vegetarian diet that comprises plant lectins is related to a greater incidence of PD compared to a diet dominated by meat consumption

[Bolt_Upright]

So if you Google "vegetarian risk Parkinson's" you will be flooded with articles saying that vegetarian is best for PD and that PD risk is lower for vegetarians. I am not disputing this.

But... I was reading this very short paper: sci-hub.st/10.1016/S0016-50...

Dietary Lectins As the Environmental "Unknown Pathogen" in Parkinson's Disease

"Luca Toti, Gregory M. Holmes, R. Alberto Travagli

In the search for environmental clues that might trigger the development of Parkinsons' disease (PD), Braak's group observed the early onset of gastrointestinal (GI) symptoms in PD patients and hypothesized that an "unknown pathogen" penetrates the GI walls and enters the central nervous system via retrograde transport through the vagus nerve, ultimately reaching nigrostriatal dopaminergic neurons to induce their degeneration. Dietary plants, in general, are rich in glycoprotein-lectins which can penetrate the wall of GI tract by endocytosis or via a lectin receptor (saccharide)-mediated mechanism. Lectins, by virtue of their permeability, could act as a chaperon for viruses and toxin(s). Moreover, a vegetarian diet that comprises plant lectins is related to a greater incidence of PD compared to a diet dominated by meat consumption. We aimed to test whether dietary lectins are the environmental clues that might trigger the development of GI impairments that are observed in the early phases of PD. Sprague-Dawley rats of either sex were gavaged daily for 5 consecutive days with fluorescent conjugated lectins from Pisum Sativum (0.1% in 150μl of PBS).

To maximize contact time and absorption, CCK (3μg/kg/ip) was injected 15min prior to the gavage to reduce gastric emptying. Control rats received a PBS solution with 0.1% lectin-free retrograde tracer. Gastric emptying was assessed, starting 7 days prior to the first gavage (baseline), using the non-invasive [13C]-octanoic acid breath test. 10-13 weeks after the treatment, the rats were anaesthetized, gastric motility and tone were recorded with strain gauges applied to the corpus surface. Tyramine (270pmoles/60nl), thyrotropin releasing hormone (TRH; 100pmoles) at the level of the dorsal vagal complex (DVC) or NMDA (5.25nmoles) at the level of the substantia nigra pars compacta or bethanechol (50μg/

kg/iv) were injected. At the conclusion of the experiment, animals were fixed for brainstem immunohistochemistry (IHC) After 13 weeks animals gavaged with a solution of lectin 0.1% (N=6) show a significant decrease in gastric emptying compared to control animals (N=4).

The gastric motility and tone results are summarized below. IHC staining shows that in lectin-conjugated treated animals, but not in control animals, labeling is present in both TH-IR +ve and TH-IR -ve DVC neurons (n=2). Our data indicate that dietary lectins induce gastric impairment that could be caused by their transport into GI-projecting brainstem areas, mimicking the early stages of the PD as hypothesized by Braak's group. Supported by: NIH DK55530"

It has this line: Moreover, a vegetarian diet that comprises plant lectins is related to a greater incidence of PD compared to a diet dominated by meat consumption.

I am trying to get more information on this.

[House2]

I think it depends on individual genetics. I personally do better with low carb/ more meat protein

[Bolt_Upright in reply to House2]

I go with no lectin or gluten plants and meat and fish (and hard cheese).

[Little_apple in reply to Bolt_Upright]

regarding hard cheese, Parmesan for example contains a lot of MSG which causes glutamate Excitotoxicity. All plants have lectins so avoiding completely is not possible

Casein can mimic gluten and cause more distress than low lectins plants.

Therefore, my only dairy is goat kefir and chèvre.

[Bolt_Upright in reply to Little_apple]

I see I can get goat cheese at Meijers. I might give it a try.

[Despe in reply to Little_apple]

Organic feta imported from Greece!

[Little_apple]

pubmed.ncbi.nlm.nih.gov/255...

[Bolt_Upright in reply to Little_apple]

Here is a full article: Diet, Digestive Health, and Autoimmunity: The Foundations to an Autoimmune Disease Food Pyramid—Part 1 2020 sci-hub.ru/10.1089/act.2020...

[Little_apple in reply to Bolt_Upright]

Have you seen this one Bolt? Its a good one.

neurodegenerative diseases are irreversible, and the related deterioration might be due to the chronic, long-lasting, and autoimmunity-induced pathology transformation. Meanwhile, advanced age, one of the main risk factors of both neurodegeneration and autoimmune disease, is characterized by an erosion of tolerance and increased reactivity to self-antigens (16–19). As such, it is assumed that PD, as one of the most common neurodegenerative disorders ranking after Alzheimer's disease (AD), is also likely to be an autoimmune disease.

After nearly three decades, a series of research results have demonstrated that both the innate and adaptive immune systems are activated in PD. Significant increases in innate immune factors, including interleukin (IL)-1, IL-2, and IL-6 and tumor necrosis factor (TNF)-α, have been detected within the substantia nigra pars compacta (SNpc) and cerebrospinal fluid (CSF) of PD patients (24, 25), and γδ T cells, the first line of defense, have also been found to be elevated within the peripheral blood and CSF (26). For specific recognition, human catecholaminergic SNpc neurons express major histocompatibility complex I (MHC-I), which enables them to present autoantigens and be more susceptible to T cell-mediated cytotoxic attack 

However, deficiency of these genes leads to a failure to maintain normal neuron function and prevent oxidative stress and inflammation damage in PD, which has also been confirmed by our previous studies (52, 53). Similarly, a failure to maintain the homeostatic immune system leads to a hyperactive autoimmune state and accelerates disease progression.

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

[Bolt_Upright in reply to Little_apple]

They fed healthy overweight folks raw broccoli sprouts for 10 weeks and IL-6 and C-Reactive Protein went way down! healthunlocked.com/cure-par...

[kaypeeoh]

Yikes. Because of prostate disease in my family I've avoided meat for 20 years. My PSA is still low but is the trade-off PD?

[Bolt_Upright in reply to kaypeeoh]

The opinion in this paper seems to be a minority opinion. I e-mailed the author for details.

[Little_apple in reply to Bolt_Upright]

pubmed.ncbi.nlm.nih.gov/345...

[park_bear in reply to kaypeeoh]

I do not buy it and nor should you. This statement in the cited paper is not accompanied by any supporting reference: “Moreover, a vegetarian diet that comprises plant lectins is related to a greater incidence of PD compared to a diet dominated by meat consumption.”

Now compare that kind of speculation to this reality: Insecticide Permethrin Associated With QUADRUPLED Risk Of Parkinson's tinyurl.com/k3vt26py

If lectins actually caused PD where are the studies showing rodents fed with lectins getting PD? Here is a study showing rodents fed with permethrin getting PD: pubmed.ncbi.nlm.nih.gov/277... Early life exposure to permethrin: a progressive animal model of Parkinson's disease

If Parkinson's were actually an autoimmune condition where are the studies saying so outright? MS is well known to be an autoimmune condition and researchers have no hesitation in saying so.

Where are all the Parkinson's models using lectins or autoimmunity to cause PD? All the Parkinson's models I know of use toxicants or genetically modified alpha-synuclein. That is because these are the things that actually cause Parkinson's.

I had been planning to hold my peace on this matter but cannot do so when others take this idea seriously.

[kaypeeoh in reply to park_bear]

pubmed.ncbi.nlm.nih.gov/331...

[park_bear in reply to kaypeeoh]

Interesting. It looks like autoimmunity is an issue. That said I stand by my comments re lectins.

[Bolt_Upright in reply to park_bear]

Thanks Park Bear. I always appreciate your opinion.

I think Lectins are part of the problem, at least for some people.

Did you know that even though a pitch can throw a baseball 95 MPH, the fastest they can move any body part is 15 MPH? To get a ball to 95 MPH they have to add a bunch of 15 MPH movements together (wrist, forearm, upper arm, shoulder, torso, upper legs, lower leg, ankle). That is what I heard.

I think the reason they can't give rodents PD with Lectins is because rodents can't get PD. Only humans can get PD. None of the animal models are giving animals PD.

[park_bear in reply to Bolt_Upright]

I disagree. The A53T mouse produces the same defective alpha synuclein as humans with this mutation and ends up with the same Parkinson's symptoms. Researchers who are really serious about demonstrating a treatment works for Parkinson's are free to use this mouse. One example of this kind of work is this cinnamon study: link.springer.com/article/1...

We can debate the fidelity of various toxicant animal models, but that debate is hardly worth having as most of these kinds of studies use pre-treatment, which invalidates the model from the get-go.

[Bolt_Upright in reply to park_bear]

Here is that full cinnamon article: Reduction of Lewy body pathology by oral cinnamon 2020 ncbi.nlm.nih.gov/pmc/articl...

[Little_apple in reply to Bolt_Upright]

Together, these results highlight a new therapeutic property of cinnamon and suggest that cinnamon and NaB may be used to halt the progression of α-synucleinopathies.

??Is benzoic acid, naturally found in cinnamon, the same thing as man made sodium benzoate? Based on the quote below, sounds like it is. Sodium benzoate is the sodium salt version of Benzoic acid.

“Upon oral administration, cinnamon markedly reduced the level of insoluble α-syn in nigra, hippocampus and brain stem of A53T mice. We also demonstrated that sodium benzoate (NaB), a metabolite of cinnamon, a widely used food additive and a FDA-approved drug for glycine encephalopathy, was also capable of reducing α-syn deposits in A53T mice. In addition, both cinnamon and NaB treatments showed improvement in their motor and cognitive “

Note: This is a bit of a leap but taking cinnamon with vitamin C might increase cancer risk. Sodium Benzoate is in cinnamon and cranberry.

Sodium benzoate is not known to be carcinogenic on its own. However, there have been concerns by the FDA that when both vitamin C (ascorbic acid) and sodium benzoate are mixed, they form benzene, a known human carcinogen. Benzene is also formed when potassium benzoate is combined with vitamin C.

From my reading, I believe that sodium benzoate is the main ingredient of cinnamon that is believed to reduce A-syn in mice. But, sodium benzoate has downsides

“Itis believed that benzoate can be transformed by decarboxylation into toxic benzene, especially in combination with vitamin C, and then become a compound of high toxicity, mutagenicity, and teratogenicity [17]. There are also reports that sodium benzoate has a weak genotoxic effect. “

“another study, its effect on the induction of apoptosis was observed [25]. In addition, inhibition of antioxidant enzymes, decreased levels of glutathione (GSH), increased levels of nitric oxide (NO), and inflammation (increased in IL-6 and TNF α) were noted. ”

Note: apoptosis is similar but not the same as autophagy. It is cinnamons stimulating if apoptosis that is said to be one of its therapeutic effects in PD. But increasing inflammation and reducing glutathione is obviously detrimental

“Another in vivo study confirmed its negative effects on the liver, as evidenced by an increase in the serum liver enzymes (alkaline phosphatase, aspartate aminotransferase (AST)) (the doses of sodium benzoate were 30, 60, 120 mg/kg b.w./day) [45].

Furthermore, some studies have undertaken evaluation of the therapeutic properties of benzoate in PD. Mutations in the DJ-1 protein are presumed to be associated with the pathogenesis and occurrence of PD [172]. It was mentioned previously that sodium benzoate in a mouse model of intracerebral hemorrhage had a beneficial effect on DJ-1 levels [80]. In another study, it increased the levels of this protein by modulating the mevalonate pathway in primary mouse and human astocytes, as well as in human neuronal cells [173]. Additionally, the compound increased the expression of other PD-related genes, such as Parkin, PINK1, LRRK2 and HtrA2, while suppressing the expression of α-synuclein. The researchers suggest that this compound could alleviate nigrostriatal damage in PD. In an animal model of PD (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model), sodium benzoate was also shown to affect levels of glial cell-derived neurotrophic factor (GDNF) [174]. It stimulated the increase in GDNF expression in mouse and human astocytes via CREB, but in vivo also had a beneficial effect on the levels of this factor in the substantia nigra pars compacta (SNpc). Thus, the compound improved locomotor activity in mice and also had a neuroprotective effect restoring the innervation of the striatum. It should be noted that the mouse model of MPTP PD has limitations [175]. One is that it is the effects of acute/post-acute administration of MPTP are spontaneously reversible over time. However, it is a good model for screening and also for studying the mechanism of action of the substance. In another study, sodium benzoate was shown to stimulate dopamine production by dopaminergic neurons by affecting the expression and protein levels of tyrosine hydroxylase [176]. As previously mentioned, locomotor improvement occurred in the animals. Disturbed trypofan metabolism is also observed in PD [165]. In these patients, there is an increased degradation of it. As mentioned above, sodium benzoate has a beneficial effect by inhibiting its degradation [56].

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

Benzoic acid is used as a preservative in a wide variety of foods. Benzoic acid retards the growth of yeast and moulds, the effective agent being the undissociated acid.

NOTE: Bc the active ingredient in cinnamon , Benzoic acid, is such a potent antimicrobial, it is my layman conclusion that is should not be used daily and certainly not indefinitely. As with Berberine, Allicin , it should be used for a time then take a break and resume. Its benefits are countered by concerns of liver toxicity , increased oxidative stress etc.

[Bolt_Upright in reply to park_bear]

PS: I like that newer article. Glad I am still taking 2.2 grams of Ceylon Cinnamon every day. Thanks!

[Little_apple in reply to park_bear]

Is ”Parkinson’s” a process culminating in manifestations of symptoms we associate with “Parkinson’s” or is this Parkinson’s the symptoms that define it? Parkinson’s pathology is a process, a cascade that leads to the symptoms that have been labeled as Parkinson’s. Mice can be afflicted with a process that leads to the Parkinson’s symptoms but, the important distinction is that the complexity of the disease process is not replicated accurately in mice so to deduce that “well, the mice have Parkinson’s because they were given Parkinson’s inducing chemicals” is a huge oversimplification of a very complex and multifaceted process. There is not and never will be a Parkinson’s “off switch” just as there is not one “on switch.”

AS aggregating and misfolding is part of the disease but it is not “the disease.” It can not be so easily deduced and therefore can not be so easily replicated.

[park_bear in reply to Little_apple]

There certainly is an on switch - healthy rodents exposed to permethrin do get Parkinson's, as do humans..

If there are no studies showing rodents exposed to lectins get Parkinson's, the simple explanation is that lectins don't cause Parkinson's.

[Little_apple in reply to park_bear]

you are over simplifying this. What is your purpose in holding so fervently on to your belief that lectins do not play a roll in PD? What benefit is there to your stance?

Gut dysfunction contributes to PD. Well established. Lectins can contribute to gut barrier permiability which is associated with bbb permiability which is associated with PD pathology. This is proven.

I should not invest more in this conversation as it derails my efforts to learn when I end up in entanglements with those who refuse to abandon beliefs.

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

We discuss the limitations and utility of current models, issues regarding translatability, and future directions for developing animal models of these human disorders.

nature.com/articles/s41593-...

If, as you assert, the animal models of PD are such an accurate depiction of PD , then why are the treatments so rarely translatable?

“It is now apparent that PD is not only a disease of the dopamine system but also includes many neuronal subtypes, alterations in diverse neuronal circuitries and considerable functional decline of the peripheral nervous system [7]. Hence, PD is a multi-system and multi-faceted syndrome manifesting and progressing uniquely for each patient. The cause (environment and/or genetics) and the site (central nervous system and/or periphery) from which neurodegenerative processes are initiated are likely as multi-faceted as the symptoms and the disease course [8, 9].”

Note; multi system and multi faceted.

I’m finding this interesting

link.springer.com/article/1...

And if as you have repeatedly asserted, PD is not autoimmune then can you show anything debunking the position that autoimmunity contributes to PD? To say that something is autoimmune is not to say it is ONLY autoimmune.

Covid pandemic, being a virus is, is obviously the transmission of a virus. But does that mean that the pandemic is ONLY about “the virus.” Of course not. Just as PD is not only about AS and can therefore be reliably replicated in animal models, Covid and peoples susceptibility to it and the degree to which is affects them is much more complex than just the virus itself. Lack of Metabolic flexibility, co-morbidities , inflammation, etc etc etc make it much more complex than just a virus.

I’m prone to wasting my time on here. It is a destructive weakness of mine to not be better at just walking away from silly arguments. I overly abhor mistruths being spread and so here I am again, dumping previous time in to silly arguments when I know I should focus on science and learning.

That’s said, inability to let go of our fixed beliefs keeps progress from being made.

No, a mouse model of PD is not an accurate depiction of PD and PD pathology most definitely includes autoimmune response.

The End

[Bolt_Upright in reply to Little_apple]

Well researched and written Little Apple. I think a little debate among well meaning friends is a good thing, and we are all friends here. Both you and Park Bear are in my nightly prayers.

I did not realize I was going to create a kerfuffle saying rodents don't get PD. I recently heard a doctor talking about animal models and saying none of the animal models are very trustworthy as only humans get PD. Monkeys don't even get PD.

I Googled "only humans get Parkinson's" and got: "Despite the importance of animal models to the understanding of potential pathogenic mechanism in PD (5), there is no naturally occurring parkinsonism in non-human species: PD is a specific human disease.May 1, 2017"

Parkinson Disease: An Evolutionary Perspective 2017 ncbi.nlm.nih.gov/pmc/articl...

"PD is Specifically Human

Many neurological diseases can be found in non-human mammals (9–12) both acquired and hereditary (such as myelopathy, brain tumors, epilepsy, muscular dystrophy, and narcolepsy, to mention a few). However, Alzheimer disease and PD are considered specific to Homo sapiens (13–15). While there are useful animal models of PD including MPTP and alpha-synuclein-overexpressing transgenic mouse models, which may recapitulate important clinical features of the human disorders (5, 14), especially in aged monkeys (16, 17), no spontaneous akinetic-rigid syndrome is known to occur in wild mammals including non-human primates.

Several lines of evidence serve to explain why PD appears to be restricted to the human species. The major motor manifestations of PD are the consequence of degeneration in the dopamine-synthesizing neurons of the mesostriatal neuronal pathway (1, 13). In particular, the dopaminergic fields in the striatum of neurons from the substantia nigra pars compacta (SNpc) can be far more extensive than those of other neurotransmitter types (18). The elegant anatomical studies of Matsuda and colleagues illustrated that the magnitude of the SNpc-to-neostriatum relationship whereby the axon of a single tyrosine hydroxylase-positive dopaminergic neuron in the rat occupies up to 6% of the volume of the striatum (18). Conversely, the arborization of the human mesostriatal neurons occupies a much larger volume of striatum compared to other vertebrates. Vernier and colleagues suggested that the peculiar phenotype of the dopamine mesencephalic neurons, selected during vertebrate evolution, and reshaped in the human lineage, has rendered these neurons particularly prone to oxidative stress (13). Bolam and Pissadaki also stressed the enormous expansion of the human dopamine mesencephalic neurons onto the striatum compared with other mammals (19, 20). Some figures are impressive: the volume of the striatum has increased by approximately 300-fold from rats (20 mm3) to humans (6,280 mm3), but the number of dopaminergic neurons in the SNpc has increased by only 32-fold (rats, 12,000; humans, 382,000) (19). Thus, human dopamine nigral neurons must give rise to axons 10 times the size and 10 times the number of synapses compared to rats (19, 20). Pissadaki and Bolam elegantly proposed that this axonal architecture creates high-energy demands on dopamine-producing nigral neurons to maintain cell functions including the propagation of action potentials (19, 20). As these authors suggested, the nigral neurons are on the edge of an energetic catastrophe (19). Hence, an evolutionary bottle neck was reached with the expansion of the massive (and unmyelinated) nigrostriatal axonal arborization. This peculiar nigral overload may partly explain the selective fragility of the human dopaminergic mesencephalic neurotransmission and the unique presence of PD in humans (13, 19, 20).

Finally, it is relevant to note that this phylogenetically overloaded system needed to regulate very complex motor behaviors. Motor control among mammalians became progressively more sophisticated as hominids developed such skilled motor behaviors as stone tools manufacturing (21). The basal ganglia are known to be critical for the acquisition, improvement, and sustainability of skilled motor behaviors (22, 23)."

[Little_apple in reply to Bolt_Upright]

☺️. You are a kind soul Bolt.

PB can join the club of people who I’ve pissed off. PB, I respect you. But the facts will always lead the way and none of this is personal. I’m wrong a lot. And when I’m shown I’m wrong I’m grateful because that means I am growing. Being wrong in my held beliefs is worse than being naive. Wrong will send you on the wrong path but worse is the naive who you convince with a failed argument and bring with you. At least with naive you stay at the crossroads. (So long as one is aware of their naivety) I digress…. I’ve left multiple times bc of deeply frustrating myself with wasting time on exchanges that have caused me extreme emotional distress due to my inability to handle people doing the verbal equivalent of throwing rotten tomatoes at me. Not implying that that is in any way what has occurred in this exchange as we have in my mind, respectfully disagreed. But it has in the past and the name calling and degrading hurt me mostly bc so few gave a hoot including the moderators. But, here I am resurfacing again because I’m desperate to learn.

Anyways, high lectin foods are absolutely most definitely a problem for many people and the lectins benefit no one. If the needed nutrients can be gotten via low lectin alternatives that is absolutely and definitely optimum.

[LAJ12345]

or is it a lack of b12?

[Bolt_Upright in reply to LAJ12345]

Good thinking!

[Little_apple in reply to LAJ12345]

Good point! Vegetarian diet can (not saying always nor definitively) can lead to insufficient nutrients needed for neuro protection.

B12 , omega 3 (flax is very low in bioavailability and you would need an extreme volume of algae omega 3) , Carnitine is needed for the process that enables omega 3 to be utilized , etc

But, all that being true, it is PROVEN that for at least some people, lectins cause gut permiability. Gut permiability increases BBB permiability.

I was a vegetarian for 13+ years. I’m just an N of 1. My story is long and it is relevant but I’m not going to over share. End point, I have a lot of personal experience in this area.

[PalmSprings]

I really appreciate your contributions to this site. Thanks

[rebtar]

I would put stress at the front of the line. For me. But clearly stress, genetics, toxins, autoimmunity from whatever the specific triggers are….each of us has a particular constellation of symptoms…and causative factors.

All of us here are well intentioned, and debate can be constructive but can also trigger stress. Please be kind when you choose to debate, kind words can go a long way towards allowing ideas to be heard. We don’t need to agree. Thanks to all who contributed information and especially to those who were kind in doing so.

❤️

[Little_apple in reply to rebtar]

The stress of the exchanges I previously had on here are why I keep leaving. The emotional toll was not worth it for the information learned. Upon reflection I realize I am now communicating with my shield up in defense because I am still very bruised from the name calling and attacks that got very personal and cruel and no one, No One defended me even though I was scientifically correct. I am approaching communications on here as someone who is worn and bruised but determined to learn.

[kaypeeoh]

Articles prove vegetarian diet is best. Other articles prove meat diet is best. Other say avoid dairy. Maybe assuming there's no cure and a mixture of foods is better but not perfect. Researchers live by "Publish or Perish". I've seen plenty of studies that were eventually proven to be just plain wrong. So I eat a mixed diet, low in meat and dairy but not purely vegetarian. Occasionally have crackers and cheese. Rarely have BBQ pork ribs.

[kaypeeoh]

Copied from WebMD: A lectin, also known as the “antinutrient” is a type of protein that binds to certain carbohydrates. Just about every organism in the world, from plants to animals to microbes, contains lectins.

[Little_apple in reply to kaypeeoh]

The amount of lectins in these different plants varies greatly. For example, compare an almond with a pecan or, a tomato with asparagus. All contain lectins. Gluten, a lectin, is the worst offender. No one needs dietary gluten.

Regarding the different camps; The Dairy Bad camp, the Meat Bad camp, the Vegetarian Bad camp, all have valid points and all are wrong when taking those valid points and arriving at a generalization.

Dairy for example; lumping goat kefir in with nonfat ice cream is just plain stupid. Lumping factory farm chicken fried in seed oils with grass fed beef is just stupid. It is so much more complex than that.

You are very correct in stating that there is no cure and a mixture is best. To add to the complexity, our biomes change and our guts can go through times of greater distress and then require a different approach then once healing has occurred.

But this is a fact; no one needs grains to be healthy. That is a fact. Grains are optional and I believe the downsides out way the good.

drdavisinfinitehealth.com/

drpeterosborne.com/

Both of these doctors have very good info on this subject.

Please, to those that think I’m wrong, tell me with solid science not dogma.

[kaypeeoh in reply to Little_apple]

So if the problem is not lectins, maybe it's glutens?

[Little_apple in reply to kaypeeoh]

gluten is a lectin

[Bolt_Upright in reply to kaypeeoh]

Lectins can not be digested and they break through the gut barrier and introduce insults into the bloodstream.

[AaronS]

Hey Bolt, I'm currently meat and fruit and vegetables only, no sugar, no grain, no dairy, no peanuts, no wheat. I have just heard a brief snippet of a Podcast where it was mentioned that a 72 hour fast has huge benefits all throughout the body in cases where, people with MS showed good success on managing their symptoms. So I want to Implement fasting if I can. Any calorie restriction/low carb type diet will help us out. The thing is let's be honest they are quite hard to 1: start up properly and 2: maintain strictly.

Regards

Aaron

[Bolt_Upright in reply to AaronS]

I agree about the challenge. A little easier for me as I have Asperger's. Good luck and may God bless you.

[Ponieboy]

I find vegetarians better with gravy. Ketchup makes them taste funny.

Sorry couldn't resist

[JayPwP]

Good find Bolt

[WhyRBD]

do you still have a copy of the paper and could you send to me. The link is bad

[Bolt_Upright in reply to WhyRBD]

This link will work: sci-hub.st/10.1016/S0016-50...

[WhyRBD in reply to Bolt_Upright]

nope - can you email me a pdf

[Bolt_Upright in reply to WhyRBD]

Sent!