A Toxin That Travels From Stomach to Brain May Trigger Parkinson’s

A Toxin That Travels From Stomach to Brain May Trigger Parkinson’s

Summary: A new study reports the combination of a toxic herbicide and lectins may trigger Parkinsonism after the toxins travel from the stomach to the brain.

Source: Penn State.

Combining low doses of a toxic herbicide with sugar-binding proteins called lectins may trigger Parkinsonism — symptoms typical of Parkinson’s disease like body tremors and slowing of body motions — after the toxin travels from the stomach to the brain.

In a study with rats, researchers at Penn State College of Medicine found that after ingesting paraquat, a once widely used herbicide that has been banned in the U.S. since 2007, along with lectins — sugar-binding proteins found widely in nature — the animals developed Parkinsonism.

According to Thyagarajan Subramanian, professor of neurology and neural and behavioral sciences and co-author on the study, the findings — recently published in the journal Parkinson’s Disease — offer clues to how and why Parkinson’s disease develops, and offer a model to test new medications in the future.

“This study gives solid evidence that lectins, while in the presence of certain toxins, may be one potential culprit for the cause of Parkinsonism,” Subramanian said. “Additionally, this animal model can be a tool in the future to continue developing new medications and treatments for Parkinson’s disease.”

The researchers were able to track the formation and spread of a misfolded protein called alpha-synuclein, which previous research has linked with Parkinson’s.

“We were able to demonstrate that if you have oral paraquat exposure, even at very low levels, and you also consume lectins — perhaps in the form of uncooked vegetables, dairy or eggs — then it could potentially trigger the formation of this protein alpha-synuclein in the gut,” Subramanian said. “Once it’s formed, it can travel up the vagus nerve and to the part of the brain that triggers the onset of Parkinson’s disease.”

R. Alberto Travagli, professor of neural and behavioral sciences and senior author of the study, said that while toxins like paraquat have been suspected of contributing to Parkinson’s for decades, the scientific evidence was small. While paraquat was linked with Parkinsonism in previous studies, those experiments typically used high doses of paraquat that humans were not likely to encounter in real life.

Additionally, lectins, which are used in medications to help deliver substances into the brain or stomach, also have been associated with certain rare forms of Parkinsonism. But the researchers weren’t sure if it was the lectins themselves that were causing Parkinsonism, or if they were helping different substances get into the body that then triggered the symptoms.

“Experimenting with the lectins together with the toxin makes sense, because lectins are used in pharmacology to chaperone other substances into the body,” Travagli said. “So it makes sense that the two can be combined and used to make the toxicity more potent, even though the amount of toxin is very low.”

Using a rat model, the researchers exposed the animals daily to small doses of paraquat and lectins for seven days. After stopping the treatment, the researchers waited two weeks. Then, the researchers did a variety of tests to measure problems with motor function and other symptoms typical of Parkinsonism.

stomach

The researchers observed a decrease in motor function that was consistent with Parkinsonism. But to confirm that the symptoms were related to Parkinsonism and not another cause, Travagli said he and the other researchers did several additional tests.

“After observing that these animals did indeed show symptoms of Parkinsonism, we wanted to double check and make sure we weren’t looking at animals that had these symptoms for another reason,” Travagli said. “We administered levodopa, which is a common medication for Parkinson’s disease. We saw a return to almost normal types of motor responses, which was a clear indication that we were looking at some sort of Parkinsonism.”

Additionally, the researchers said when the vagus nerve was disconnected from the stomach prior to exposure to paraquat and lectins, the animals were protected from Parkinsonism, confirming the route of the alpha-synuclein from the gut to the brain.

In the future, Travagli and Subramanian said they will explore whether interventions in the form of diet modifications or medications that interfere with the transport of alpha synuclein from the stomach via the vagus nerve could be used to help prevent or slow the development of Parkinsonism in this rat model. This includes a natural substance called squalamine which has been shown to remove alpha synuclein from the gut and is now in clinical trials for the certain symptoms associated with Parkinson’s disease.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Laura Anselmi, research associate; Cecilia Bove, doctoral student in neuroscience; F. Holly Coleman, lab manager; K. Le, research technologist; Megha Subramanian, research technologist; and Kala Venkiteswaran, assistant professor of neurology, also worked on this research.

Funding: This research was supported by the National Institutes of Health, the Michael J. Fox Foundation for Parkinson’s Disease and the Tobacco Settlement Fund.

Source: Katie Bohn – Penn State
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Ingestion of subthreshold doses of environmental toxins induces ascending Parkinsonism in the rat” by L. Anselmi, C. Bove, F. H. Coleman, K. Le, M. P. Subramanian, K. Venkiteswaran, T. Subramanian & R. A. Travagli in Parkinson’s Disease. Published September 27 2018.
doi:10.1038/s41531-018-0066-0

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Abstract

Ingestion of subthreshold doses of environmental toxins induces ascending Parkinsonism in the rat

Increasing evidence suggests that environmental neurotoxicants or misfolded α-synuclein generated by such neurotoxicants are transported from the gastrointestinal tract to the central nervous system via the vagus nerve, triggering degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and causing Parkinson’s disease (PD). We tested the hypothesis that gastric co-administration of subthreshold doses of lectins and paraquat can recreate the pathology and behavioral manifestations of PD in rats. A solution containing paraquat + lectin was administered daily for 7 days via gastric gavage, followed by testing for Parkinsonian behavior and gastric dysmotility. At the end of the experiment, brainstem and midbrain tissues were analyzed for the presence of misfolded α-synuclein and neuronal loss in the SNpc and in the dorsal motor nucleus of the vagus (DMV). Misfolded α-synuclein was found in DMV and SNpc neurons. A significant decrease in tyrosine hydroxylase positive dopaminergic neurons was noted in the SNpc, conversely there was no apparent loss of cholinergic neurons of the DMV. Nigrovagally-evoked gastric motility was impaired in treated rats prior to the onset of parkinsonism, the motor deficits of which were improved by L-dopa treatment. Vagotomy prevented the development of parkinsonian symptoms and constrained the appearance of misfolded α-synuclein to myenteric neurons. These data demonstrate that co-administration of subthreshold doses of paraquat and lectin induces progressive, L-dopa-responsive parkinsonism that is preceded by gastric dysmotility. This novel preclinical model of environmentally triggered PD provides functional support for Braak’s staging hypothesis of idiopathic PD.

NAC, activated charcoal , sleep and parasites

ParasitesParasites, another cause of IBS symptoms, can cause diarrhea, constipation, gas, bloating, cramps, nausea, poor digestion, fatigue, muscle aches, bleeding, rectal itching, and abdominal pain. Parasites cannot live without you.

If you are embarking on a natural treatment for Candida, fungi or parasites, remove all sources of natural sugar from you diet, including sources like honey and fruits. … Diatomaceous Earth– This is a naturally occurring substance that has amazing ability to kill parasites, yeast and parasite eggs.

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3 Signs You May Have Intestinal Parasites (and what to do about it) –

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Always stay away from tobacco, alcohol, coffee, and black tea as they may slow our body from being able to get rid of parasites. Essential nutritional supplements for cleansing parasites: New Chapter Berry Greens to alkalize the intestinal tract and to make the environment unsuitable for parasitesNAC(N-Acetyl-L-Cysteine) …

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Visceral fat, genes, heart disease and how the stomach talks to the brain

Who is prone to visceral fat?

The tendency to accumulate visceral fat is governed by genetic, ethnic, and gender differences. For example, people who inherit two copies (one from each parent) of a mutation in a gene involved in fat metabolism are more likely to have higher amounts of visceral fat than people with just one copy. Those without any copies of the gene mutation are less likely to develop heart disease — even if they become obese. Natives of India and South Asia have a higher-than-average propensity for abdominal obesity. And white men and black women tend to accumulate more visceral fat than black men and white women.

Fat and aging

With age, people tend to lose muscle tissue, especially the type of specialized muscle fibers that produce quick bursts of speed and power. Fat frequently accumulates within the remaining muscle tissue, causing your body fat percentage to increase even when your weight remains constant. This scenario is closely linked to bodywide inflammation and diabetes risk. It may also explain why your BMI measurement doesn’t provide a true reflection of your health risks.

Evidence suggests that waist circumference and waist-to-hip ratio are better indicators of metabolic health than BMI. Even among people with the same BMI, those who have a large waist (defined as more than 40 inches for men and 35 inches for women) have a significantly higher risk. In addition, people who tend to carry their weight in their hips and thighs (a “pear” shape) have lower waist-to-hip ratios and are less prone to heart disease than people with abdominal obesity (an “apple” shape); see “Measuring your midsection.”

Measuring your midsection

To measure your waist accurately, exhale and wrap a measuring tape around your bare abdomen just above your navel (belly button). Don’t suck in your gut or pull the tape tight enough to squeeze the area.

To compute your waist-to-hip ratio, first measure your hips by putting the tape measure around the widest part of your buttocks. Keep the tape measure level. Then, divide your waist size by your hip size.

Measurements that signal high risk Waist (inches) Waist-to-hip ratio
Women 35 or more 0.9 or more
Men 40 or more 1.0 or more

What should you do about visceral fat?

People with abdominal obesity — even if they’re not overweight — can lessen their heart disease risk with regular exercise and healthy eating habits. “Reducing the total amount of fat in your body frees up storage space for fat particles in places that are associated with less metabolic risk,” says Dr. Mantzoros. That’s why losing as little as 7% of your total weight helps lower heart disease risk: the most dangerous visceral fat disappears first.

 

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Connie’s comments:
  1. Get adequate sleep at night
  2. Do strength training
  3. Use music – toning relaxation music for brain health
  4. Eat colored whole food and get quality supplements at:

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Lectin, gluten, stomach, fasting, toxins, wheat, and foods

By Dr Mercola

From an evolutionary standpoint, any creature, including plants, has a built-in imperative to grow, thrive and propagate. Plants, being rooted into the ground, cannot outrun a predatory insect. Instead, plants use chemistry for self-defense. One of the plant kingdom’s self-defense systems is lectins — not to be confused with lecithin or leptin.

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Lectins are plant proteins, sometimes called sticky proteins or glyca-binding proteins, because they seek out and bind to certain sugar molecules on the surface of cells. There are many types of lectins, and the main difference between them is the type of sugar each prefers and binds to.

Some — including wheat germ agglutinin (WGA), found in wheat and other grass-family seeds — bind to specific receptor sites on your intestinal mucosal cells and interfere with the absorption of nutrients across your intestinal wall. As such, they act as “antinutrients,” and can have a detrimental effect on your gut microbiome by shifting the balance of your bacterial flora — a common precursor to leaky gut.

“I like to think of it as they hack into our communication system, or any predator’s communication system,” Gundry says. “For instance, in insects, they attack a sugar called sialic acid which, among other things, sits between the endings of nerves. One nerve talks to the other nerve by acetylcholine jumping through that space.

Sialic acid allows that to happen. Lectins bind to sialic acid and so interrupt nerve transmission. If you think about it, paralyzing an insect is a great defense system because if the insect can’t move, bingo, you’ve solved the problem. One of the things I’ve learned through the years through my patients is we’re just a giant insect to a plant.

What may happen to an insect fairly instantaneously by eating some plant lectins may take years in us, who are giant insects, to manifest. It may manifest as neuropathy, it may manifest as brain fog, arthritis or heart disease. But the longer I do this, the more I’m convinced that almost every disease process … can be traced back to … plant lectins.

That’s a long-winded explanation for how plants don’t like us. They absolutely don’t want to be eaten. They’ve had 400 million years to work out defense systems — a really long time.”

The Role of Your Microbiome

One of the things that struck me about Gundry’s approach is that it targets the mitochondria and the microbiome, both of which are vital for optimal health. Few physicians, even those in the integrative medicine field, fully understand the importance of mitochondrial function, but Gundry certainly does. And, while the human genome has received a majority of the scientific attention, the bacterial microbiome genome is actually far more important. As noted by Gundry:

“Our microbiome is, I think, our early warning system, because about 99 percent of all the genes that make up [the human body] are actually nonhuman, they’re bacterial, viral and fungal … [from which] we’ve uploaded most of the information about interacting with our environment … because the microbiome is capable of almost instantaneous changing and information processing that we actually don’t have the ability to do.

We’re beginning to realize … that the microbiome is not only how we interact with plant materials … like lectins, but probably more importantly, our microbiome teaches our immune system whether a particular plant compound is a friend or foe [based on] how long we’ve known that plant compound.

There are lectins in everything. But the longer we’ve interacted with lectins and the longer our microbiome has interacted with them, the more our microbiome kind of tells our immune system, ‘Hey, guys, it’s cool. We’ve known these guys for 40 million years. Chill out. They’re a pain, but we can handle them.’

From an evolutionary perspective, if you look at modern foods — say the grains and the beans, which we started interacting with 10,000 years ago, which is a blink of time — our microbiome [regards them as] foreign substances … [T]here’s no lectin speed dating in evolution.”

The Importance of Mitochondrial Function

With regard to mitochondria, “mitochondrial flexibility is one of the unique things that make us human,” Gundry says, comparing the human race to a “fat-storing ape.” Whether you ascribe to the evolutionary theory or not, humans and apes have many genetic similarities, but the ability to store fat is a unique human feature. No other great apes can do that.

Chimps, gorillas and orangutans carry 3 percent body fat. Few humans could ever achieve that low of a body fat percentage unless we were near death from starvation.

“The reason we’re designed to [store fat is to] be able to access fat for fuel,” Gundry says. “The reason why [humans] have been able to take over all parts of the world … [is] because we can cycle back and forth, having our mitochondria use fat for fuel or glucose for fuel. We’re designed to shift very quickly … even within 24 hours.

[Most people] no longer have that metabolic flexibility [because] we’ve been constantly bombarding our mitochondria with an overload of glucose as a fuel, and that really underlies, I think, most disease processes.”

How Intermittent Fasting Boosts Mitochondrial Flexibility

One of the strategies Gundry recommends and uses to improve his own metabolic flexibility is intermittent fasting. For nearly a decade now, he’s been fasting for 22 hours a day, five days a week, from January through June 1, which means he eats all his calories for the day during a two-hour window. On the weekends, he eats lunch and dinner.

“I don’t eat breakfast. I don’t eat lunch. I eat my calories between 6 and 8 o’clock at night. I do that because my wife and I are at home at that time. If I was really smart, I would [eat] earlier in the day, but, you know, you’ve got to be practical in one way or another …

In summer, I’ll have a smoothie with some MCT oil in it, half an avocado, some romaine lettuce, spinach, half a lemon and a little bit of vanilla or stevia. Then I won’t eat lunch. At dinner, same sort of thing, I try to pack all of my calories in between 6 and 8 o’clock at night … 

[June 1], I finished my winter fast, if you will. Now, why do I do that? [Historically], food was a rare thing to find [during the winter]. Again, our metabolic advantage is we’re really good at starvation. It’s what allowed us to survive.

We know that during food scarcity, not only do our mitochondria rev up, but more importantly, our entire immune system and genetic monitoring basically says, ‘Look, times are tough. We don’t know when the next good food supply is going to come. We’ve got to make it through to that next period. We’re going to look at every cell in our body. We’re going to look at whether they’re pulling their own weight.

Are they odd? Are they not very fuel-efficient? We’re going to jettison that. We’re going to create apoptosis until these cells commit suicide.’ It’s kind of like if we were in a hot air balloon and we’re heading for the mountain and we’re going to crash, we’ve got to start throwing things overboard to get more lift.

I think that’s a fundamental principle that you’ve known for a number of years and that I’ve certainly preached for a number of years. The more we understand that that’s how successful aging occurs and study successful agers, one of the things that’s fascinating, particularly in an animal model, is that this intermittent fasting, this challenging [your mitochondria], is the way to do it.”

Although I used to do 14- to 16-hour intermittent fasts, because I felt that it was wise to increase glycogen stores prior to strength training, I have come to realize that’s not true. In fact, it’s counterproductive, as carbs after strength training can increase insulin and diminish IGF-1 response and blunt the anabolic stimulus. So now I am fasting for 18 to 20 hours a day and do all my strength training in a fasted state.

That may sound challenging, but I can confidently assure you, from personal experience, that once you are fat adapted there are no cravings. Additionally, I recently interviewed Dr. Dale Bredesen, who wrote the book “The End of Alzheimer’s: The First Program to Prevent and Reverse Cogntive Decline,” in which he discusses how ApoE4 is a genetic risk factor for Alzheimer’s but ONLY if you don’t intermittent fast. If you do, it will likely actually decrease your risk for the disease as its biological function is to allow us to go for longer periods of time without food.

The Importance of Ketogenic Cycling

Gundry also understands the importance of cycling in and out of nutritional ketosis. While your body is still burning sugar as its primary fuel, you’ll want to be quite strict about not going over your net carb allotment. But once your body has regained the metabolic flexibility to burn fat, it’s really important to cycle in and out or on and off.

I suggest doubling, tripling or even quadrupling your net carbs two days a week, because the metabolic “magic” actually happens during the refeeding phase. As noted by Gundry:

“You have to look at it evolutionarily. It really was feast or famine. When we hit large amounts of food, whether it was a fruit tree or whether it was honey or a wildebeest or a mastodon, there was no food storage system. People tend to forget that nobody walked out of their cave and said, ‘What’s for breakfast?’ There was no refrigerator to have organic berries in every day.

When we chanced upon fuel, then our beautiful design [allowed us to] eat large quantities of [food] and store it as fat. Because, very shortly, whether it was a period of drought, whether it was a period of winter, we were going to regress. I’d like people to think of circadian rhythms. Obviously, we have a 24-hour clock. We have a moon clock. We have seasonal clocks.

What I like people to think of is that we have a period of every year where [we’re in] a growth cycle … That’s the time of growth and it’s a time to reproduce. Then there’s a time of involution, whether it’s a tree dropping its leaves, whether it’s an animal hibernating.

That’s the time where we kind of take stock of everything. That yin and yang, that flow that would happen every year on seasonal basis has completely been lost. We have to have periods where we consume excess calories, then we have to have periods where the exact opposite happens.

Years ago, after my first book came out, I was invited to Phoenix, Arizona, by a blogger named John Kiefer. Kiefer said you should burn fat for fuel most of the time. But every week, you should have what’s called “carb nite loading.” He chanced upon this by accident, but he made a career out of it. I picked his brain and he picked my brain. I think he’s absolutely right.”

Lectins Are Strongly Associated With Autoimmune Diseases of All Kinds

Since we just talked about carb-loading at least once or twice a week (once you’ve regained the ability to burn fat for fuel), it’s worth stressing that these ought to be healthy carbohydrates, and ideally lectin-free. While intermittent fasting and eating a ketogenic (high-fat, low-carb, moderate protein) diet will dramatically reduce your risk of chronic disease, lectins may still cause trouble. One of the primary issues is autoimmune diseases.

“One of the things I talk about in the book that really made me hyper-focused on lectins was a friend of mine who was a very early adopter of my first program. I call him Tony in the book. Tony had really bad vitiligo. That’s … where the [skin] pigmentation is lost. Vitiligo is an autoimmune disease.

What happens is we attack the pigment-forming cells in our skin called melanocytes. Melanocytes are actually modified neural cells. They migrate from the neural crest to our skin in embryonic development. When Tony started my program, a few months later, he came up to visit me. He said, ‘You’re not going to believe this. My vitiligo is gone.’ I’m looking at him and I’m going, ‘Wow. That’s impressive.’

He said, ‘How did that happen?’ I could have said, ‘Well, this is a very anti-inflammatory diet. It’s high in antioxidants.’ But because I’m a researcher, I said, ‘No. That’s too simple.’ I said, ‘Melanocytes. Neural Cells. What’s the target of lectins in insects? Neural cells! Could it be that lectins are why [his body is] attacking his neural cells? What I’ve done is I’ve removed lectins from his diet.’

I lost track of him for a number of years. I was on a health panel in New York City two years ago. I saw him and he’s covered with vitiligo again. I said, ‘What happened?’ He says, ‘You know. I fell off [the diet]. I really need to get back on.’ I said, ‘This is a great experiment. Come on. Here’s the list. Go for it.’

We were just on a panel at Harvard two months ago. He’s chairing the panel. He says, ‘I’ve got to show you — everybody — the vitiligo’s gone because I took lectins back out of my diet. It sounds silly but here’s the proof.'”

Molecular Mimicry

One way by which lectins cause harm is through molecular mimicry. They resemble proteins in the thyroid gland, in your joint spaces and in nerves. They mimic myelin sheath proteins.

The reason why lectins will in one person cause vitiligo or psoriasis, and in another attack the thyroid or cause rheumatoid arthritis, is still unknown. What is known is that one of the underlying factors in all of these disease processes is the penetration of the gut wall by lectins and their co-travelers, lipopolysaccharides (LPSs), also known as endotoxins, which tend to elicit very strong immune responses.

“One of the things I found in all my autoimmune patients is they had profoundly low levels of vitamin D … Interestingly, when you finally seal the gut … all of a sudden, their vitamin D levels went sky high and I could back down on the dosage.

Vitamin D is essential to tell the stem cells at the bottom of the crypts in the villi to grow and divide. Without vitamin D stimulating them, they just sit there and don’t repair the gut. I think plants are so intelligent, it’s shocking. I think one of the plant strategies is that if you have low vitamin D, because you can’t absorb it, then you can’t repair your gut. You’re a horrible predator. You won’t reproduce. You won’t walk.

Vitamin D is really one of the keys to autoimmune disease. Lectins are the other key. I’ve been blessed by knowing thousands of autoimmune patients who I call “canaries,” because they react almost instantaneously to lectins. It’s interesting. Everybody has their own certain lectin or lectins that they really react to.

This morning I had a woman who has rheumatoid arthritis. Her rheumatoid markers or anti-CCP3 markers have gone up. Her IL-17 had gone up. I said, ‘All right. What are you doing? What’s going on?’ She said, ‘No, no. I’m perfect. I know your list backwards and forwards.’ I said, ‘No. There’s something.'”

A Sample Case History of Crohn’s Disease

As it turns out, she’s been eating raw (unpeeled) almonds, and almond peels contain lectins. Another patient’s markers went up after going on a cashew binge, forgetting that cashews are an American bean and hence high in lectins. The answer for autoimmune patients, Gundry says, is to remove lectins from the diet and add vitamin D, which together will help “heal and seal” the gut, thereby preventing the autoimmune response.

“I mention a young woman who has Crohn’s disease in the book. Her well-meaning doctor at the Mayo Clinic told her that food had nothing to do with Crohn’s disease. She had been cured of Crohn’s disease with my program. He told her it was the placebo effect. We still laugh at that one. She ate a couple of Christmas cookies after she got off the phone with him.

Of course, it was like throwing a bomb in her stomach. She had horrible cramps and diarrhea. We skyped and she said, ‘Why don’t doctors see this?’ Like I talk about in the book, we can’t see unless our eyes are open …

I was lucky enough that when I met the guy who changed my life, Big Ed, who cleaned out his arteries with diet and supplements, [I had] my eyes open. I said, ‘This is not chance. How did [he] do this?’ Luckily, because of my evolutionary background, I was able to piece it together.”

Which Foods Have the Most Problematic Lectins?

Lectins are found in many of our most cherished foods, such as: 2,3

Potatoes Eggplants Tomatoes Peppers Goji berries Lima beans
Cashews Peanuts Sunflower seeds Chia seeds Pumpkin seeds Kidney beans
Squash Corn Quinoa Soybeans Wheat Lentils

Another common lectin is the A1 casein protein, found in most of today’s dairy cows. I’ve talked a lot about the benefits of raw milk on my site. The devil’s in the details however, and aside from being high in sugar, even raw dairy may cause problems if it has A1 casein.

“Casein A2 is the normal protein in milk, besides whey. It’s present in sheep, goats and water buffalos. But, most of the cows in the world are now casein A1 producers. They make a lectin-like protein called casein A1, which is metabolized in our gut to make beta-casomorphin, which is a very interesting thing. They can attach to the beta cell of the pancreas and incite an autoimmune attack on the pancreas.

I and others are pretty convinced that [many cases] of Type 1 juvenile diabetics is because of the casein A1 in milk. I’ve been convinced through the years that not only is it the problem, but people who think they’re lactose intolerant or that milk gives them mucus, it’s the casein A1 … Raw milk is great, as long as it came from the right cow … [Some] Jerseys are A1 and [some are] A2. Holsteins are A1.”

More and more people are now starting to recognize this, and there are even grassroots movements pushing for A2 milk in California and Ohio. Jeni’s Ice Cream gets all her milk from Snowville Creamery, which is an A2 farm. “I’ve actually talked to those people. They get it,” Gundry says. There have even been attempts to introduce A2 milk on a larger scale, but each attempt has been crushed by the American Dairy Council, for obvious reasons.

Wheat — Going Beyond Gluten

Wheat germ agglutinin (WGA) is another problematic lectin, found in wheat. Compared to WGA, gluten is a minor problem. According to Gundry, WGA is one of the most efficient ways to induce heart disease in experimental animals. WGA binds to insulin receptor sites. Normally, a normal hormone will dock on a receptor site, give its information and then release. Pseudo hormones like WGA, on the other hand, dock on the receptor permanently. Gundry explains:

“If they hit the insulin receptor on a fat cell, they turn on lipoprotein lipase and pump sugar into the fat cell, turning it into fat constantly. In muscle cells, the exact opposite happens.

They’ll attach to the insulin receptor in the muscle cell [and] block insulin from delivering sugar into the cell. I see so many long-distance runners who are carboholics, who look like concentration camp survivors because they’re really cachectic and sarcopenic because they block the insulin receptors in their muscles …

The lectins, like WGA and galactans in beans are miraculous ways of making us store fat … [T]he only way we’ve ever been able to fatten an animal for slaughter is to give them grains, beans and some antibiotics. If that’s how we fatten animals, that’s how we fatten us. It works really well.”

Not All Bread Is the Same

If you’ve ever traveled to Europe, you may have indulged in some bread and noticed you didn’t experience the same type of problems you have when eating bread in the U.S. The reason for this is because the lectins are removed when you use traditional methods of raising bread, which is still popular in Europe.

“Europe [has] always used traditional methods raising bread. They use yeast or sourdough. Yeast and bacteria are actually pretty good at breaking down the gluten molecule and other lectins,” Gundry explains.

Europe also does not permit the use of glyphosate to desiccate wheat, which has become common practice in the U.S. Glyphosate is also used on many conventional grains, including beans and flax, so it’s in the animal meats we eat, it’s in our baked goods, and even in wine produced in the U.S. According to Gundry, glyphosate potentiates gluten to people who are not even gluten-sensitive, and interferes with your liver’s ability to manufacture the active form of vitamin D.

Glyphosate also chelates important minerals, disrupts the shikimate pathway, decimates your microbiome and increases leaky gut, which allows more of the LPSs into your bloodstream. Since it works synergistically with the lectins, it really delivers a double-whammy.

“[Glyphosate] hits cytochrome P450. It’s one of the reasons the Europeans are so far [ahead] on health,” Gundry says. “It’s one of the reasons why so many of my patients can go to Europe, eat their traditional diet and think they’re cured and now they can start eating bread. They come back and eat a piece of bread and, bam — the whole thing starts all over again.”

On Vegetarianism and Other Diets

As mentioned, Gundry was a professor at Loma Linda University, a Seventh Day Adventist facility. Seventh Day Adventists are typically vegetarians, and while not an Adventist, Gundry did eat a vegetarian diet for about 15 years during his time there.

“I’ve never been sicker in my life. I used to weigh 228 pounds despite running 30 miles a week and running half marathons on the weekend and going to the gym one hour every day, wondering why I had high blood pressure, prediabetes and heart disease … Quite frankly, we have a fabulous orthopedic department at Loma Linda, because grains are pretty doggone mischievous for that.

Through the years, I’ve been good friends with the head of the Adventist Health Studies, a cardiologist. One of the things I’ve learned from following the Adventists and following Gary Fraser is that … certain animal proteins do contribute to aging. In the Adventist health study, the vegan Adventists have the longest life span. Behind them are the lacto-ovo vegetarians, then behind them are the pescetarians. Then finally, there are the real cheaters who eat chicken …

It is interesting that the longest living of the Adventists, who are very long-living, are the vegans. I take care of a lot of vegans because of my association with Loma Linda. As a general rule, the vegans are some of the unhealthiest people I have met. The reason is they’re grain- and bean-itarians. They are not vegetable eaters.

I have nothing against a high vegetable diet … The other thing we see in the vegans is they somehow think they will convert short-chain omega-3 fats into EPA, the long-chain omega-3 fats. They absolutely and positively do not.

Our brain is about 70 percent fat; 50 percent of that fat is DHA. There are beautiful longitudinal studies showing people with the highest omega-3 index have the largest brains as they age, and the largest areas of memory in the hippocampus. People with the lowest levels of omega-3 index have the most shrunken brains and the smallest areas of memory. Vegans have no excuse anymore. There’s algae-based DHA.”

Fruit and Berries — Seasonal Treats

Gundry’s first rule is that what you stop eating is more important than what you start eating. “It’s absolutely true,” he says. “If you take away certain foods, you’ll be amazed [to find] that it’s certain foods that are the troublemakers.” His second rule is, take care of your gut microbiome. Rule No. 3 is “fruit might be as good as candy.” While he doesn’t expound on the importance of burning fat for fuel in his book, that’s really part of the equation. Once you’re able to burn fat, fruit can be a healthy carbohydrate to add once or twice a week.

“Exactly. I think part of the problem is the vast majority of Americans are insulin-resistant. One of the things that people should realize is that the modern fruit has been bred for sugar content … One of the things I ask people to do initially is give fruit the boot.

Fructose is a major toxin. We take fructose directly to our liver and detoxify it into triglycerides and uric acid. It always amazes me the number of people with gout who consume more concentrated fruit, like wine or beer. Beer is one of the underlying reasons that they have gout.

The other thing people should realize is that fructose is a direct renal toxin. The more fructose I can get out of people, the better. Having said that, once you get to a point where you have metabolic flexibility, I think things like berries are probably one of the best ways to carbohydrate load on the day you decided to do that … Sweet potatoes are great as well, [and] I’m a big fan of taro root.

Years ago [in June] … my wife and I were at a Santa Barbara farmers market. I was taking these gorgeous organic peaches and putting them into my bag. She says, ‘Hey, wait a minute. Aren’t you the guy who says give fruit the boot?’ I said, ‘Yeah, yeah. But it’s June and it’s time to eat fruit.’ She says, ‘OK, smart guy. Let’s do this. This summer, we’re going to give up fruit to see what happens’ …

So, we gave up fruit for one summer. We didn’t change anything else in our diet. My wife lost 6 pounds and I lost 8 pounds. It brought home to me that, again, our ancestors and the reason we have two-thirds of our tongue devoted to sweet taste is we are great fruit predators. Fruit was only available once a year. We utilized that fruit to gain weight for the winter … [Now] we can have it 365 days a year, but that’s not normal. So, always keep that in mind.”


Connie: Eat gluten free, avoiding refined and processed foods.

Use Distributorship ID #: USW9578356 when ordering at:

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Colon and rectal cancer incidence is rising among Gen X and millennials

Earlier this year, researcher Rebecca Siegel of the American Cancer Society published a startling report showing that colon and rectal cancer incidence is rising among Gen X and millennials while falling in older generations.

On Tuesday, after delving further into the data, she and her co-authors identified “a true and perplexing escalation in disease occurrence.” In a paper in JAMA, the Journal of the American Medical Association, they report that deaths from colorectal cancer are increasing for young and middle-aged Americans — though the increase appears, at least so far, to be confined to white men and women.

The U.S. mortality rate for colorectal cancer for ages 20 to 54 fell from 6.3 per 100,000 in 1970 to 3.9 in 2004. It then began to go up by 1 percent annually. By 2014, the rate was 4.3 per 100,000.

Breaking the numbers out by race reveals the  trend, with the outlook becoming better for blacks and people of other races but not for whites.

The mortality rate for whites had been declining for decades, but it began to climb starting in 2004, going from 3.6 per 100,000 to 4.1 per 100,000 in 2014. For blacks, it went down to 6.1 per 100,000 in 2014. While that’s still higher than for whites, the trend is heading in the right direction. For other races, mortality rates declined until 2006 and remained stable through 2014.

Siegel noted that the racial patterns are “inconsistent” with trends in major risk factors for colorectal cancer. These include obesity, which is increasing among all races and would suggest colorectal cancer rates should be going up among all races, too.

 


The mortality rate for white Americans declined for a number of years but began to rise again in 2004. In comparison, the rates for black Americans has declined. (JAMA)

The data, which encompass almost  250,000 people, come from the National Center for Health Statistics and information it collects from death certificates. They raise more questions on whether the country’s screening standards should be revisited. Current guidelines call for regular screening for colorectal cancer to begin at age 50.

The analysis of mortality rates contained another surprise: They are also rising for white men and women in their 50s despite the actual cancer incidence decreasing and screening recommended for this age group for decades. In contrast, the mortality rates for blacks in their 50s has declined since 1993.


Contact Connie or join us at the Health Care Network Alliance to stop cancer with whole foods, exercise, sleep and supplementation that affects the gene expression to effect health, vitality and youth. motherhealth@gmail.com or text 408-854-1883 to tailor fit supplementation based on your health.

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Cancer screening protocol for patients with Li-Fraumeni syndrome

tp53.JPG

In a new study from the National Cancer Institute (NCI), part of the National Institutes of Health, researchers found a higher than expected prevalence of cancer at baseline screening in individuals with Li-Fraumeni syndrome (LFS), a rare inherited disorder that leads to a higher risk of developing certain cancers. The research demonstrates the feasibility of a new, comprehensive cancer screening protocol for this high-risk population.

The study was led by Sharon A. Savage, M.D., of NCI’s Division of Cancer Epidemiology and Genetics (DCEG), and was published with a companion meta-analysis on August 3, 2017, in JAMA Oncology.

LFS is most often caused by germline, or hereditary, mutations in a tumor suppressor gene known as TP53. The disorder results in many kinds of cancers — including bone and soft-tissue cancers (sarcomas), breast cancer, brain tumors, and cancer of the adrenal gland — that frequently occur at young ages. Individuals with LFS have an approximately 50 percent chance of developing cancer by age 40, and up to a 90 percent chance by age 60. Many patients with LFS develop more than one primary cancer over their lifetimes.

Dr. Frederick Pei Li and Dr. Joseph F. Fraumeni, Jr., first described LFS at NCI in 1969. “Researchers at the NCI have evaluated families with LFS extensively to better understand how germline mutations in TP53 influence risk, and how best to prevent cancers or treat them at the earliest possible stage,” said Dr. Fraumeni, Scientist Emeritus and Founding Director of DCEG. “However, because of the broad spectrum of cancers in LFS families, it has been challenging to put in place universally accepted cancer strategies.”

To address this gap in clinical care, researchers modified a cancer surveillance protocol from a previously published study and screened 116 LFS patients with germline TP53 mutations using a variety of tools including whole body, brain, and breast MRI, as well as mammography, colonoscopy, bloodwork, and abdominal ultrasound. The study only used modalities that do not utilize ionizing radiation for imaging, since patients with LFS appear to be radiosensitive.

They found that 40 trial participants (34 percent) had abnormalities on baseline screening examination with whole body, brain, or breast MRI that required further evaluation. Eight of these patients (7 percent) were diagnosed with a new primary cancer. All but one of the cancers found through screening were fully removed with surgery. In contrast, the non-MRI techniques used in the trial did not lead to a diagnosis of cancer at baseline screening.

“For high-risk populations, like families with LFS, personalized prevention approaches like this are critical to the early detection of the many kinds of cancers seen in this group,” Dr. Savage explained. “This protocol, along with other published studies, offers patients with LFS a new road map for early cancer detection going forward.”

The meta-analysis, published in the same issue of the journal, involved 578 participants with LFS in 13 cohorts at multiple research centers around the world. Similarly utilizing rapid whole body MRI, the investigators had an overall detection rate of 7 percent for new primary cancers, confirming the results of the study conducted at NCI.

“The findings from this international team effort further demonstrate the utility of whole body MRI screening for individuals with LFS,” Dr. Savage said. “With long-term follow-up, additional refinement, and through international collaborations, we hope to establish a screening regimen that could extend and improve the lives of this unique population.”

About the National Cancer Institute (NCI): NCI leads the National Cancer Program and the NIH’s efforts to dramatically reduce the prevalence of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI website at cancer.gov or call NCI’s Contact Center (formerly known as the Cancer Information Service) at 1-800-4-CANCER (1-800-422-6237).

https://www.nih.gov/news-events/news-releases/nci-study-shows-feasibility-cancer-screening-protocol-patients-li-fraumeni-syndrome