Is Parkinson's disease a lifestyle diseas... - Cure Parkinson's

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Is Parkinson's disease a lifestyle disease? 1. Parkinsonian lifestyle (higher risk).

parkinsonshereandnow profile image

(Excerpt from the book I am writing now. I hope you find it useful).

Is Parkinson's disease a lifestyle disease?

1. Parkinsonian style

(increased risk of developing the disease)

I have less and less doubts about the existence of a "Parkinsonian" way of life, which predisposes and increases the risk of developing the disease (especially from the fifth or sixth decade of life onwards) and which coincides in many respects with that which possibly aggravates it once the disease has been diagnosed.

My father was considered a typical Parkinsonian case, almost 100%. He could have been one of those listed in the medical literature: family history, psychological trauma in childhood, sedentary life and obesity, history of hepatitis, drank well water in his village during his childhood, anaphylactic shock, chronic insomnia, phobic anxiety, abuse of drugs in general and of strong antibiotics, as well as the use of neuroleptics, intestinal disorders, unhealthy nutrition all his life (rejection of vegetables and fruits, excess of fried foods, sweets, etc.) and many other things.

In spite of everything, he lived 18 years with the diagnosed disease. And even in the last few years, he would sit up in his armchair to do breathing exercises when the nutritional changes made him experience some improvement.

In 2003, the first major crack opened in the wall of our ignorance and arrogance (both form a very strong cement). The news of the recommendation made by the scientist Luc Montagnier (Nobel Prize for Medicine in 2008) to Pope John Paul II, who was suffering from Parkinson's disease, about the consumption of fermented papaya extract to combat the Parkinson's disease he was suffering from, due to its richness in antioxidants.

Another such piece of news came from Brazil. A team of Brazilian researchers, led by neurologist Dr Cicero Galli Coimbra, reportedly achieved surprising results by giving high-dose vitamin B2 (riboflavin) to their patients (90mg three times a day) and eliminating red meat from their diet. The improvements in their mobility abilities were up to 71%.

Then we understood almost nothing. Antioxidants and vitamins... Since all the patients were taking levodopa and were regular red meat eaters, it is possible that much of the improvement in mobility was due to the fact that the meat removed from the diet no longer hindered the drug from reaching the brain. We later learned that riboflavin (vitamin B2) activates vitamin B6 (pyridoxal phosphate), which is essential for the synthesis of dopamine from dopa, stimulates glutathione and energy synthesis in mitochondria (ATP).

In Dr. González Maldonado's book ("El extraño caso...") we read about the existence of psychogenic parkinsonism (largely produced by the mind). Then we learned that in almost all types of Parkinsonism or parkinsonism, the mind possibly plays an important role.

The first studies we learned about were about:

The increased risk of Parkinson's related to diet poor in vitamin E (Golbe, 1988, 1990) and to excessive consumption of dairy products (Chen 2002).

The existence of drugs that produced Parkinsonism or aggravated existing Parkinsonism (books by González Maldonado, Martí-Massó 1988, Nguyen 2004).

Psychogenic Parkinsonism (Lang 1995).

The danger of pesticides, with high percentages of parkinsonism among Amish populations (Racette 2009); or of manganese from the steel alloy industries in Brescia, Italy (Lucchini 2007), which prevents the hydroxylation of tyrosine, the precursor of natural dopa; the apparent lack of preventive efficacy of vitamin E (DATATOP study), etc.

Vitamin E also occupied many hours of reading and debate. It is now known to be composed of four tocopherols and four tocotrienols (alpha, beta, delta and gamma). There are a few more forms, but they are not of interest for this commentary.

The DATATOP study was conducted only with alpha-tocopherol (2000 IU per day for two years) and not with tocotrienols, part of natural vitamin E which has potent neuroprotective effects (Sen 2004, Osakada 2004, Khanna 2006). This would explain why the diet rich in full vitamin E is protective and not the one used in the studies with only part of the vitamin. Another aspect to consider is whether vitamin E was supplemented with fat (it is fat-soluble and without fat cannot be assimilated by the body).

The fact that drinking coffee (Benedetti 2000) or smoking (Hernan 2002, Grandinetti 1994) was significantly protective against Parkinson's, and that among non-coffee drinkers the risk was five times higher (Hu 2007), either because of caffeine or vitamin B3 (Hellenbrand 1996, Ross 2000), and among non-smokers the risk was higher (40 %) and that the protective effect depended on time and number of cigarettes, also attracted our attention.

This does not mean that smoking is good, but that nicotine is a substance to be taken into account. Nicotine patches are already used to treat Parkinson's disease (Dr Villafañe in Paris).

Dr Caroline Tanner's research in 2002, with tobacco and twins, was one of our constant references in the following years.

Later, I gathered more studies, which, together with those already known, reinforced our conviction that there was a lifestyle that clearly increased the risk of developing the disease:

Depression increases the risk of Parkinson's threefold (Shen 2013). And insomnia increases the risk of depression.

Phobic anxiety (Weisskopf 2003).

Sleep disorders that affect the REM phase increase the risk as well. 45% end up suffering from Parkinson's or other neurological diseases related to dopamine (Iranzo 2006, 2009, 2014).

Sedentary lifestyles and lack of exercise (Xu 2010).

Obesity (Abbot 2002) multiplies the risk by a factor of 3.

Excess saturated fats (Peers 1997).

Drinking little water throughout life (Ueki 2004) or drinking well water in early life (Barbeau 1987).

High cholesterol (Hu 2008) and type 2 diabetes (Hu 2007) also increase the risk.

Chronic constipation years or decades earlier (Petrovitch 2009, Savica 2009, Gao 2011).

In my opinion, the various studies cited above would point to the possibility that Parkinson's is, not only but to a large extent, a multi-carrier disease: before and during treatment, deficiencies of magnesium, zinc, vitamin D, vitamin B6, vitamin B3, dopamine, GABA, norepinephrine, epinephrine, tyrosine hydroxylase, tryptophan, glutathione, etc. (Karobath 1971, Charlton 1997).

Not drinking coffee, not smoking (although not recommended because of its many negative health effects), increases the risk of Parkinson's disease. Although it is not clear whether it is only caffeine and nicotine, or whether the way of life associated with habits (a more playful view of life) is also important.

Dr. Werbach's book "Textbook of Nutritional Medicine", which we bought from a famous online bookstore in the USA, made us look at the studies in a different way.

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parkinsonshereandnow
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21 Replies
park_bear profile image
park_bear

I believe my Parkinson's is due to exposure to the pesticide permethrin, the active ingredient in household insect foggers (“flea bombs”). See my writing here for details:

Parkinson's and Pesticides

tinyurl.com/y8tckmx4

Coffee was discussed here:

healthunlocked.com/parkinso...

I only share one of the 14 predisposing factors listed for the poster's father.

I question the designation of well water as a predisposing factor, because well water is highly variable and can be of excellent or poor quality. In addition, even city water supplies may come from wells.

parkinsonshereandnow profile image
parkinsonshereandnow in reply topark_bear

As you know, the EGCG in green tea is generally effective against almost all toxicants that cause parkinsonism, including rotenone, paraquat, maneb, etc. Perhaps matcha tea combined with the supplement Teavigo (EGCG extract), which is widely used in Japan, could help. Alphalipoic acid, coenzyme Q10, vitamin C, theoretically protect the vulnerable points: mitochondria, blood-brain barrier, liver, etc.

Well water before the massive use of pesticides in agriculture was healthy. Now it is a risk almost everywhere, especially where there are greenhouses and crops that use a lot of chemicals.

Today's big city is also a neurodegenerative risk factor (chemical pollution, noise, stress, fear, loneliness...). It should not be, because there are areas of cities where the danger is not so great.

park_bear profile image
park_bear in reply toparkinsonshereandnow

>"As you know, the EGCG in green tea is generally effective against almost all toxicants "

EGCG failed in a recent trial for MSA and caused liver toxicity in some subjects at levels thought to be safe ( EGCG has also caused liver failure in people taking it as a supplement).

atm.amegroups.com/article/v...

"positive therapeutic effects found in multiple pre-clinical models, including rodent (26) and non-human primate (27) models of synucleinopathy have built the case for the recent PROMESA clinical trial of EGCG in patients with MSA, which unfortunately failed to show a protective effect (28)... Clear hepatotoxicity was observed in two patients who had to drop out of the trial... Despite promising initial data in test-tube, cell-culture, and animal models, polyphenols, including EGCG, have not fulfilled their promise in clinical trials testing them in various proteinopathies"

Published January 2020.

------------------

Regarding water, why should water pulled out of a river the any better than water from a well?

parkinsonshereandnow profile image
parkinsonshereandnow in reply topark_bear

What I know best is vitamin C, which gave me back my normal life as an allergic asthmatic and I have been free of medication for almost 20 years. Although there is no clear evidence according to multiple studies...

On every aspect of vitamin C there are studies with opposing results. Sometimes they border on the tragicomic and the studies are gigantic in resources and study subjects, for example on possible benefits for the heart: in men yes but in women no; in women yes but in men no; in men and in women yes; in men and in women no; etc.

So I have learned to evaluate the results taking into account who is doing them and how many years he/she has been working on this subject.

There are hundreds of studies that deny any benefit of vitamin C for colds and flus. Despite the unsurpassed work of Professor Hemila and the Ran study in 2018 (a meta-analysis including nine randomised, placebo-controlled trials conducted from 1950 to 2001...), the public continues to be misinformed. After Hemila, there is no excuse.

I stand by the Japanese and Israeli researchers on green tea and EGCG. Mandel, Levites and colleagues must have been thrilled by that 2020 study after a lifetime of studying EGCG and not noticing that it damaged the liver.

We walk in quicksand...

park_bear profile image
park_bear in reply toparkinsonshereandnow

This guy ended up needing a liver transplant after taking EGCG.

bbc.com/news/stories-45971416

According to this review, EGCG doubles the risk of liver toxicity:

ncbi.nlm.nih.gov/pmc/articl...

"The summary odds ratio, estimated using a meta-analysis method for sparse event data, for intervention compared with placebo was 2.1 "

------------------

Vitamin C is quite safe. I take 5 to 10 g daily.

genesurf profile image
genesurf in reply topark_bear

Jim McCants, the man who needed a liver transplant, was taking high doses of EGCG along with other supplements: bbc.com/news/stories-45971416 . He lost a court case in 2019: "McCants took a long list of supplements, some of which were associated with liver problems" blog.cvn.com/breaking-kroge...

The complete quote from the study you cited paints rather a different picture than you implied: "The summary odds ratio, estimated using a meta-analysis method for sparse event data, for intervention compared with placebo was 2.1 (95% confidence interval: 0.5–9.8). The few events reported in both groups were elevations of liver enzymes. Most were mild, and no serious liver-related adverse events were reported. Results of this review, although not conclusive, suggest that liver-related adverse events after intake of green tea extracts are expected to be rare."

Finally, the report you cited in an earlier comment about hepatotoxicity? The two patients were only 4% of the treatment group, and they were taking 1200mg EGCG which is three to six times the normal dose. neurologyadvisor.com/topics...

A typical 400mg Green Tea Extract capsule contains 200mg of EGCG. It's fine. Keep the EGCG dose low enough and there are unlikely to be problems.

genesurf profile image
genesurf in reply togenesurf

Even if it's safe at normal dosages, though, is EGCG helpful? The outcome of the PROMESA trial suggests not.

However, a closer look into the high-dose PROMESA failure shows that EGCG might be doing something positive:

"Interestingly, in a sub-group of patients who participated in a MRI sub-study, substantially lower striatal volume loss was observed compared to the placebo, suggesting that EGCG treatment exerted a neuroprotective effect and/or modulated neuroinflammation in these patients, which may or may not be related to its direct interaction with α-synuclein.

Sub-acute toxicity also might have contributed to the failure of the trial. Clear hepatotoxicity was observed in two patients who had to drop out of the trial whereas other adverse effects were not significantly different between the EGCG and placebo groups, yet sub-acute toxicity due to covalent modification of amino groups might have interfered with brain processes without being detected as overt adverse effects and led to a lack of improvement of disease symptoms. An interesting possibility is that mannitol, which was used as a placebo, did not work as a real placebo and inhibited α-synuclein aggregation, as has been reported recently in vitro (34), masking the effect of EGCG.

It is also possible that target engagement was achieved yet the treatment was applied too late in the disease to be effective."

ncbi.nlm.nih.gov/pmc/articl...

Based on this, I think a EGCG supplement (dosed low enough to avoid elevated liver enzymes) may still be useful.

park_bear profile image
park_bear in reply togenesurf

"Clear hepatotoxicity was observed in two patients"

pubmed.ncbi.nlm.nih.gov/312...

Out of 47 who received:

"one hard gelatin capsule (containing either 400 mg epigallocatechin gallate or mannitol) orally once daily for 4 weeks then one capsule twice daily for 4 weeks, and then one capsule three times daily for 40 weeks,"

So 1200 mg daily was too much.

"There was no evidence of a difference in the mean change from baseline to week 52 in motor examination scores on UMSARS between the epigallocatechin gallate (5•66 [SE 1•01]) and placebo [mannitol] (6•60 [0•99]) groups"

In other words the mannitol did better than high-dose EGCG, without the toxicity concerns.

genesurf profile image
genesurf in reply topark_bear

Mannitol did not provide "substantially lower striatal volume loss" though.

Probably both are good in different ways. I would be interested in a study combining both.

MBAnderson profile image
MBAnderson

I wholeheartedly disagree with any insinuation that lifestyle should be cited for having PD -- for the reason that people don't have a choice to live in a toxic free environment or to be well educated about nutrition from young age.

Yes, everything you said is true about sedentary lifestyle, diet, pharmaceuticals, trauma, etc., etc. possibly contributing, but it's unrealistic to expect people to be so well-informed about those issues at an age where putting them into practice would do any good.

As you know, Parkinson's is more heavily clustered around industrial areas and farm areas where the environment is saturated with toxins. (The chemical engineers who designed those compounds knew perfectly well they're extremely damaging to people.)

Huge portions of the world's population are barely able to feed themselves from one day to the next much less control these variables. Anything that is beyond their control is not a lifestyle choice.

This contributes to people believing they brought it on themselves -- which is hardly constructive.

parkinsonshereandnow profile image
parkinsonshereandnow in reply toMBAnderson

I don't think anyone has brought Parkinson's on themselves.

I substituted a famous cola drink for my father's "light" version with aspartame (neurotoxic), in the belief that it was good for him (sugar for sweetener). I didn't know that at the time.

Tell people that they can use turmeric with black pepper, curry (India has 4 times less Alzheimer's than the US possibly because of the use of this spice compound), tomato and peppers as neuroprotectors, green tea....

If there were no alternative, perhaps. But I refuse to accept that since it is difficult to change things, we should not report that there are solutions and hope...

Long-term use of levodopa causes psychosis. The antidote is vitamin B3. Do we say so, or do we let sufferers continue to reach that stage helplessly?

I put the responsibility on governments, foundations and associations that should run information campaigns on TV, in prime-time series and in blockbuster movies...

park_bear profile image
park_bear in reply toparkinsonshereandnow

>Long-term use of levodopa causes psychosis.

Evidence?

parkinsonshereandnow profile image
parkinsonshereandnow in reply topark_bear

There is plenty of evidence.

But before mentioning it, I would like to say that for me the written testimony of a doctor of the prestige of neuropsychiatrist Abram Hoffer is a sufficient starting point. If, in addition, it is confirmed by dozens of studies and classic texts in Neurology, even better.

Niacin reduces the side effects of l-dopa medication. Says Abram Hoffer, MD, PhD: [L-dopa becomes] "L-dopamine {which] is oxidized into dopachrome in the brain; this is toxic to cells and is an hallucinogen. Many patients given too much became psychotic. And because it is toxic to brain cells, it also hastens the onset of more degeneration and even death. Therefore it is not surprising that, like adrenochrome, it can cause psychotic reactions. Niacin protects the body against the toxic effect of adrenochrome. For this reason I have used it in conjunction with the l-dopa to protect these patients. The presence of dopachrome (oxidized dopamine) increases the need for niacin, which must be replaced. The other nutrient that is now standard treatment is coenzyme Q10, using up to 1200 milligrams daily." (Foster HD and Hoffer A (2004). The two faces of L-dopa: benefits and adverse side effects in the treatment of Encephalitis lethargica, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis. Medical Hypotheses).

A few studies:

Moskovitz (1978). Levodopa-induced psychosis: a kindling phenomenon. Am J Psychiatry.

Scharf (1978). Dream phenomena induced by chronic levodopa therapy. J Neural Transm.

Klawans (1988). Psychiatric side effects during the treatment of Parkinson's disease. J Neural Transm Suppl.

Friedman (1991). The management of the levodopa psychoses. Clin Neuropharmacol.

Factor (1995). Combined clozapine and electroconvulsive therapy for the treatment of drug-induced psychosis in Parkinson's disease. J Neuropsychiatry Clin Neurosci.

Svetel (1997). [Clozapine in the treatment of adverse psychiatric manifestations of long-term therapy with levodopa]. Srp Arh Celok Lek.

García-Escrig (1999). [Levodopa-induced psychosis in patients with idiopathic Parkinson disease]. Med Clin (Barc).

ssrs profile image
ssrs in reply toparkinsonshereandnow

How much B3 should a Parkinson’s patient take daily? My husband takes sinemet. He just stated taking it 1 month ago.

I definitely appreciate your research and I always gain something from your posts. Although there are many lifestyle factors that contribute to the onset and progression of PD, I think that referring to it as a "lifestyle disease" does not serve any purpose other than to make people with PD feel they are being blamed for their disease.

parkinsonshereandnow profile image
parkinsonshereandnow in reply to

Thank you, cclemonade.

But that can happen because until now (although there are studies on this, they have been neglected), there was nothing to oppose it. It comes from one of the many errors in the way Parkinson's was viewed at the time when there was nothing to prevent it, slow it down or improve the symptoms.

The diagnosis was a shock and the progression inexorable.

Epidemiology frees us if it teaches us the "antidotes", just like Epigenetics.

Epidemiology: NAC, resveratrol or EGCG from green tea are capable of alleviating and slowing down the damage of a stroke, how could they not repair any problem of previous years not so serious.

Epigenetics: vitamin B12 is able to regulate the main "hereditary Parkinson's" gene, LRRK2. And so magnesium, sulphur or vitamin D3?

It would be like not talking about the time of pregnancy as a future neurological risk for the baby so as not to blame the mother or the genes so as not to blame the ancestors. It seems to me to be the way to find solutions.

There are things that depend on the patient, on their carers, on society (pesticides, drugs that induce parkinsonism or DIP, etc.).

I would never mention the shadows of levodopa if there were no solutions or antidotes.

I would never talk about a pro-parkinsonian lifestyle, if there wasn't a preventive and an anti-parkinsonian one.

I was saving it for the book, but since it is published in Spanish, I see no reason not to publish it in English as well.

AaronS profile image
AaronS

Can't wait to read the final product mate 👍

parkinsonshereandnow profile image
parkinsonshereandnow in reply toAaronS

Thank you, AaronS. I will try to finish it as soon as possible.

In the meantime:

2. Non-Parkinsonian lifestyle (lower risk of developing the disease).

healthunlocked.com/parkinso....

3. Antiparkinsonian lifestyle.

healthunlocked.com/parkinso....

What is certain is that we live in an increasingly hostile environment and that Professor Dorsey spoke of a Parkinson's "pandemic" in 2018 (even though it is not an infectious disease). Between 1990 and 2015 there are twice as many sufferers.

Nutrients are preventive and antidotal. If we get an effective and adjustable "protocol" for each patient, they could lead a normal life and would be dependent on certain nutrients and doses for the rest of their lives. It would not be a high price to pay to lead as normal a life as possible (Dr. Costantini's therapy seems to me to be the most effective so far and the one I would take if I had Parkinson's or had recommended it to my father).

Erniediaz1018 profile image
Erniediaz1018

Gracias por este impresionante trabajo, espero con anticipación

sharoncrayn profile image
sharoncrayn

You need a better understanding of US PD drug history and treatment. It takes a long time for the FDA(US) to approve any drug, but PD drug therapy began long before your suggestion of 2003 in the US.

H&Y published their seminal works on PD in the 1950s.

L-dopa was first used in a US PD clinical trial in 1961. Merck patented Sinemet in 1961 for PD...approved by the FDA in 1975. Kroll developed selegiline for PD in the early 1960s with US clinical trials beginning in 1970...approved by the FDA in 1989.

Currently in the US we have 54 PD prescription drugs with 2 new ones approved in 2019... MYOBLOC (rimabotulinumtoxinB) and NOURIANZ(istradefylline),

Sharon

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