Discovery of previously unknown mechanism may someday aid in battle against Alzheimer’s


The body’s ability to adapt to changing conditions and shifting physiologic demands is essential to its survival. To ensure cellular performance and the health of the entire organism, each cell must be able to dispose of damaged or unnecessary proteins.

Now, a study from the Blavatnik Institute at Harvard Medical School (HMS) shows that intense exercise, fasting, and an array of hormones can activate cells’ built-in protein-disposal systems and enhance their ability to purge defective, toxic, or unneeded proteins.

The findings, published Feb. 19 in PNAS, reveal a previously unknown mechanism that is triggered by fluctuations in hormone levels, which signal changes in physiologic conditions.

“Our findings show that the body has a built-in mechanism for cranking up the molecular machinery responsible for waste-protein removal that is so critical for the cells’ ability to adapt to new conditions,” said Alfred Goldberg, senior author on the study and professor of cell biology at the Blavatnik Institute.

Cellular housecleaning in disease and health

Malfunctions in the cells’ protein-disposal machinery can lead to the accumulation of misfolded proteins, which clog up the cell, interfere with its functions, and, over time, precipitate the development of diseases, including neurodegenerative conditions such as amyotrophic lateral sclerosis and Alzheimer’s.

The best-studied biochemical system used by cells to remove junk proteins is the ubiquitin-proteasome pathway. It involves tagging defective or unneeded proteins with ubiquitin molecules — a process known as the “kiss of death” — marking them for destruction by the cell’s protein-disposal unit, known as 26S proteasome.

Past research by Goldberg’s lab has shown that this machinery can be activated by pharmacological agents that boost the levels of a molecule known as cAMP, the chemical trigger that initiates the cascade leading to protein degradation inside cells, which in turn switches on the enzyme protein kinase A. The lab’s previous research found that cAMP-stimulating drugs enhanced the destruction of defective or toxic proteins, particularly mutant proteins that can lead to neurodegenerative conditions.

The new findings, however, reveal that shifts in physiological states and corresponding changes in hormones can regulate this quality-control process independent of drugs. Goldberg’s lab previously focused on reining in overactive protein breakdown — excessive protein removal that can cause muscle wasting in cancer patients or give rise to several types of muscle atrophy. In fact, a proteasome inhibitor drug Goldberg and his team developed to tamp down protein-disposal activity has been widely used to treat multiple myeloma, a common blood cancer marked by abnormal protein accumulation and overworked proteasomes.

The team’s latest work, by contrast, is focused on developing therapies that do just the opposite — invigorate the cell’s protein-disposal machinery when it is too sluggish. These newest findings open the door, at least conceptually, to precisely such treatments.

“We believe our findings set the stage for the development of therapies that harness the cells’ natural ability to dispose of proteins and thus enhance the removal of toxic proteins that cause disease,” said study’s lead investigator, Jordan VerPlank, a postdoctoral research fellow in cell biology at the Blavatnik Institute. Such treatments may not necessarily involve the design of new molecules, but instead stimulate the cell’s built-in capacity for quality control.

“This is truly a new way of looking at whether we can turn up the cellular vacuum cleaner,” Goldberg said. “We thought this would require the development of new types of molecules, but we hadn’t truly appreciated that our cells continually activate this process.

“The beauty and the surprise of it is that such new treatments may involve churning a natural endogenous pathway and harnessing the body’s pre-existing capacity to perform quality control,” he said.

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It is already well known that exercise has many salutary effects, but the researchers said the new findings hint at the possibility that exercise and fasting could also help reduce the risk of developing conditions associated with the accumulation of misfolded proteins, such as Alzheimer’s and Parkinson’s. That possibility, however, remains to be explored, the team noted.

In their experiments, the researchers analyzed the effects of exercise on cells obtained from the thigh muscles of four human volunteers before and after vigorous biking. Following exercise, the proteasomes of these cells showed dramatically more molecular marks of enhanced protein degradation, including greater levels of cAMP. The same changes were observed in the muscles of anesthetized rats whose hind legs were stimulated to contract repeatedly.

Fasting — even for brief periods — produced a similar effect on the cells’ protein-breakdown machinery. Fasting increased proteasome activity in the muscle and liver cells of mice deprived of food for 12 hours, the equivalent of an overnight fast.

In another round of experiments, the researchers exposed the liver cells of mice to glucago, the hormone that stimulates production of glucose as fuel for cells and tissues during periods of food deprivation or whenever blood sugar levels drop. The researchers observed that glucagon exposure stimulated proteasome activity and enhanced the cells’ capacity to destroy misfolded proteins.

Exposure to the fight-or-flight hormone epinephrine produced a similar effect. Epinephrine, also known as adrenaline, is responsible for stimulating the liver and muscle to mobilize energy reserves to boost heart rate and muscle strength during periods of physiologic stress. Liver cells treated with epinephrine showed marked increases in cAMP, as well as enhanced 26S proteasome activity and protein degradation. Epinephrine exposure also boosted proteasome activity — a marker of protein degradation — in the hearts of living rats. Similarly, when researchers exposed mouse kidney cells to vasopressin — the antidiuretic hormone that helps the body retain water and prevents dehydration — they observed higher levels of protein degradation as well.

Taken together, these findings demonstrate that the rate of protein degradation can rise and fall swiftly in a variety of tissues in response to shifting conditions, and that such changes are mediated by fluctuations in hormone levels. This response was surprisingly rapid and short-lived, the scientists noted. For example, exposure to the antidiuretic hormone triggered protein breakdown in kidney cells within five minutes and subsided to pre-exposure levels within an hour, the experiments showed. The findings show that the diverse set of hormones that stimulate cAMP appear to share a common mechanism that alters the composition of cells. These have long been known to modify gene expression, but this latest research reveals they also play a critical role in cellular housecleaning by disposing of proteins that are no longer needed.

A new twist on a classic concept

The new findings build on observations about the physiologic effects of hormones first made by HMS physician Walter Cannon nearly a century ago and elegantly captured in his book “The Wisdom of the Body” (1932). Some of Cannon’s most notable work includes defining the mechanism of action of epinephrine and its role in the fight-or-flight response. Epinephrine is one of the hormones whose action on the protein-disposal machinery is now illuminated by Goldberg’s latest work. In a symbolic coincidence, Goldberg’s lab occupies the very space where Cannon made his observations on the same hormone a hundred years ago.

“We think ours is truly a neoclassical discovery that builds on findings and observations made right here, in this very building, nearly a century ago,” Goldberg said.

Breakthrough discovery: Scientists have found where Alzheimer’s starts – in a set of inflamed immune cells


Image: Breakthrough discovery: Scientists have found where Alzheimer’s starts – in a set of inflamed immune cells

Over 5.5 million Americans – mostly over the age of 65 – are battling Alzheimer’s disease, a debilitating condition that kills more people than breast cancer and prostate cancer combined. Alzheimer’s progressively destroys memory and other cognitive functions, causing confusion, anxiety and heartache. The number of people fighting this disease has increased by a staggering 89 percent since 2000.

Now, an exciting new study by researchers from the University of Bonn, Germany, claims to have uncovered the cause of this incurable disease, and the team hopes that their discovery will lead to a breakthrough in treatment within the next decade.

Scientists have understood for some time that Alzheimer’s is associated with a build-up of amyloid plaques in the brain. Amyloid plaques are a sticky build-up which accumulates on the outside of neurons, or nerve cells. While amyloid is a protein that naturally occurs throughout the body, in Alzheimer’s patients this protein divides improperly, creating a form of amyloid which is toxic to neurons in the brain.

Most human trials for Alzheimer’s treatments have focused on trying to target these plaques. All have failed.

The new research is exciting in that it has revealed the root cause of this amyloid plaque build-up: Inflammation in immune cells called microglia, which make up between 10 and 15 percent of all brain cells, and which act as the brain’s first line of immune defense.

Inflammation directly fuels the characteristic amyloid plaque build-up which autopsies have revealed in the brains of Alzheimer’s patients.

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The Daily Mail recently reported:

For years inflammation has been suspected of having a role but the exact nature of its involvement has been hard to pin down – until now.

The researchers found the microglia release specks of a protein called ASC in response to it. They stick to the amyloid beta protein – boosting its production. …

ASC reside in a vital inflammatory pathway called the NLRP3 inflammasome which damages brain cells.

The researchers found that this process takes place right from the earliest stages of the disease, and that when an antibody was used in laboratory tests to prevent ASC from binding to the amyloid protein, the damaging, sticky amyloid plaque build-up was prevented.

The research team is excited about the possibility of developing a chemical treatment which can directly target inflammasomes, and hope that an Alzheimer’s “cure” might be on the horizon within the next five to 10 years.

Of course, any such chemical cure is likely to carry a slew of side effects, and will more than likely be very costly.

On the other hand, the knowledge that inflammation is the root cause of Alzheimer’s is very powerful, because inflammation can be avoided and even reversed. (Related: Six healthy habits effective for preventing Alzheimer’s disease.)

An article published by Harvard Medical School, for example, noted:

Doctors are learning that one of the best ways to quell inflammation lies not in the medicine cabinet, but in the refrigerator.

The article noted that while inflammation serves the purpose of protecting your body against threatening invaders, inflammation can sometimes persist for long periods of time, even when no such threat exists. It added:

That’s when inflammation can become your enemy. Many major diseases that plague us—including cancer, heart disease, diabetes, arthritis, depression, and Alzheimer’s—have been linked to chronic inflammation.

One of the most powerful tools to combat inflammation comes not from the pharmacy, but from the grocery store.

The foods we eat we will either cause or prevent inflammation; it’s as simple as that.

Foods that cause inflammation include refined carbohydrates, fries and other junk food, soda, processed meats, margarine, and conventionally farmed meat that has been subjected to routine antibiotic and hormone treatments.

On the other side of the spectrum, foods that actively fight inflammation include most of the foods that form part of the Mediterranean diet, including tomatoes, olive oil, green leafy veggies, fatty fish like salmon and tuna, and fresh, organic fruit.

Discover the latest information and breakthroughs at Alzheimers.news.

https://www.brighteon.com/embed/5848224213001

Sources for this article include:

DailyMail.co.uk

Alz.org

Health.Harvard.edu

Tau Tracer May Aid Diagnosis in Alzheimer’s


A new radioactive tracer molecule that binds to the Alzheimer’s protein tau has been developed that may help in diagnosis and monitoring of the disease, as well as in the development of new drugs for the condition.

The compound, known as 18F-RO-948, being developed by Roche, is the subject of two articles published in the December issue of the Journal of Nuclear Medicine.

“This is a second generation radiopharmaceutical that binds to the tau protein found in Alzheimer’s patients,” lead author of one of the articles, Dean Wong, MD, PhD, Johns Hopkins University School of Medicine, Baltimore, Maryland, commented to Medscape Medical News.

“Tau accumulation seems to correlate better with cognitive impairment than amyloid, and it is therefore thought to be a better predictor of cognitive decline,” he said.

Wong explained that a first generation tau radiotracer has been available for some time but that compound has high off-target binding; that is, it also binds to other areas of the brain not associated with Alzheimer’s.

“This new compound is much more specific for tau, and so will allow much more specific imaging of the extent of the disease,” he said.

The Roche compound joins another second generation tau radiotracer developed by Merck. Wong described the two compounds as complementary to each other “with different strengths and weaknesses.”

“The development of his compound will help in understanding the pathophysiology of Alzheimer’s progression and help identify different subtypes of the disease. It will also help in the development of new anti-tau drugs by monitoring if they are reaching their target and assessing their effectiveness,” he said.

“These compounds could also help the earlier diagnosis of Alzheimer’s,” he added. “In future, they could form the basis of a screening test in high risk individuals.”

 

In the first article, the researchers led by Wong recruited 12 patients with Alzheimer’s disease, seven younger healthy controls, and five older healthy controls for brain PET scans. An additional six older healthy controls were recruited for full-body scanning.

The study was divided into three parts. In the first part, three designated tau tracers were tested, 11C-RO-963, 11C-RO-643, and 18F-RO-948, and 18F-RO-948 showed the best results.

In the second part of the study, researchers tested 18F-RO-948 with additional brain imaging in five patients with Alzheimer’s and five older controls, with follow-up of previously seen patients to evaluate the potential progression of tau protein tangling after an average span of approximately 16 months.

The third part of the study examined six older control patients who underwent whole-body scanning. Researchers looked at 80 different regions of the brain to evaluate how well the tracers were taken up by the brain, how well they penetrated the tissue, and how specifically they bound to the tau protein.

They found that healthy brains retained little to no tracer, whereas the brains of those with Alzheimer’s showed tau to be in regions of the brain consistent with previously reported postmortem data on filamentous tangles.

18F-RO-948 is a promising radiotracer for imaging tau pathology in Alzheimer’s disease,” the investigators write. “The tracer shows good brain uptake, has no apparent brain-penetrant radiolabeled metabolites, has a good kinetic profile, shows little or no retention in cognitively normal controls and a distribution in Alzheimer’s subjects consistent with published postmortem data.

“It is our hope that tools such as 18F-RO-948 will allow us to gain a better understanding of the pathophysiology of Alzheimer’s and, in the context of drug development, select patients for clinical trials, confirm the mechanism of action of drugs targeting pathologic tau, and monitor the effects of disease-modifying therapies regardless of whether they target tau directly,” they conclude.

In the second article, the team examined the detailed quantification of 18F-RO-948 tau binding in 11 patients with Alzheimer’s disease, five young cognitively normal controls, and five older cognitively normal controls, and verified that the compound showed reproducible results.

The noodles that are linked to chronic inflammation, weight gain, Alzheimer’s and Parkinson’s


ramen noodles

Instant noodles are a popular go-to lunch or dinner for those who are strapped for time (or cash), like college students. While you probably don’t consider them a health food, you may think they’re not that bad, or, at least, not as bad as eating a burger and fries or a fast-food burrito.

In a first-of-its-kind experiment, however, Dr. Braden Kuo of Massachusetts General Hospital may make you reconsider your love of instant noodles (assuming you have one).

He used a pill-sized camera to see what happens inside your stomach and digestive tract after you eat ramen noodles, one common type of instant noodles. The results were astonishing…

Video URL:https://youtu.be/IQlNv2Au-Lg

Ramen Noodles Don’t Break Down After Hours of Digestion

In the video above, you can see ramen noodles inside a stomach. Even after two hours, they are remarkably intact, much more so than the homemade ramen noodles, which were used as a comparison. This is concerning for a number of reasons.

For starters, it could be putting a strain on your digestive system, which is forced to work for hours to break down this highly processed food (ironically, most processed food is so devoid of fiber that it gets broken down very quickly, interfering with your blood sugar levels and insulin release).

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When food remains in your digestive tract for such a long time, it will also impact nutrient absorption, but, in the case of processed ramen noodles, there isn’t much nutrition to be had. Instead, there is a long list of additives, including the toxic preservative tertiary butyl hydroquinone (TBHQ).

This additive will likely remain in your stomach along with the seemingly invincible noodles, and no one knows what this extended exposure time may do to your health. Common sense suggests it’s not going to be good…

Five Grams of Noodle Preservative, TBHQ, Is Lethal

TBHQ, a byproduct of the petroleum industry, is often listed as an “antioxidant,” but it’s important to realize it is a synthetic chemical with antioxidant properties – not a natural antioxidant. The chemical prevents oxidation of fats and oils, thereby extending the shelf life of processed foods.

It’s a commonly used ingredient in processed foods of all kinds (including McDonald’s chicken nuggets, Kellogg’s CHEEZ-IT crackers, Reese’s peanut butter cups, Wheat Thins crackers, Teddy Grahams, Red Baron frozen pizza, Taco Bell beans, and much more).

But you can also find it in varnishes, lacquers, and pesticide products, as well as cosmetics and perfumes to reduce the evaporation rate and improve stability.

At its 19th and 21st meetings, the Joint FAO/WHO Expert Committee on Food Additives determined that TBHQ was safe for human consumption at levels of 0-0.5 mg/kg of body weight.1

However, the Codex commission set the maximum allowable limits up to between 100 to as much as 400 mg/kg, depending on the food it’s added to.2 (Chewing gum is permitted to contain the highest levels of TBHQ.) In the US, the Food and Drug Administration requires that TBHQ must not exceed 0.02 percent of its oil and fat content.3

So there’s quite a discrepancy in supposedly “safe” limits, but it’s probably best to have little or no exposure to this toxicant, as exposure to five grams can be lethal and, according to A Consumer’s Dictionary of Food Additives, exposure to just one gram of TBHQ can cause:4

  • Nausea and vomiting
  • Ringing in the ears (tinnitus)
  • Delirium
  • Sense of suffocation
  • Collapse

While TBHQ is not suspected to be a persistent toxicant, meaning your body is probably able to eliminate it so that it does not bioaccumulate, if you eat instant noodles your body might be getting prolonged exposures. This is concerning, to say the least. According to the Environmental Working Group (EWG), based on animal studies health hazards associated with TBHQ include:5

  • Liver effects at very low doses
  • Positive mutation results from in vitro tests on mammalian cells
  • Biochemical changes at very low doses
  • Reproductive effects at high doses

Eating Instant Noodles Linked to Metabolic Syndrome

If you’re still considering ramen noodles for lunch, you should know a new study published in the Journal of Nutrition found that women who consumed more instant noodles had a significantly greater risk of metabolic syndrome than those who ate less, regardless of their overall diet or exercise habits.6

Women who ate instant noodles more than twice a week were 68 percent more likely to have metabolic syndrome — a group of symptoms such as central obesity, elevated blood pressure, elevated fasting blood sugar, elevated fasting triglycerides, and low levels of HDL cholesterol.

Having three or more of the symptoms increases your risk of developing diabetes and cardiovascular disease. Past research also analyzed overall nutrient intake between instant-noodle consumers and non-consumers, and found, as you might suspect, that eating instant noodles contributes little value to a healthy diet.

The instant noodle consumers had a significantly lower intake of important nutrients like protein, calcium, phosphorus, iron, potassium, vitamin A, niacin, and vitamin C compared with non-consumers.7 Those who ate instant noodles also had an excessive intake of energy, unhealthy fats and sodium (just one package may contain 2,700 milligrams of sodium).8

What Else Is in a Package of Instant Noodles?

Aside from a lot of sodium and the preservative TBHQ, what else is found in a typical serving of instant noodles?

Prevent Disease reported:9“The dried noodle block was originally created by flash frying cooked noodles, and this is still the main method used in Asian countries, though air-dried noodle blocks are favored in Western countries. The main ingredients of the dried noodle are wheat flour, palm oil, and salt. Common ingredients of the flavoring powder are salt, monosodium glutamate, seasoning, and sugar.

Benzopyrene

…In June 2012, the Korea Food and Drug Administration (KFDA) found Benzopyrene (a cancer-causing substance) in six brands of noodles made by Nong Shim Company Ltd. Although the KFDA said the amounts were minuscule and not harmful, Nong Shim did identify particular batches of noodles with a problem, prompting a recall by October 2012.”

Monosodium Glutamate (MSG)

The monosodium glutamate (MSG) in instant noodles is reason enough to avoid them. MSG is an excitotoxin, which means it overexcites your nerve cells to the point of damage or death, causing brain dysfunction and damage to varying degrees — and potentially even triggering or worsening learning disabilities, Alzheimer’s disease, Parkinson’s disease, Lou Gehrig’s disease, and more.

Glutamic Acid

Part of the problem is that free glutamic acid (MSG is approximately 78 percent free glutamic acid) is the same neurotransmitter that your brain, nervous system, eyes, pancreas, and other organs use to initiate certain processes in your body. Not to mention, MSG is also used to fatten up mice for scientific study. Yes, MSG is the perfect obesity drug. If you want to achieve your ideal body weight and health, avoid MSG at all costs.

Return to Whole, Living Foods for Optimal Health

Occasionally eating a package of instant noodles clearly won’t kill you, but when you make a habit of substituting convenience foods for real food, it’s only a matter of time before health problems will likely develop.

Instant noodles are a prime example of the types of processed foods you want to avoid as much as possible, as they are virtually guaranteed to make you sick and fat if you indulge too much (and “too much” may be as little as a couple of times a week).

Processed foods encourage weight gain and chronic disease because they’re high in sugar, fructose, refined carbohydrates, and artificial ingredients, and low in nutrients and fiber. Processed foods are addictive and designed to make you overeat; they also encourage excessive food cravings, leading to weight gain.

Eating processed foods also promotes insulin resistance and chronic inflammation, which are hallmarks of most chronic and/or serious diseases. On the other hand, people have thrived on vegetables, meats, eggs, fruits, and other whole foods for centuries, while processed foods were only recently invented.

Ditching processed foods requires that you plan your meals in advance, but if you take it step-by-step as described in my nutrition plan, it’s quite possible, and manageable, to painlessly remove processed foods from your diet.

You can try scouting out your local farmer’s markets for in-season produce that is priced to sell, and planning your meals accordingly, but you can also use this same premise with supermarket sales.

You can generally plan a week of meals at a time, making sure you have all ingredients necessary on hand, and then do any prep work you can ahead of time so that dinner is easy to prepare if you’re short on time (and you can use leftovers for lunches the next day, so you don’t have to resort to instant noodles).

One of World’s Biggest Drug Companies Just Abandoned Alzheimer’s And Parkinson’s Research


Pfizer, the world’s third largest drug maker, has announced it is ending research to discover new medications for Alzheimer’s and Parkinson’s disease.

The move, which will eliminate hundreds of research positions across the pharmaceutical giant’s roster, casts an even darker shadow outside the company – dashing the hopes of millions affected by neurological disorders, whose dreams of finding a treatment just got that much more desperate.

“As a result of a recent comprehensive review, we have made the decision to end our neuroscience discovery and early development efforts and re-allocate [spending] to those areas where we have strong scientific leadership and that will allow us to provide the greatest impact for patients,” the company said in a statement to NPR.

Job reductions primarily in Massachusetts and Connecticut are expected to occur across the next several months, although the company is continuing research into rare neurological diseases, and plans to launch a venture fund committed to neuroscience.

To many, though, those gestures won’t replace the loss of some 300 neuroscientists and associated staff in an organisation that bills itself as “the world’s largest research-based pharmaceutical company”.

“Any decision impacting colleagues is difficult,” the company’s statement reads.

“[H]owever, we believe this will best position the company to bring meaningful new therapies to market, and will bring the most value for shareholders and patients.”

Of course, value for shareholders is one thing; but for patients, especially those affected by neurological diseases (and their families), it’s quite another, as critics of Pfizer’s new direction are eager to make clear.

“[W]ith no new drug for dementia in the last 15 years, this will come as a heavy blow to the estimated 46.8 million people currently living with the condition across the globe,” says the head of research at the UK’s Alzheimer’s Society, James Pickett.

“Every three seconds someone in the world develops dementia and, with this number set to rise, there has never been a more important time for such life-saving research.”

That’s especially so since the best, mostly ineffective medications we have for conditions like Alzheimer’s are in fact the products of research from decades ago.

While there are strong hopes they can be improved upon – and treatments for Parkinson’s and other neurological conditions too – until more research is done, a hoped-for, effective replacement won’t materialise.

“The current medication for Alzheimer’s disease is approved, essentially, because it’s better than nothing. There’s nothing else at the moment,” neuroscientist Joseph Jebelli told NPR last week.

“These drugs were pioneered in the ’70s and ’80s and they treat the symptoms, as opposed to the underlying biology.”

 Of course, one company announcing the closure of one wing of medical research doesn’t signal the end of other scientists working in that field – but in light of Pfizer’s dismaying decision, some commentators are wondering what this means for the rest of the big pharma landscape in terms of neuroscience research.

“It’s really alarming to see such a large pharmaceutical company deciding to abandon research into the brain and central nervous system,” chief scientific officer at the Parkinson’s Foundation, James Beck, told the Los Angeles Times.

“[H]aving Pfizer exit does not augur well for what other companies are likely to do.”

That’s especially so since Pfizer’s decision follows a series of clinical failures by other companies pursuing Alzheimer’s research – developments that can be extremely costly for the companies invested in the trials.

We’ll have to wait and see what happens here – and hope the companies committing to this research keep focussed on what’s really at stake here.

“[N]euroscience research is high risk, in that failure for pharmaceutical companies comes at a high price,”Alzheimer’s Research’s director of policy, Matthew Norton, told The Times.

“[But] the potential benefits of success to the millions of people around the world living with dementia are too great to ignore.”

A Pungent Life: The Smells in My Head


I am in my kitchen smelling dirt. Three new plants — a white kalanchoe and two red begonias — sit on a stand at my window. It is April, nearly a decade ago, and I have bought them because it is finally spring. I admire their small, dense flowers and green, waxy leaves.

But I hadn’t planned on their powerful, raw smell. Working around the house, I try to think about something else. When I go upstairs, the smell follows me, earthy, pushy, almost wet. I wonder how it is that I can smell three small houseplants on the floor below.

That afternoon, at the grocery, I can’t shake their dank odor. Could the smell somehow have gotten into my clothes? A day later, miles away at my doctor’s office in Manhattan, I am shocked that it smells there, too. But she has no potted plants.

I finally get it. This assertive smell, my uninvited companion for almost two days, is inside my head, not out. Mortified, I think I must smell. Talking to friends, I cover my mouth with my hand. I brush my teeth more often, swish mouthwash compulsively. But my husband says I smell fine — no bad breath. I finally call my doctor.

I discover that I suffer from phantosmia. “Osmia,” from the Greek osme, means “smell.” Coupled with “phanto” (like “phantom”), it refers to an illusory sense of smell. I smell a smell when no odorant is present.

Inevitably, medical tests followed. I had an M.R.I. of my brain (ruling out a tumor), then a CT scan of my sinuses (looking for infection), and finally, an EEG (olfactory hallucinations do occur in epilepsy). The results were negative, and two rounds of antibiotics (was there a hidden nasal or sinus infection?) constituted my only — and fruitless — treatment.

One day a year later I realized that the earthly smell was finally gone. But to my dismay a new smell immediately took over. My husband had burned a big pot of chili. Burned chili became my new default odor. At least it smelled better than dirt.

Then, about seven years ago, a trip to Provence erased the chili. Lavender wafted in the air, becoming my new smell du jour. Southern France’s lavender-infested landscape — dried bouquets, scented soaps and candles, even flavorings for food — trailed me back home. Some might think me lucky — lavender is hugely popular. But I hated this smell that had squirmed its way into my brain.

I tried in vain to fool my nose. Holding lemons under my nose didn’t kill the odor. Smearing pungent perfumes and lotions around my nose didn’t work either. A powerful odor like ammonia might trump the lavender for a moment, but that cure is worse than the disease.

Sometimes I can’t tell whether a smell is inside or outside my head. Walking my dog, I cried as I smelled manure, convinced it would lodge in my head. At home, I rejoiced that the stink was gone. The next day, the horrid smell reappeared at the same spot. This time I noticed the warning sign: gardeners had spread fertilizer. Only then did I know the smell was real.

Avoiding gruesome odors is my first line of defense. There’s a coffee shop nearby that I simply won’t enter. It’s jam-packed with wooden barrels of reeking coffee beans; locals complain they can smell the roasting blocks away. I send my husband to buy coffee while I wait in the car with the windows up.

I’ve tried the opposite tactic, going out of my way to imprint favorite perfumes, fresh flowers, that wonderful bakery smell. Alas, my phantosmia specializes in the disagreeable.

That is typically the case, I now know. Dr. Donald Leopold, chairman of the department of otolaryngology at the University of Nebraska Medical Center in Omaha, has studied smell disorders for 30 years. In phantosmia, Dr. Leopold says, both the upper nasal passages and the brain play a part, especially the brain, “where the actual smell perception is generated.”

Almost always the patient has lost some ability to smell. Dr. Leopold says that the brain, “which has a propensity to make smell,” overcompensates by offering up odors, usually disagreeable ones, that may have existed previously but were suppressed. It appears that certain “traffic cop” neurons, which had worked to exclude such odors, turn off.

Though Dr. Leopold assures me that “treatment is available,” I haven’t tried the nasal saline drops, antidepressants, antiseizure medicines or sedativesrecommended by one doctor or another. Mainly I try to think past the phantosmia, forcing my attention elsewhere. If that fails, I try to laugh at it, more absurd than awful. I win more of these skirmishes than one might expect.

I learn that this disorder is best kept private. Some friends squirm when they hear about it, as if I were crazy. For that matter, phantosmia is linked to certain psychiatric disorders (schizophreniadepressionAlzheimer’s), but I don’t have them. I do wonder, though, what it means to hallucinate smell. Those neurological explanations aren’t entirely satisfying. There’s nothing plainer than the nose on my face, but nothing more mysterious, either.

Source:nytimes.com

Scientists Have Finally Discovered Why Consuming Red Meat Causes Cancer


Many people grew up being urged to eat pork, beef, and dairy products for their health, but in recent years have received advice to cut back on animal products especially red meat. 

According to a number of studies, the consumption of red meat is linked with increased risk for cancer(s), atherosclerosis (heart disease), stroke, Alzheimer’s, and even Type II Diabetes…  But until now, researchers have not exactly understood why.

As The Telegraph reports, scientists from the University of California in San Diego believe it mainly has to do with sugar. 

While humans, as omnivores, can tolerate eating meat (and have been doing so for many years, but not in the quantity witnessed today) there is unique sugar named Neu5Gc, found in most mammals but not in humans, that triggers an immune responsewhich causes inflammation.

Mice were used for the study which found that all the evidence linking Neu5Gc to cancer was circumstantial or indirectly predicted from experimental setups. According to the scientists, this is the first time they mimicked the exact situation in humans through feeding non-human Neu5Gc and inducing anti-Neu5Gc antibodies. This increased spontaneous cancer in mice.

This sugar can be found in red meats (pork, beef, and other livestock), cow’s milk and certain cheeses. Because the human body is not capable of producing this sugar naturally when the sugar is absorbed into the tissues, it is perceived as a foreign invader and activates the immune system. It is suspected that over time, the chronic inflammation caused by the immune system response plays a role in the development of cancer.

Thus, those who consume red meat on a regular basis are likely to suffer a stronger reaction than those who ingest red meat occasionally.

Source:http://livetheorganicdream.com

Study: Metformin Linked to Higher Risk of Alzheimer’s and Parkinson’s


Metformin and Alzheimer's disease

A recent study found that the use of metformin in people with diabetes increased their risk for developing dementia and Parkinson’s Disease.

This may be surprising as not too long ago, we reported on a different study which found the opposite–that using metformin might lower the risk for dementia in older men.

The study from Taiwanese researchers was presented on March 29, 2017 at The 13th International Conference on Alzheimer’s and Parkinson’s Diseases in Vienna Austria by Dr. Yi-Chun Kuan from the Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.

The researchers found that long-term use of metformin may raise the risk of neurodegenerative disease in those with type 2 diabetes.

How Harmful Might Metformin Be to the Brain?

As reported by Medscape Medical News, Yi-Chun Kuan and team conducted a cohort study to follow a total 9,300 patients with type 2 diabetes in Taiwan for up to 12 years. They checked records for these patients from the National Health research database of Taiwan including 4,651 who had metformin prescriptions and 4651 matched controls who didn’t take any metformin.

Dr. Kuan told Medscape they adjusted for age, sex, and diabetes severity and that despite this, “the cumulative incidences of Parkinson’s and dementia were significantly higher for our metformin cohort” at 12 years.

In fact, the risk for Parkinson’s disease or Alzheimer’s dementia went up over 50 percent during a 12 year period in those who took metformin when compared to those who did not. Researchers also found that “outcome risks increased progressively with higher dosage and longer duration of treatment.”

Dr. Yi-Chun Kuan said, “We’d heard about a possible protective effect from metformin. However, we found the reverse,” and she added that large-scale, prospective studies would need to be done in other countries to get clarification of the results.

Another detail the researchers noted was that outcomes increased the longer a patient was on metformin and the higher the metformin dose they took, “especially with use for more than 300 days and doses greater than 240 g.”

A limitation of the study was that the patients on metformin might also be taking other diabetes drugs like insulin or sulfonylureas and Dr. Kuan said that she and her team would like to follow up on these other possible associations.

There was also no word on what the patient’s HbA1c levels were to help indicate the state of diabetes management nor an explanation on how factors were controlled for, as medical consultant, Dr. Larry Ereshefsky told Medscape.

Could a B12 Deficiency Have Anything to Do With It?

Recently, metformin has been shown to possibly cause B12 deficiency, particularly in those who take it longterm. One of the side effects of a B12 deficiency is neuropathy, or nerve damage.

A serious B12 deficiency has been known to also cause side effects like cognitive difficulties such as memory loss.

While this study still needs a follow-up, if you are concerned about metformin or your B12 levels, talk to your health care provider who can provide testing and if needed, guidance on how to get your B12 levels up.

Source:www.diabetesdaily.com

‘Minibrains’ Could Help Drug Discovery For Zika And For Alzheimer’s


 This image is from lab-grown brain tissue — a minibrain — infected by Zika virus (white) with neural stem cells in red and neuronal nuclei in green.

Some tiny clusters of brain cells grown in a lab dish are making big news at this week’s Society for Neuroscience meeting in San Diego.

Known as “minibrains,” these rudimentary networks of cells are small enough to fit on the head of a pin, but already are providing researchers with insights into everything from early brain development to Down syndrome, Alzheimer’s and Zika.

At a Sunday press conference at the neuroscience meeting, researchers said minibrains are helping them figure out how the Zika virus can disrupt human brain formation in the early stages of fetal development.

Minibrains are highly organized structures that actually start out as human skin cells. They are then coaxed in the lab to become neural stem cells, then to differentiate into some of the different types of cells found in a real brain.

What makes these lab-grown structures so useful is that they replicate part of the cell diversity and connectivity of the human brain, said Dr. Thomas Hartung, a researcher and experimental toxicologist at the Johns Hopkins Bloomberg School of Public Health in Baltimore.

“These cells are communicating,” Hartung said. “These neurons are talking to each other.”

As a result, the minibrains can help researchers answer questions that couldn’t be answered by studying animal brain tissue. “We need human systems to tell us about humans, and that’s why this is such a big step forward,” Hartung said.

The first minibrains were developed a few years ago by scientists in Europe. Since then, researchers at a handful of institutions around the world have begun cranking out these experimental structures.

At Johns Hopkins, Hongjun Song has been working to streamline the process and make minibrains that are closer to the real thing in the way they respond to viruses, for example.

When I visited Song’s lab recently, he took me to a small, windowless room at Hopkins that has a powerful air filtration system, to show me the result of his team’s effort. He opened an incubator the size of a dorm fridge and pointed to a device inside that was only slightly larger than a cell phone.

The device contains a complete factory for these organoids, he said; the system was built by three high school interns using a 3-D printer.

The lower half looks like a miniature muffin pan with a dozen separate compartments. “We can grow up to 10 minibrains in each one,” Song said.

The top half resembles a mechanized Lego project. A small motor powers gears connected to a dozen plastic shafts. They gently stir a precise mixture of cells, nutrients, and growth factors in each compartment.

The minibrains that emerge after several months in the incubator are barely big enough to see with the naked eye, said Dr. Guo-Li Ming, a professor of neurology at Hopkins who is married to Song and collaborates with him on this research.

“It’s basically like a ball of cells clustering together,” she said. “But if you open it up you really see something very similar to the early embryonic brain.”

Though it has only a tiny fraction of the number of cells of an actual brain, a minibrain grows much the way a real brain does during early pregnancy. And that has helped researchers solve a medical mystery involving the Zika virus.

When Zika began making headlines last year, scientists suspected the virus could interfere with brain development in the womb. “But you can’t study that in a mouse,” Ming said, because mice have very few of the developing brain cells that are most vulnerable to Zika infection.

A student suggested that Ming and Song use minibrains to figure out what was happening. So the couple contacted Hengli Tang, a research biologist they knew at Florida State University, who was studying the Zika virus.

That call led to studies of minibrains that showed precisely how the infection was attacking certain neural cells, especially at a point in development equivalent to the first trimester of pregnancy. “It was turning [these cells] into a viral factory,” Song said.

As a result, the minibrains infected with the virus early in their development actually decreased in size, which may help explain why a human fetus infected with the Zika virus early in pregnancy sometimes develops into a baby with a very small brain.

Members of the Hopkins team are presenting details of their Zika findings this week at the neuroscience meeting, and are already planning minibrain studies of other disorders, including autism, schizophrenia and Alzheimer’s.

Elsewhere during the neuroscience meeting, scientists are presenting minibrain research as a model in brain cancer and in developmental disorders, including Down syndrome and Rett syndrome.

Minibrains’ greatest potential, though, may be for testing new drugs for brain disorders, Hartung said. Drug testing with animals has often proved misleading because animal brains just aren’t like human brains, he explained.

“One company after the other failed on things like stroke, multiple sclerosis, [and] also neurodegenerative diseases like Alzheimer’s and Parkinson’s,” Hartung said.

Those failures involved drugs that worked when tested in animals, but failed on people, Hartung said. So he has begun working with pharmaceutical companies to see whether minibrains might offer a better model.

One obstacle to the widespread use of minibrains in research may be public acceptance of the idea that scientists should be growing “brains” in the lab. But people would be less concerned, Hartung said, if they understood the differences between these very small, lab-grown structures and a real brain.

For one thing, minibrains stop growing when they still have only about 20,000 cells. A human brain has many billions. And these clumps of cells, he explained, have no way of learning or becoming conscious.

Nutritional Ketosis Diet May Be Key for Optimal Health


Cancer Prevention

Story at-a-glance

  • Obesity and heart disease, Alzheimer’s and cancer have something significant in common — they’re all rooted in insulin and leptin resistance
  • By eating a high-quality fat, low-carbohydrate diet, you achieve nutritional ketosis; a metabolic state in which your body burns fat rather than glucose as its primary fuel.
  • Maintaining nutritional ketosis may have health benefits in diseases such as obesity, diabetes, cancer, epilepsy, Alzheimer’s, Parkinson’s, ALS, MS, autism, migraines, traumatic brain injuries, polycystic ovary syndrome and much more

Obesity and top killers such as diabetes, heart disease, Alzheimer’s and cancer have something significant in common — they’re all rooted in insulin and leptin resistance.

In other words, the underlying problem is metabolic dysfunction that develops as a result of consuming too many net carbohydrates (total carbs minus fiber) and/or protein. Sugars found in processed foods and grains are the primary culprits, and the standard American diet is chockfull of both.

Once you develop insulin and leptin resistance, it triggers biochemical cascades that not only make your body hold on to fat, but produce inflammation and cellular damage as well.

Hence, whether you’re struggling with weight and/or chronic health issues, the treatment protocols are the same. This is good news, as it significantly simplifies your approach to improving your health. You won’t need a different set of strategies to address each condition.

In short, by optimizing your metabolic and mitochondrial function, you set yourself squarely on the path to better health. So how do you correct these metabolic imbalances? Your diet is key. The timing of your meals can also play an important role.

Nutritional Ketosis May Be Key for Optimal Health

By eating a healthy high-fat, low-carbohydrate and low- to moderate-protein diet, you enter into what is known as nutritional ketosis: a state in which your body burns fat as its primary fuel rather than glucose (sugar). Mounting research suggests nutritional ketosis is the answer to a long list of health problems, starting with obesity.

In fact, emerging scientific evidence suggests a high-fat, low-net carb and low- to moderate-protein diet (in other words, a diet that keeps you in nutritional ketosis) is ideal for most people.

In fact, endurance athletes are turning away from conventional high-carb strategies and adopting this way of eating because it boosts physical stamina and endurance.

Beyond insulin resistance and type 2 diabetes, there are a number of applications for nutritional ketosis, including as a treatment for seizures, especially in kids who are unresponsive to drugs, and in neurological conditions such as Alzheimer’s and Parkinson’s. Cancer is another area where ketogenic diets show great promise.

Other benefits include fewer hunger pangs and a dramatic drop in food cravings once you’ve made the shift from burning sugar to burning fat as your primary fuel. Being an efficient fat burner may also boost your longevity. Researchers have identified about a dozen genes associated with longevity.

According to Jeff Volek, Ph.D., a registered dietitian and professor in the Human Science Department at Ohio State University, who has done enormous work in the field of high-fat, low-carbohydrate diets and has authored several books on this topic, the primary function of one of these genes is to cripple the degradation of branched-chain amino acids (BCAAs), such as leucine.

Preventing this degradation can help preserve your muscle mass.1 BCAAs have other benefits as well: In a number of studies involving middle-aged animal models, adding BCAAs increased muscle and cardiac mitochondrial biogenesis (the creation of new mitochondria), improving both health span and longevity.

Interestingly, BCAAs are very similar in structure to ketones — energy molecules created by your liver from fats — and ketones seem to be preferentially metabolized.

In other words, ketones spare those branched-chain amino acids, leaving higher levels of them in circulation while also helping you retain muscle mass and promoting longevity.

Ketones — A Healthy, Clean-Burning Fuel

The primary reason that so many people are overweight and/or in poor health these days is that the Westernized diet is overloaded with non-fiber carbs as the primary fuel, which in turn inhibit your body’s ability to access and burn body fat.

High-quality fats, meanwhile, are a far preferable fuel, as they are utilized far more efficiently than carbs. When you burn fat as your primary fuel, your respiratory quotient (the amount of oxygen you need) typically goes down,2 which is a sign that your metabolism is running more efficiently.

How to Enter Into Nutritional Ketosis

The most efficient way to train your body to use fat for fuel is to remove most of the sugars and starches from your diet, and that’s true for everyone, whether you’re an elite athlete or a sedentary diabetic. At the same time, you’ll want to replace those carbs with healthy fats.

A dietary intake of about 50 grams or less per day of net carbs while also keeping protein low-to-moderate is usually low enough to allow you to make the shift to nutritional ketosis (the metabolic state associated with an increased production of ketones in your liver; i.e., the biological reflection of being able to burn fat).

This is only a generalization, as each person responds to foods in a different way. Some people can enter into full ketosis while eating as much as 70 to 80 grams of non-fiber carbs. Others, especially if you’re insulin resistant or have type 2 diabetes, may require less than 40 grams, or even as little as 30 grams per day, to get there.

To find your personal carb target, it’s important to measure not just your blood glucose but also your ketones, which can be done either through urine, breath or blood.

This will give you an objective measure of whether or not you’re truly in ketosis, rather than just relying on counting the grams of carbohydrates you consume. Nutritional ketosis is defined as blood ketones that stay in the range of 0.5 to 3.0 millimoles per liter (mmol/L).

That said, using a nutrient tracker will radically improve your ability to understand how much and what kind of foods help you to keep to your ketogenic diet nutrient targets while also helping you to assess the nutrient value of your food choices.

My first choice is Cronometer.com/mercola. That’s my upgrade to the basic Cronometer nutrient tracker, and the default is set to macronutrient levels that will support nutritional ketosis.

Avoid Milk and Consider MCT Oil

Aside from added sugars and grains, it is best to avoid milk for the time being, as it can be difficult to stay in ketosis if you eat or drink a lot of it.

The galactose in milk is a carbohydrate and you can easily exceed your net carb allotment by drinking a single glass of milk. Casein, the primary protein in milk, can also trigger or contribute to inflammation.

When you keep net carbs low, your body switches to burning fat for fuel and your liver begins to convert some of that fat into ketone bodies. This is endogenous production, meaning that they are made by your body from your fat stores or from the fats in the foods that you eat.

You can boost your level of ketones by taking them in supplement form, but these exogenous ketones (made in a lab, not in your body) are not likely to be as beneficial unless you are already “low carb.” Food oils such as medium chain triglyceride (MCT)  coconut oil can also be used to mildly increase ketone levels.

Ketogenic Diet Has Long Track Record of Use for Epileptic Seizures

Authority Nutrition reviews 15 health conditions shown to respond favorably to a ketogenic diet,3 and that’s likely a short list.

Based on my understanding of mitochondrial health and metabolic function, a vast majority of health conditions could fall into this category. One of the conditions for which a ketogenic diet has the longest and best documented track record is epilepsy.

This diet has been effectively used to treat drug resistant epileptic seizures since the 1920s,4 and studies have confirmed it’s helpful for both children and adults.

In my view, it would be wise to implement a ketogenic diet as a first-line therapy, but in conventional medicine, it’s typically not considered or recommended unless the patient fails to respond to medication.

Even then, this conversation may have to be initiated by the patient, or the parent of a child with seizures. As noted in the featured article:5

“Research shows that seizures typically improve in about 50 percent of epilepsy patients who follow the classic ketogenic diet. This is also known as a 4:1 ketogenic diet because it provides four times as much fat as protein and carbs combined.

The modified Atkins diet (MAD) is based on a considerably less restrictive 1:1 ratio of fat to protein and carbs. It has been shown to be equally effective for seizure control in most adults and children older than two years of age.”

Nutritional Ketosis Improves Your Brain Health

Your brain will work better in general when burning fat rather than glucose, as fat has been shown to be both neurotherapeutic and neuroprotective. While fats are unable to cross the blood brain barrier, ketones, being water-soluble fats, can cross it and feed your brain. They also appear to lower markers of systemic inflammation, such as IL-6 and others. Many times, improved cognition and mental acuity are among the first things people notice when entering nutritional ketosis.

Ketones are the preferred source of energy for your brain in general, but especially for those affected by diabetes, Alzheimer’s, Parkinson’s and maybe even ALS, because in these diseases certain neurons have become insulin resistant or have lost the ability to efficiently utilize glucose, which causes the neurons to die off. When ketones are present, these neurons have a better chance of surviving and thriving.

In one study, Parkinson’s patients who followed a 4-to-1 ketogenic diet experienced, on average, a 43 percent improvement in their symptoms after one month.6 For Alzheimer’s, supplementing with MCT oil appears to be particularly beneficial.7,8

Studies also support the use of nutritional ketosis for autism. As noted in the featured article, “Autism shares some features with epilepsy, and many people with autism experience seizures related to the over-excitement of brain cells.” Research shows nutritional ketosis helps dampen this excessive activity; in one pilot study,9 a majority of autistic children showed improvement after following a cyclical ketogenic diet for six months.

Unlike blood glucose, blood ketones do not stimulate an insulin surge. They also do not need insulin to help them cross cell membranes, including neuronal membranes. Instead, they use simple diffusion, so they can even enter cells that have become insulin resistant. This is likely one of the reasons nutritional ketosis works so well for a variety of neurological problems and diseases. It even shows promise for:

  • Migraine headaches: Following a ketogenic diet for four weeks has been shown to reduce migraine frequency and lower the use of pain medication.10,11
  • Traumatic brain injuries: Animal studies suggest it can help reduce brain swelling, improve motor function and speed up recovery, although it appears more effective in the young than the old. Human studies still need to validate these findings.12

Metabolic Conditions Improve on Ketogenic Diet

Nutritional ketosis is also indicated for obesity, metabolic syndrome (prediabetes) and diabetes. This is not surprising, considering the fact that one of its beneficial effects is correcting insulin resistance. If you meet at least three of the following criteria, you may be diagnosed with metabolic syndrome: abdominal obesity, elevated triglycerides, low HDL cholesterol, high blood pressure and/or elevated fasting blood sugar. Nutritional ketosis has been shown to improve most of these.

Nonalcoholic fatty liver disease (NAFLD), which is strongly associated with obesity, type 2 diabetes and metabolic syndrome, has also been shown to improve on a low-carb diet high in healthy fats. In one study,13 obese men diagnosed with metabolic syndrome and NAFLD showed significant improvement in their weight, blood pressure, liver enzymes and liver fat after four months on a ketogenic diet; 21 percent completely resolved their NAFLD.

Glycogen storage disease (GSD) and glucose transporter 1 (GLUT1) deficiency syndrome are two other conditions for which a ketogenic diet is a literal life saver. GSD is characterized by a lack of an enzyme that helps store glucose as glycogen or break glycogen down into glucose. The exact form of the disease depends on which enzyme in question that’s lacking. As noted by Authority Nutrition:

“GSD patients are often advised to consume high-carb foods at frequent intervals so glucose is always available to the body. However, early research suggests that a ketogenic diet may benefit people with some forms of GSD, [for example] GSD III, also known as Forbes-Cori disease … [and] GSD V, also known as McArdle disease … “

In GLUT1 deficiency syndrome (a rare genetic disease), you lack a protein that helps shuttle blood sugar into your brain. Seizures and impaired motor skills are two common symptoms that typically manifest shortly after birth. The benefit of a ketogenic diet is quite apparent in this case, as ketones do not need this protein in order to enter your brain. Hence ketones are an ideal fuel for GLUT1 deficient people, allowing their brains to function more normally.

Hormonal and Nervous System Disorders May Improve on Ketogenic Diet

Your hormone regulation and nervous system may also benefit from being an effective fat burner. Polycystic ovary syndrome (PCOS) and multiple sclerosis (MS) are two conditions that appear to respond well to this switch in primary fuel. PCOS, which puts women at an increased risk of developing insulin resistance, diabetes, infertility, coronary artery syndrome, lipid disorders (such as elevated cholesterol and high blood pressure) and possibly breast cancer, is characterized by:

  • Hyperinsulinemia (insulin resistance with elevated serum insulin levels)
  • Increased androgen (male hormone) production, causing facial hair and/or acne
  • The complete or almost complete lack of ovulation
  • Obesity

In one study,14 women diagnosed with PCOS who followed a ketogenic diet for six months lost an average of 12 percent of their body weight and reduced their fasting insulin by an average of 54 percent. Levels of sex hormones also showed improvement, and 2 of the 11 women were able to get pregnant despite a history of infertility.

MS, an autoimmune disease, results in damage to the myelin sheath (the protective nerve covering), causing symptoms such as numbness, loss of balance and declining motor function, as well as vision and memory problems. As noted in the featured article: “One study15 of MS in a mouse model found that a ketogenic diet suppressed inflammatory markers. The reduced inflammation led to improvements in memory, learning and physical function.”

Nutritional Ketosis May Be the Key to Cancer Prevention

Cancer is a devastating disease, and today it’s hard to find anyone whose life hasn’t been affected in some way by this disease. In fact, it’s become one of the leading causes of death around the world. What’s worse, the medical profession is largely ignorant of the fact that most cancers are rooted in metabolic and mitochondrial dysfunction, and hence the conventional prevention recommendations do little to nothing to quell the tide of cancer diagnoses.

It is my belief, as well as that of many of the experts I have interviewed, that over 90 percent of cancer cases are either preventable or treatable. The key is recognizing that cancer is really a mitochondrial metabolic disease, rooted in poor diet choices combined with a toxic lifestyle.

Viewing cancer as a metabolic disease — opposed to a disease of damaged DNA, which is a downstream effect of mitochondrial dysfunction — gives us the power to control this dysfunction by carefully choosing foods and nutrients and employing strategies that help optimize the biochemical pathways that suppress cancer growth while simultaneously stimulating mechanisms to push it into remission.

Nutritional ketosis has received a lot of attention by cancer researchers in recent years, and many studies show it has great potential not just as a form of cancer prevention but also treatment — in combination with other treatments such as chemotherapy and radiation.16 Research is looking at whether non-toxic metabolic therapies and drug cocktails may be just as effective, with less toxicity.

In fact, according to Dr. Thomas Seyfried, who is one of the leading academic researchers of nutritional interventions for cancer, the mechanism by which the ketogenic diet manages cancer is far clearer and more readily understood than the way the ketogenic diet manages epileptic seizures. This is ironic considering that it’s barely recognized, let alone applied, within oncology circles, while it’s been an accepted treatment for epilepsy since the 1920s.

The central premise is that since cancer cells need glucose and insulin to thrive, lowering the glucose level in your blood though carb and protein restriction literally starves the cancer cells. Additionally, low protein intake tends to dampen the mTOR pathway that is often responsible for accelerating cell proliferation.

Correcting Metabolic Dysfunction and Optimizing Mitochondrial Health Paves the Way for a Long, Healthy Life

I have come to recognize that mitochondrial dysfunction is at the core of what is causing your system to go haywire. You have thousands of mitochondria in nearly all of your cells and they generate around 90 percent of the energy you need for health and survival.

When large numbers of them cease to function properly, your body can no longer function as intended, setting you up for developing any number of diseases. For some, it may manifest as diabetes or heart disease; in others, it shows up as cancer or some form of neurodegenerative disease.

The remedy lies in optimizing your mitochondrial function and correcting the metabolic dysfunctions of insulin and leptin resistance. Here, we have focused on the benefits of a ketogenic diet, which means eating foods high in healthy fats, with moderate protein and low net carbs (think non-fiber carbs).

The choices you make in dietary fats are really critical, as fatty acids contribute to the formation of cellular membranes, and it’s virtually impossible to have optimal biological function with impaired cell membranes. So dietary fat serves two purposes; first, as a fuel, but also as the building blocks for the structural components of your body.

Most Americans unknowingly consume large quantities of harmful fats, like processed vegetable oils, which contribute to your deterioration over time. So when I talk about dietary fats, I’m referring to natural, unprocessed fat, found in whole foods like seeds, nuts, butter, olives, avocado, coconut oil, raw cacao or cacao butter. But also remember that MCT oil has some great health benefits as well.

Other Strategies That Promote Healthy Fat Burning

Two other strategies that will help you make the transition from burning sugar to burning fat as your primary fuel are:

Extended or intermittent fasting, such as Peak Fasting. Intermittent fasting is an alternative to extended fasts. While I used to recommend skipping breakfast and making lunch your first meal, I eventually learned that for most, skipping dinner is a far more effective strategy.

This is because you are the least metabolically active while you are sleeping, so the last thing you want to do is add fuel you don’t need in the evening. Doing so will simply generate excess dangerous free radicals.

However, this may be enormously challenging for most people to implement. It’s easy for most people in nutritional ketosis to skip breakfast because they’re not hungry anyway but skipping dinner may seem more like a hardship. Most people view breakfast as an obligation and dinner as more of a social event. If you can’t skip dinner, allow at least three to six hours between this last meal and bedtime.

The challenge then becomes to determine the most appropriate time to eat your breakfast. I wear a 24-hour glucose monitor and I have learned that I can pin-point the ideal time to break my fast by tracking my glucose. You can, too, even without this specialized monitor. Simply measure your glucose at regular intervals in the morning, and when you notice your glucose level rising, even though you haven’t eaten, it’s a sign you’re undergoing gluconeogenesis.

Basically, your body is starting to break down protein (muscle), turning it into glucose. This is not a healthy process, so when this occurs, you’ll want to eat something to avoid muscle degeneration. In my experience, that will typically occur after 16 hours of fasting or so, although it’s highly individual. If you’re a competitive athlete, this strategy may not be appropriate, but it could work for most average people.

Exercising is a great way to increase mitochondrial repair and regeneration as it is a potent stimulus of PGC1 alpha which is likely the most potent stimulus in your body for mitochondrial biogenesis.

Source:.mercola.com

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