believe that in the future, the MP will become largely a preventative treatment. At the first sign of a symptom, or if a person lives with someone who is ill, they will likely be put on the MP. Some healthy people may choose to do the treatment just to ensure that they don’t accumulate any bacteria and remain healthy. In fact, that’s what my sister is currently doing. Although she doesn’t have any symptoms she is taking Benicar and minocycline to kill any bacteria she may have picked up from me or any bacteria that she picks up from food or other sources. She is doing very well and manifests with such a low level of immunopathology that it doesn’t affect her daily life at all. The reason healthy people can use the MP as a preventative treatment is because the medicines have such excellent safety profiles.
So I encourage people to use the MP as a preventative already and I also encourage people who are symptomatic to start the MP at the earliest date – when their bacterial loads are at the lowest point. The treatment will be much easier and quicker under such circumstances.
Best,
Amy
Hi Joseph,
One more thing. MRSA is a growing health concern and certainly on the rise, so if Elecampane root treats it 100% effectively why would this be the case? Do you have any peer-reviewed studies that confirm the statistic that Elecampne root eliminates MRSA so effectively?
Thanks,
Amy
Dallas Raty June 1st, 2009 at 9:12 am 22
I was surprised to find out a few months ago that Vitamin-D in the body is not just one chemical, but a series of metabolites. What is usually called Vitamin-D (i.e. 25-D) is not even the most active form.
This is relatively new knowledge. Historically it’s been (25-D) alone that’s been measured in most research.
I think most people will be surprised, as I was, to learn about the several different forms of Vitamin-D. It will also be surprising to most people to learn that it’s the (1,25-D) form that activates the immune system, and that the (25-D) form tends to switch it off.
In some chronic diseases, concentrations of the more active form (1,25-D) is elevated, even though the concentration of the well-known form (25-D) may be depressed. In such cases, how can we continue to think that there is a Vitamin-D “deficiency”? There is an abundance of (1,25-D) compared to normal levels in healthy people.
In view of the fact that concentrations of (25-D) and (1,25-D) are not always at a constant ratio, coupled with the fact of (1,25-D)’s potency, it seems researchers ought to be testing for both metabolites, i.e. (25-D) and (1,25-D), not just one, if they want to truly understand what’s really going on.
In the case of this Parkinson’s study, it is too bad that we don’t have the (1,25-D) data. Amy brings up a very needed point. There is strong evidence from the MP cohort, in-silico VDR studies, and elsewhere, to link vitamin-D supplementation as a major suspect in the progression of Parkinson’s disease. If we had (1,25-D) data on those patients, in addition to the (25-D) data, we might very well find that there is no deficiency of active Vitamin-D (1,25-D) at all.
I hope researchers will take note!
Furthermore, if (25-D) tends to switch off the immune system, then studies that show low levels of (25-D) in the presence of chronic disease should be interpreted anew. Instead of that being an argument “for” supplementation of Vitamin-D, it becomes an argument “against”. That is, more (25-D) would tend to compromise the patient’s immune system even more.
In the past, the world has held the idea that “the” sunshine vitamin, (25-D), increased immune response, and therefore, if (25-D) was low when patients were ill, that implied supplementation was needed. However, that argument gets turned around by in-silico studies that show (25-D) deactivates the Vitamin-D nuclear receptor.
I hope researchers will take note!
Thank you Amy for posting this article on Parkinson’s and milk, — or we may say, on positive steps to make Parkinson’s research better.
Thank you Dallas,
I agree with your reasoning. I do think that it is very, very important that the medical community begins testing both 25-D and 1,25-D in patients and that they understand the differences between the two secosteroids.
Best,
Amy
sandra June 12th, 2009 at 6:48 pm 24
I’ve read that MS and Parkinson’s are more common in northern latitudes and symptoms are worse in winter indicating a protective role for vitamin D. Is that bogus info?
I drink unfortified milk, but I do try to get sunlight for natural D and take cod liver oil in winter… is this harmful according to MP?
Why would humans have evolved to make D from sunlight if this could be damaging? Wouldn’t degenerative disease suppossedly caused by D have been common among our early ancesters (who spent more time outside) and less so today as we spend more time inside and use sunscreen?
Or are natural sources of D OK?
Crafty Hunter June 12th, 2009 at 6:49 pm 25
Oh, brother. On a trivial level, this reminds me of how butter (in moderation) is bad for you … no, wait, good for you … no, wait, bad … no, wait, good. Other random memes are the startling and unexpected discovery of jumping genes, and of how bacteria after all are the root cause of ulcers. Another meme is the six blind men and the elephant.
One wonders realistically what level of development of real-time biological monitoring of humans and analysis of actual drug components (including food additions such as different forms of vitamin D) will be required to properly evaluate the effect of environmental influences (foodstuffs, sunlight, drugs, etc.) on disease conditions. All I see now is high-level guesswork, here today and gone tomorrow, with a few exceptions such as the undeniable effect of antibiotics on disease-causing bacteria, and some surgeries.
As for the person who commented on natural substances, chemicals is chemicals (sic). Cheese fat is a chemical. Your tinkletoes are made of chemicals. Aspirin is a chemical, and so is the protein in a banana. It’s all chemicals. What matters is the exact reaction by living organisms to any chemical or combination of chemicals, such as a hamburger or a herb or a synthetic substance meant for treatment of disease.
Hi Sandra,
I am so glad you asked about latitude studies. Have a look at the relevant Knowledge Base article:
http://mpkb.org/doku.php/home:pathogenesis:vitamind:latitude
One thing I don’t point out in that article is that people in Northern latitudes are more likely to take immunosuppressive drugs. Those in tropical countries tend to be poorer and cannot afford interferon, penicillins, TNF-alpha drugs, etc.
According to the Marshall Pathogenesis, supplementing with vitamin D (synthetic, natural, D2, D3, etc.) is harmful – at least over the long-term. Moderate sun exposure is fine obviously.
Sunscreen doesn’t have a huge effect on vitamin D production. Look at the studies referenced here:
http://mpkb.org/doku.php/home:lifestyle:light:skin_protection#effect_of_sunscreen_on_vitamin_d_production
There is currently no evidence that the vast majority of chronic diseases haven’t been around for at least millenia. Manifestations of both arteriosclerosis and cardiac disease can be observed in mummies of ancient Egypt. Ötzi the Neolithic Iceman who lived around 3300 BC was found to have arthritis. Et cetera.
Whether our ancestors spent more time outside is debatable. I asked a current professor of history from Princeton how much time Neolithic man spent outside in the sun. He said there was not enough evidence either way.
Hope this helps.
Best,
Paul
Hi Crafty:
Indeed, the dueling recommendations can get a little old.
The problem with making our case that vitamin D is harmful is that the negative effects of taking a secosteroid takes several years, sometimes even decades, to be realized. For the record, we agree that some/many people who take supplemental vitamin D feel better in the near term. It’s that pesky long-term which is cause for concern.
I wish this weren’t so. That way our discussion would be much more straightforward.
Best,
Paul
Daniel June 15th, 2009 at 5:54 pm 28
Parkinson’s disease is related to low levels of the neurotransmitter dopamine in the body. Vitamin D promotes the synthesis of dopamine (along with epinephrine and norepinephrine). I find it difficult to understand why you think that drinking milk fortified with vitamin D would cause a disease that occurs due to insufficient dopamine levels.
To be more specific, it seems unlikely that a vitamin/hormone that increases dopamine levels would be implicated in a disease caused by low dopamine levels. The more likely explanation, as pointed out by the doctor who posted the first response to this article, is that some other factor is involved. It could be possible, for example, that too much dairy calcium interferes with the body’s normal ability to regulate and use vitamin D.
Vitamin D promotes the synthesis of dopamine (along with epinephrine and norepinephrine).
I’m sure it could for short periods of time, but how is it doing that? More importantly, how is it affecting the disease over long periods of time such as the length of this study?
You know, anabolic steroids promotes the synthesis of muscle. If short-term benefit were all that was important, we should be giving underweight elderly regular doses of Dianabol.
Clearly vitamin D and anabolic steroids are vastly different, but there’s a point here, namely that you give a person a powerful substance and it has effects beyond what is immediately apparent.
In my opinion, our essential difference is over whether bacteria cause Parkinson’s. The NIH says 9 of every 10 cells in the human body are bacterial. Only 1% of these have been characterized. I think it’s fair to say these bacteria cause Parkinson’s disease. If I could show you that bacteria cause disease and that interfering with bacterial die-off reduces symptoms of symptoms of disease, then I think I could make a pretty good case that vitamin D exacerbates Parkinson’s.
I take issue with even a guess that calcium causes Parkinson’s. Why not vitamin D? After all, we already know that vitamin D intake is correlated with brain lesions (and that lesions are themselves associated with Parkinson’s). Note that with regard to the vitamin D-lesion study, only vitamin D intake, and not calcium consumption, was shown to be significantly positively associated with brain lesion volume.
Best,
Paul
Vitamin D promotes neurotransmitter synthesis because that is one of its many roles in a normally-functioning body – along with regulating calcium. A healthy 25-hydroxyvitamin D level is correlated with proper neurological and psychological functioning. In other diseases (like Parkinson’s) where a dopamine dysregulation is implicated – schizophrenia, for instance – there are studies that show elevated serum calcium levels, depressed magnesium levels, and depressed vitamin D levels.
We have been in the sun for tens of thousands of years, and virtually all life on this planet is absolutely dependent on sunlight for its continued existence. It is well known, anecdotally and scientifically, that Vitamin D boosts the immune system… a treatment protocol that suppresses a naturally-sourced, endogenous immunoprotective hormone is laughable.
If you people want to stick your head in the sand (literally) and ignore that sunlight is good for people, then that’s your choice. When you realize, after a few decades of fruitless work supported only by ‘in silico’ models, that your life could have been spent doing other things, don’t blame me…
Daniel,
Vitamin D can’t do all its usual good things when the vitamin D system is dysregulated due to disease. This is explained in other articles.
There are diseases like Sarcoidosis where (1,25,D) levels are “not” lock-step linked to (25,D). It is (1,25-D) that is the “active” form which activates the VDR. Many researchers are still following the assumption that the two are always proportionally related, and therefore measuring (25,D) is all that matters. However, there are known exceptions, so why should we keep using a failed assumption?
The MP has in-silico findings which point this out. Other people use in-silico, too. But the MP has an on-going in-vivo study going, too, where people are getting well, not just palliated.
Please don’t be too quick to side-step understanding the new in-silico findings. Read on.
Hi Daniel,
I understand that you are butting heads with new research when you hear about our current research on vitamin D but please at least try to be somewhat open-minded.
We could get into a long argument about why 25-D supplementation would or would not be good for a Parkinson’s patient but our answer to that question (which is no!) can be found in our published papers. Those of us at ARF have made a concerted effort to publish our findings on vitamin D so that we don’t have to repeat it over and over again to naysayers like yourself. I can tell you have not read any of our publications and I urge you to do so.
If you continue to remain steadfast with your views on vitamin D then perhaps you would like to engage directly with Dr. Marshall, or perhaps attend one of our many talks on vitamin D at conferences around the world where we are presenting our findings and join in the debate there.
The primary focus of this site is to help patients who want to use the Marshall Protocol as a means to recover from their diseases. I spend my time helping such people who are open-minded to our research.
For the record, we do not advocate sun avoidance. Light sensitivity is common in our patients but the goal of every MP patient is to once again return to a place where they can tolerate healthy amounts of sun. Read more here:
http://bacteriality.com/2008/02/23/misconceptions/#8
Please let me bury my head in the sand if you truly think that’s what I’m doing. Meanwhile, ARF chaired the entire session on vitamin D at the 2008 International Congress on Autoimmunity in Portugal, and we are starting a large clinical trial in China with researchers from around the world who are very receptive to our work. At the moment I need to focus on our collaborations with them.
Thanks,
Amy
Daphne Sproule August 6th, 2009 at 6:03 pm 34
I live in Edmonton, Alberta, Canada and was diagnosed with stage 3 Sarcoidosis of the lungs in 2008. I am presently in my 3rd month taking Prednisone (30 mg/day) — I am SO confused trying to make sense of what to do and what not to do to effectively improve/cure my condition. I did approach my lung specialist with the MP, and he hadn’t heard of it before but did some research on it. He had a few issues with it due to the fact that no clinical trials were available and thought that the doses of Benicar were too high for me, so he wasn’t comfortable putting me on the program. I have not been able to find much information on why not to take Vitamin D, etc., so am left in limbo. There’s not much info out there on Sarcoidosis, let alone what to do about it…
Hi Daphne,
Sorry to hear your have sarcoidosis. I understand how confusing it must be to get a diagnosis of sarcoidosis and hear conflicting views on how to best treat it.
I strongly discourage you from taking Prednisone to treat your disease. The following article discusses the negative effects of Prednisone and will give you a more specific idea of why you might not want to take it.
http://mpkb.org/doku.php/home:othertreatments:corticosteroids
If you opt not to go the Prednisone route, I believe the MP is the choice that makes the most sense. There’s strong evidence for bacteria in sarcoidosis and our other patients using the MP to target these bacteria are doing quite well.
I’m sorry we can’t give your doctor the Phase III data he wants, but we are beginning a clinical trial at West China Hospital, the largest clinical hospital in the world and a center for the Cochrane Collaboration.
http://mpkb.org/doku.php/home:arf:072109
In order to better understand our views on vitamin D, take a look at this article.
http://mpkb.org/doku.php/home:pathogenesis:vitamind
Here’s an article on Benicar safety:
http://mpkb.org/doku.php/home:protocol:olmesartan:safety
You may want to show your doctor our organization’s peer-reviewed papers and presentations:
http://mpkb.org/doku.php/home:publications
Ultimately, the manner in which you treat your sarcoidosis is up to you. If you read enough about the Marshall Protocol and feel it is the best treatment option for your condition and your doctor does not believe it is the right treatment option, you should consider finding another doctor.
Here is an article that talks about how to find a doctor who might be supportive.
http://mpkb.org/doku.php/home:starting:physician:finding
Good luck!
Best,
Amy
Claire August 18th, 2009 at 8:21 pm 36
Thank you Amy and Paul for the great article and for your efforts to help raise concern about D.
Claire
P.S. I certainly hope Daniel takes you up on your suggestion that he read the MP related research, as this comment alone “there are studies that show elevated serum calcium levels, depressed magnesium levels, and depressed vitamin D levels” let me know that he had not. Had he, he may have put forward a more powerful argument–that is, if one exists.
In cases of sarcoidosis, why not consider lab work for:
All vitamin and mineral levels?
Infectious microbes?
Heavy metals, biotoxins, and exotoxins?
Food intolerances?
Instead of prednisone (or ancillary to) why not consider fish oil, ginger, curcumin, boswellia, rosmarinic acid, and a list of other natural
anti-inflammatory agents?
Amy, in response to your previous comments:
From personally reading hundreds of reports on using samento and cumanda to treat Lyme, babesia, and other microbes, a most common comment is that it does indeed exacerbate symptoms purportedly via the Herxheimer reaction of pathogen die off. The elecampane research mentioned concerning MRSA has been conducted by Susan O’Shea, a research student at Cork Institute of Technology (CIT), Ireland.
The Cork Institute of Technology evolved from the Royal Cork Institution in 1807 , and the Crawford Municipal Technical Institute which was founded in 1912. It seems like a legitimate institution. Furthermore, elcampane has been demonstrated effective against mycobacteria by Cantrell CL, Abate L, Fronczek FR, Franzblau SG, Quijano L, Fischer NH in “Antimycobacterial eudesmanolides from Inula helenium and Rudbeckia subtomentosa,” Planta Medica, 1999 May;65(4):351-5, reporting that “elcampane root extracts exhibited significant activity against Mycobacterium tuberculosis.” A National Library of Medicine “Pubmed” search on antimycobacterial plants returns over one hundred research journal articles. Antimycobacterial phytochemical agents have a considerable research literature.
There are many effective natural cures. In the USA physicians face malpractice lawsuits if their protocol is not FDA approved. An FDA approval , and the necessary machinations to bring a new drug to market, is currently estimated to cost one Billion dollars. Who is going to finance studies for all the natural cures that are inexpensive and non-patentable, and therefore, not profitable? USA medical practice is based on profit, not on health.
Hi Joseph,
Wow, that’s a lot of supplements! Maybe some of the supplements lead to a bacterial die-off reaction, but then again something like fish oil has definitely been shown to slow immune activity:
http://mpkb.org/doku.php/home:othertreatments:efas
I’m sure you would disagree, but, compared to Benicar and the MP antibiotics, we know relatively little about how these supplements affect the immune system.
Besides, our problem is not in generating an immune response. Almost every sick patient on the MP has been able to generate a pronounced a die-off reaction.
So, we’re right now we’re not interested in supplements. We’re interested in using medications that have clearly defined actions at the molecular level.
As for the tests you mention, those tend to be rather expensive and most patients can’t afford them.
Best,
Paul
Hi Paul, My budget health insurance covers all those tests, since they are not exotic but fundamental tests. Due to out of control medical costs, out of pocket for anything is getting more difficult; but that is another discussion topic. The premise for testing for essential vitamins, minerals, and fatty acids, is the same for testing for vitamin D in many ways. They are called vitamins and essential because they are the fundamental parameters of a healthy metabolism. I find it incredulous that few doctors care about the overall health of patients; naturopaths and orthomolecular medical doctors are notable exceptions.
My goal is inexpensive practical cures; however, most diseases are much less expensive to prevent. Eating the right foods, and perhaps a few inexpensive supplements, can restore metabolism to a healthy homeostasis, once illuminated by some diagnostic testing.
For example, it is much better to take a few tablespoons of coconut oil, eat tomatoes, consume whole dark grapes (skin and seeds), and use knotweed shoots in salad to PREVENT candida (coconut fatty acids, lycopene and resveratrol kill candida), than to try to remove candida once it has penetrated the intestinal epithelium and taken up residence in blood and organs.
I am not arguing against the MP at all.
First, I am just suggesting for those not already suffering from mycobacterial over growth, there are dietary, herbal, and supplements that have been scientifically researched to have antimycobacterial properties, which can be logically expected to provide an inhospitable internal environment for mycobacteria to get a foothold.
Secondly, does MP have a 100% cure rate? Perhaps for those not cured by MP alone, an ancillary enhancement using a combination of MP and aforementioned nutraceuticals would improve the cure rate for those intractable outliers.
For example, at a meeting of the American College of Chest Physicians on October 29, 2008 by Gilda Sapphire Erguiza, M.D. of the Philippine Children’s Medical Center and Daniel Rauch, M.D. of the New York University Langone Medical Center, their results of a study in treating mycobacterium tuberculosis, a combination of coconut oil and antibiotics was found to be more effective than antibiotics alone.
Your point about immune suppressing effects of fish oil is significant. In various protocols for a variety of diseases, at particular stages of disease progression, the use of immune system enhancement can be contraindicated. To intuitively suggest that immune enhancement is invariably the correct course, while intuitively plausible, is not scientifically correct. While fish oil is established to contribute to the prevention of heart disease, cancer, and depression; depending on the protocol to treat a disease chosen, fish oil may, or may not be appropriate as an ancillary treatment.
Take care, Joe
Of further interest, the herb Artemisia, a traditional remedy for infection, is from my readings, probably the most common herb used by the Lyme community to treat comorbid mycoplasma infection. It has scientifically proven to be effective against several mycoplasma species.
Also Dr. Virginia Livingston, working here in Newark at Saint Michael’s Hospital in the 1950s eventually developed an autogenous vaccine for a cell wall deficient bacteria.
Her work has been updated by Dr. Alan Cantwell, who implicated cell wall deficient mycoplasma species in scleroderma, sarcoidosis, sarcoma, and Hodgkin’s.
The widespread plant phenol hydroxytyrosol has demonstrated antimycoplasmal activity, and has been suggested as an ancillary treatment for those with antibiotic resistant mycoplasmas.
Livingston VW, Alexander-Jackson E Mycobacterial forms in myocardial vascular disease. J Am Med Womens Assoc. 1965 May;20:449-52.
Al-Momani W, Abu-Basha E, Janakat S, Nicholas RA, Ayling RD. (2007). In vitro antimycoplasmal activity of six Jordanian medicinal plants against three Mycoplasma species. Trop Anim Health Prod. 2007 Oct;39(7):515-9.
Livingston VW, Alexander-Jackson E (September 1965). “An experimental biologic approach to the treatment of neoplastic disease; determination of actinomycin in urine and cultures as an aid to diagnosis and prognosis”. J Am Med Womens Assoc 20 (9): 858–66.
Livingston VW, Livingston AM (June 1974). “Some cultural, immunological, and biochemical properties of Progenitor cryptocides”. Trans N Y Acad Sci 36 (6): 569–82.
Wuerthele-Caspe V, Alexander-Jackson E, Anderson JA, Hillier J, Allen RM, Smith LW (December 1950). “Cultural properties and pathogenicity of certain microorganisms obtained from various proliferative and neoplastic diseases”. Am. J. Med. Sci. 220 (6): 638–46.
Cantwell AR Jr, Craggs E, Swatek F, Wilson JW. Unusual acid-fast bacteria in panniculitis. Arch Dermatol. 1966 Aug;94(2):161-7.
Cantwell AR Jr, Wilson JW. Scleroderma with ulceration secondary to atypical mycobacteria. Arch Dermatol. 1966 Nov;94(5):663-4.
Cantwell AR Jr, Craggs E, Wilson JW, Swatek F. Acid-fast bacteria as a possible cause of scleroderma. Dermatologica. 1968;136(3):141-50.
Cantwell AR Jr, Kelso DW. Acid-fast bacteria in scleroderma and morphea. Arch Dermatol. 1971 Jul;104(1):21-5.
Cantwell AR Jr. Variably acid-fast bacteria in a case of systemic sarcoidosis and hypodermitis sclerodermiformis. Dermatologica. 1981;163(3):239-48.
Cantwell AR Jr. Bacteriologic investigation and histologic observations of variably acid-fast bacteria in three cases of cutaneous Kaposi’s sarcoma. Growth. 1981 Summer;45(2):79-89.
Cantwell AR Jr. Histologic observations of variably acid-fast coccoid forms suggestive of cell wall deficient bacteria in Hodgkin’s disease: a report of four cases. Growth. 1981 Autumn;45(3):168-87.
Pio Maria Furneri, Anna Piperno, Antonella Sajia, and Giuseppe Bisignano (2004). Antimycoplasmal Activity of Hydroxytyrosol, Antimicrob Agents Chemother. 2004 December; 48(12): 4892–4894.
Cowan, M. M. 1999. Plant products as antimicrobial agents. Clin. Microbiol. Rev. 12:564-582.
crispy November 13th, 2009 at 8:35 pm 42
On Antioxidants and incidence of disease (Paul Albert Aug 6 09): the New Scientist article you mention is worth reading by anyone interested in ia well written piece quoting people who know nothing about health and antioxidants: look at there credentials; nothing is hidden. No medical doctor is quoted ; no-one with opposite views with credentials in healthcare is interviewed. Furthermore, if bias needed to be proven, some benefits of antioxidants are acknowledged in one paragraph but the implications seem to be ignored by the author..
Let me give 1 ex of inaccuracy in this article:
A big mistake is made by one of the scientist quoted who does not understand the difference between antioxidant capacity and reducing capacity (measured by Redox potential).
This is like comparing calcium carbonate (with its known”anti-acid capacity” = buffering capacity) and the lack of high Ph in water + CaCO3 (Ph akin to redox potential).
Perhaps it’s not the best ex since CaCO3 is not soluble in water but i can’t think of abetter one now.
Antioxidants act like a buffer against free radicals (capturing them in fact).They do not affect the redox potential in SO whose redox potential is within normal values allowing life.
The chemist who gave me the same link said this article proved the free radical theory of aging and disease was invalid… He is wrong and I hope my comments helped him to understand why )he understands chemistry).
So much for this article which ignores thousands of publications linking – if not PROVING – the benefits of diets rich in antioxidants and supplementation above and beyond diet.
I am not blaming you for quoting this paper: look at it again in detail; you’ll see what I said is true and we can quote it as a biased, unscientific look at the subject of antioxidants.
RE: Vit C and UA; I assume the reduction of uric acid levels by Vit C (which I haven’t verified) is largely compensated by the antioxidant effect of Vit C. In Ph terms I’d assume Vit C is a better/stronger buffer than uric acid or that the loss of buffer from lower UA is largely compensated by increased buffer from Vit C.
I hope this doesn’t cause further confusion.
Acai is widely overrated (not the highest ORAC value!) and is expensive. I’d stick to Kiwi and berries!
I decided not to follow MP but the above is unrelated.
here is a quote from the article (New Scientist):
“Vitamin E is not an antioxidant. In fact it must be protected against oxidation,” says Angelo Azzi, a biochemist at Tufts University in Boston, Massachusetts.”
what kind of a biochemist is he?
Vit E is antioxidant BECAUSE it neutralizes (captures, as some put it) free radicals; in that process it becomes oxidized, the free radical being reduced. To remain active indeed it has to be protected against oxidation (from O2 for ex).
Vit E, acting as an antioxidant, will prevent oil from becoming rancid (try it if You don’t believe me w 2 bottles of say olive oil, 1 w added vit E and the other without exposed to natural heat and sunlight).
The large reduction of incidence of cardiovascular disease from Vit E, in some studies, speaks for itself. I don’t know why other studies failed to show similar results. Could it be a different amount of E? Or more likely the form of synthetic Vit E given – instead of MIXED TOCOPHEROLS (what I take)?
YOU have to judge for yourself and perhaps look at Life Extension magazine with many articles on Vit E and other antioxidants.
Yes, LE sells Vit and supplements (Expensive on top of that) and can be seen as having a conflict of interest BUT you MUST look at their Medical advisory board before you jump to conclusions:
Md’s, professors of medicine etc (not a journalist writing in the New Scientist probably on behalf of pharma interests!).
End of debate for me.
Crispy,
At the risk of sounding rude and in an effort to maintain clarity, I don’t support your conclusions.
Best,
Amy
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