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02/27/20

Cancer mutations can be caused by common gut bacteria. By exposing human mini-guts to a particular strain of Escherichia coli, scientist uncovered that these bacteria induce a unique mutational pattern in human DNA. This pattern was also found in colon cancer patients, implying that the bacteria induced these mutations. For the first time the researchers establish a direct link between microbes and mutations driving tumorigenesis. This might lead to new measures in colorectal cancer prevention.

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Our skin protects us from physical injury, radiation and microbes, and at the same time produces hair and facilitates perspiration. Details of how skin cells manage such disparate tasks have so far remained elusive. Now, researchers have systematically mapped skin cells and their genetic programs, creating a detailed molecular atlas of the skin in its complexity.

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An international team of researchers identifies a compound that corrects genetic abnormalities involved in the onset and progression of Huntington's disease for which there is no definitive treatment. They successfully reversed disease-causing DNA expansion mutations with no off-target effects in the lab. They hope that their discovery may help treat other DNA repeat diseases like myotonic dystrophy.

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The Nutrition Labeling and Education Act of 1990 (NLEA) mandated nutrition labeling on most packaged foods. These include canned and frozen foods, breads, cereals, desserts, snacks, beverages, and a variety of other foods that line the aisles of grocery stores. Food labels — officially called Nutrition Facts labels — are intended to help consumers choose healthy foods. It is the FDA’s responsibility to make sure that foods are properly labeled.

Over the years there have been many changes to the initial law, and to the label. The newest version of the food label rolled out on January 1, 2020 for larger food manufacturers; smaller manufacturers have until January 1, 2021 to introduce the new labels.

Here’s a rundown of features you’ll encounter on the new food labels.

Serving size

The new food label shows “servings per container” and “serving size” in a larger font size and a bolder type. Per the NLEA, serving sizes must be based on the Reference Amounts Customarily Consumed (RACCs) — that is, the amounts that people are actually eating, not what recommendations suggest they should be eating. The amounts that people eat and drink have changed since 1993, when the previous serving size requirements were published. For example, in 1993 the reference amount used for a serving of soda was 8 ounces; it will now be 12 ounces. A serving of ice cream has also increased, from 1/2 cup to 2/3 cup.

For packages that are between one and two servings, such as a 15-ounce can of soup, the label will now treat the package as a single serving, since people usually consume it at one time.

Certain foods and beverages that are larger than a single serving but could be eaten in one sitting will now display two columns: one showing calories and other nutrients per serving, the other showing the same information for the entire package.

Calories

Calories will now be displayed much more prominently on the label. But you’ll no longer see “calories from fat” on the food label, since research has shown that the type of fat in a food is more important than the amount of fat.

Added sugars

One of the biggest changes is that the new food labels will specify the amount of added sugar — sugars that are added during food processing. Added sugars are a bigger concern than natural sugars, which occur naturally in all foods that contain carbohydrates, including fruits and vegetables, grains, and dairy products.

Research shows that it is difficult to meet nutritional needs while staying within calorie limits if you consume more than 10% of your total daily calories from added sugar (added sugars will appear on the label in both grams and percent daily value). Too much added sugar can also lead to weight gain and other health problems, including diabetes and heart disease.

Dietary fiber

The FDA definition of fiber, which is used as a guideline for what appears on food labels, includes both naturally occurring fibers and fibers added to foods that show a physiological health benefit. Fiber is naturally present in vegetables, whole grains, fruits, cereal bran, flaked cereal, and flours. In addition, some nondigestible carbohydrates that are added to food also meet the FDA’s definition of dietary fiber, and are accounted for in the dietary fiber value on the new food label.

Nutrients and daily values

The list of nutrients that appear on the food label has been updated. Vitamin D and potassium will now be required; vitamins A and C will no longer be required, since deficiencies of these vitamins are rare today. Calcium and iron will continue to be required. Manufacturers must declare the actual amount, in addition to percent daily value, of vitamin D, calcium, iron, and potassium. In the old food label, manufacturers only needed to include percent daily value of these nutrients.

Daily values are reference amount of nutrients to consume or not to exceed, and are used to calculate the daily value percentages on the label. This can help the consumer use the nutrition information in the context of a total daily diet. They are based on 2,000 calories, which is a reference number of calories for general advice. Individuals may need less or more than 2,000 calories per day depending upon their specific needs.

The daily values for nutrients like fiber, sodium, vitamin D, and potassium have all been updated based on the most recent research from the Institute of Medicine, and the 2015 Dietary Guidelines Advisory Committee Report used in the development of the 2015–2020 Dietary Guidelines for Americans.

With its more realistic measure of serving size and emphasis on calories and added sugars, the new food label has the potential to help consumers make healthier food choices.

Source: FDA

The post What’s new with the Nutrition Facts label? appeared first on Harvard Health Blog.



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Researchers have used cryo-electron microscopy to elucidate for the first time the structure and function of a very small enzyme embedded in cell membranes. This enzyme builds complex sugar trees that are subsequently attached to other membrane proteins. The findings could accelerate the development of new, protein-based medications.

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The same way baking soda breaks down grease and grime, making surfaces easier to clean, researchers now show that a new therapeutic molecule can break apart communities of harmful bacteria, opening the way for bacteria-killing antibiotics to more effectively clear out infections.

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Compounds containing metals could hold the key to the next generation of antibiotics to combat the growing threat of global antibiotic resistance. Researchers, working with a network of international collaborators, have discovered 23 previously unexplored compounds containing metals such as silver, manganese, zinc, ruthenium and iridium that have antibacterial and antifungal activity.

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For the vast majority of people, the benefits of physical exercise outweigh the risks. However, for those who have inadequate training or who have underlying heart problems that may not have been detected, the risks of heart issues from extreme exercise, such as participation in marathons and triathlons, are increased.

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According to the U.S. Centers for Disease Control and Prevention,1 nearly 805,000 Americans have a heart attack each year, and 605,000 are first heart attacks. Knowing the risk factors, symptoms and how to take early action will increase your chances of survival.

However, what may look and feel like an apparent heart attack may actually be a panic attack, and according to researchers, the cost of misdiagnosing noncardiac chest pain is high.2 "It is important for physicians to be able to recognize panic attacks and to distinguish them from cardiac disease, thus avoiding unnecessary use of health care resources," one report states.3

An investigation4 published in 1996 found that 25% of emergency room patients presenting with chest pain met the DSM-III-R criteria for panic disorder, yet attending emergency department cardiologists failed to recognize patients having a panic attack 98% of the time. As noted by the authors:5

"Panic disorder is a significantly distressful condition highly prevalent in ED [emergency department] chest pain patients that is rarely recognized by physicians. Nonrecognition may lead to mismanagement of a significant group of distressed patients with or without coronary artery disease."

So, just how do you tell the two apart? Before we get into those details, let's take a look at the common signs and symptoms associated with each.

Symptoms of Heart Attack

When a heart attack starts, blood flow to your heart has suddenly become blocked and the muscle can't get oxygen. If not treated quickly, the muscle fails to pump and begins to die. While often a result of coronary heart disease, a heart attack can also be caused by a blood clot blocking an artery. Some of the most common symptoms of a heart attack include:6

Chest pain or discomfort

Upper body discomfort

Shortness of breath

Breaking out in a cold sweat

Nausea

Sudden dizziness

Feeling unusually tired

Lightheadedness

Symptoms of Panic Attack

A panic attack typically comes on abruptly, producing intense fear and a sense of impending doom or even death that is typically severely disproportionate to the situation at hand. Common symptoms include:

Hyperventilation

Chest pain

Heart palpitations

Trembling

Sweating; hot or cold flashes

Nausea

Dizziness or lightheadedness

Numbness and/or tingling sensations

Panic attacks tend to peak within 10 minutes, and most subside within 30 minutes. Few last more than one hour. It's not uncommon for people to seek medical help, thinking they're having a heart attack or are dying, when panic attacks first set in and they're unfamiliar with the symptoms.7

How to Tell Them Apart

While it can be very difficult to tell a panic attack from a heart attack, some generalizations can be made that can help tell them apart.8

  • Pain onset — The chest pain associated with a heart attack will typically start as a feeling of pressure, fullness or aching that escalates, reaching maximum severity after a few minutes, whereas the pain associated with a panic attack tends to be sharp and stabbing in the center of the chest, typically lasting only five to 10 seconds.
  • Pain location — The location of the pain also tends to differ between the two. Whereas panic-associated pain is localized in one small area of the chest, heart attack symptoms typically include pain or discomfort that radiates from the chest into other areas, such as one or both arms, abdomen, back, shoulders, neck, throat or jaw.

Don't Ignore Your Symptoms

When in doubt, seek immediate medical attention. It's better to be safe than sorry, as sudden death is the most common symptom of a heart attack. As noted by Dr. Sam Torbati, medical director of the Ruth and Harry Roman Emergency Department in an interview for Cedars-Sinai Medical Center:9

"Unfortunately, there is great crossover between the symptoms of panic attack and heart attack, making it very challenging to discern between the two without a physician assessment and testing, such as an EKG.

Common symptoms that may affect patients with either a panic or heart attack include chest pain, shortness of breath, dizziness, sweating, passing out, tingling, or a sensation of impending doom.

These shared symptoms of heart and panic attack may also be caused by other serious conditions such as blood clots, lung infection or collapse, or tear in the large vessels of the chest for patients with certain pre-existing risk factors. So when in doubt, seek immediate medical attention …

The best predictor as to whether symptoms are due to panic versus heart attack is the patient's age and previous history of panic attacks … Patients should immediately go to the ER if they have new onset chest pain (tightness, squeezing, heaviness), shortness of breath, sweating, lightheadedness, pain that radiates to the jaw or arm, or a ripping sensation in their chest or back.

Heart attacks tend to occur in middle-aged people and older age groups, so the older the person is, the lower a threshold they should have for coming to the ER right away.

Patients with pre-existing coronary artery disease and those with risk factors associated with coronary artery disease should also be evaluated immediately, including those with hypertension, diabetes, obesity, high cholesterol, or a history of smoking."

Possible Connection Between Panic Disorder and CAD

It's also worth getting your symptoms checked out even if you're certain they're due to a panic attack. Some research suggests there may in fact be a connection between panic disorder and coronary artery disease, although the exact relationship is still unclear. According to a 2008 review in The Primary Care Companion to the Journal of Clinical Psychiatry:10

"There are several reasons to consider that a relationship between panic disorder and coronary artery disease (CAD) might exist. First, panic disorder has been linked to other forms of cardiac disease.

Second, the most likely source of the chest pain during panic attacks is ischemia. Finally, there is evidence that panic disorder may be associated with cardiovascular risk factors, such as hypertension, hyperlipidemia, and smoking.

Panic disorder is associated with several cardiac abnormalities. In addition to patients with panic disorder having elevated standing heart rates, 10% have an arrhythmia.

Panic disorder is associated with increased left ventricular mass and diameter, and patients with panic disorder have poorer cardiovascular fitness as demonstrated by lower maximum oxygen consumption and decreased exercise tolerance …

Case reports have linked panic disorder to a descending aortic aneurysm and pulmonary hypertension secondary to an atrial septal defect with pulmonic valve disease. However, the strongest association is between panic disorder and mitral valve prolapse (MVP) … but MVP is not likely to be the source of chest pain.

In addition, the significance of the panic-MVP relationship is unclear … Indirect linkages via autonomic vulnerability or dysfunction have … been proposed. However, the most likely explanation is that the decreased left ventricular volume due to the tachycardia seen in panic disorder produces the MVP."

The review11 cites evidence suggesting ischemia is the cause of the chest pain felt during a panic attack, and researchers have found there's an association between panic attacks and ischemic and nonischemic chest pain alike. According to the authors, "Myocardial ischemia could cause panic attacks via increased catecholamines or cerebral carbon dioxide levels secondary to lactate."

What's more, when looking at a large managed care database, researchers found an association between panic disorder and coronary heart disease and this association remained even after controlling for covariates.12

Overall, patients with panic disorder were between 80% and 91% more likely to also have coronary heart disease. Patients diagnosed with both panic disorder and depression were, on average, 260% more likely to develop coronary heart disease than patients without those mental health problems.13

On the flip side, research14 published in 2017 also points out that "Anxiety and its associated disorders are common in patients with cardiovascular disease and may significantly influence cardiac health." According to this paper:

"Both physiologic (autonomic dysfunction, inflammation, endothelial dysfunction, changes in platelet aggregation) and health behavior mechanisms may help to explain the relationships between anxiety disorders and cardiovascular disease."

Many Women Mistake Heart Attack Symptoms for Anxiety

It's also important to realize that the symptoms of heart attack can vary from person to person and some may have very few symptoms, especially women.15 Importantly, research16,17 shows women are less likely to report chest pain when having a heart attack.

They're also less likely to suspect their discomfort is related to a heart problem. Compared to just 11.8% of men, 20.9% of women attributed their chest pain to stress or anxiety. Women also tend to describe their pain differently. They're more likely to use terms such as "pressure," "tightness" or "discomfort" in the chest rather than referring to it as "chest pain."

Doctors are also more likely to dismiss women's complaints of chest pain as being noncardiac in nature. Overall, 53% of female heart attack patients reported that their doctor did not think their symptoms were heart-related, compared to 37% of male heart attack patients.

Approximately 29.5% of women had actually sought medical help before being hospitalized with a heart attack, compared to just 22.1% of men. What these findings suggest is that women and their doctors tend to misdiagnose or dismiss symptoms of heart attack, placing women at a higher risk of death than men. As noted by the authors:18

"The presentation of AMI [acute myocardial infarction] symptoms was similar for young women and men, with chest pain as the predominant symptom for both sexes.

Women presented with a greater number of additional non-chest pain symptoms regardless of the presence of chest pain, and both women and their health care providers were less likely to attribute their prodromal symptoms to heart disease in comparison with men."

Unfortunately, the absence of chest discomfort is a strong predictor of diagnosis and treatment delays.19 For this reason, it's important to remember there are many other symptoms that might indicate a heart attack in progress, including the following:20

Anxiety attack

Back pain

Heartburn

Hot flashes

Extreme fatigue

Feeling electric shocks down on the left side of your body

Numbness and stiffness in the left arm and neck

Feeling like you have a large pill stuck in your throat

Breathe Right to Quell Panic Attacks

When it comes to panic attacks, familiarizing yourself with the function of your fight-or-flight response can be helpful to guide you toward self-help strategies that work for your unique situation.

For example, contrary to popular belief, taking deep breaths can actually worsen a panic attack, as explained by Buteyko Breathing expert Patrick McKeown. A breathing exercise that can help quell anxiety and panic attacks is summarized below.

This sequence helps retain and gently accumulate carbon dioxide (CO2), leading to calmer breathing and reduced anxiety. In other words, the urge to breathe will decline as you go into a more relaxed state.

  • Take a small breath into your nose, a small breath out; hold your nose for five seconds in order to hold your breath, and then release to resume breathing.
  • Breathe normally for 10 seconds.
  • Repeat the sequence several more times: small breath in through your nose, small breath out; hold your breath for five seconds, then let go and breathe normally for 10 seconds.

McKeown has also written a book specifically aimed at the treatment of anxiety through optimal breathing, called "Anxiety Free: Stop Worrying and Quieten Your Mind — Featuring the Buteyko Breathing Method and Mindfulness," which can be found on Amazon.com.21

In addition to the book, ButeykoClinic.com also offers a one-hour online course and an audio version of the book, along with several free chapters22 and accompanying videos.23

EFT — A Long-Term Solution to Anxiety

Energy psychology techniques such as the Emotional Freedom Techniques (EFT) can also be very effective for anxiety and panic attacks.24,25,26 EFT is akin to acupuncture, which is based on the concept that a vital energy flows through your body along invisible pathways known as meridians.

EFT stimulates different energy meridian points in your body by tapping them with your fingertips, while simultaneously using custom-made verbal affirmations. This can be done alone or under the supervision of a qualified therapist. By doing so, you reprogram the way your body responds to emotional stressors.

EFT is particularly powerful for treating stress and anxiety because it specifically targets your amygdala and hippocampus, which are the parts of your brain that help you decide whether or not something is a threat.27 EFT has also been scientifically shown to lower cortisol levels,28 which are elevated when you're stressed or anxious.

In the video above, EFT therapist Julie Schiffman demonstrates how to tap for panic attacks. Please keep in mind that while anyone can learn to do EFT at home, self-treatment for serious issues like persistent anxiety is not recommended. For serious or complex issues, you need someone to guide you through the process. That said, the more you tap, the more skilled you'll become.

Heart Attack Prevention

As for heart attacks, your best course of action is to take proactive measures to prevent them. According to a 2015 study, more than 70% of heart attacks could be prevented by implementing:29

  • A healthy diet
  • Normal body mass index
  • Getting at least 2.5 hours of exercise each week and watching television seven or fewer hours per week
  • Avoiding smoking
  • Limiting alcohol to one drink or less per day

To this I would add maintaining a healthy iron level is important for your heart, as various studies show that both iron deficiency and iron overload30 can be a significant risk factor for heart attack.

For example, a Scandinavian study31 found elevated ferritin levels raised men's risk of heart attack two- to threefold. Another32 found elevated ferritin raised the risk of a fatal heart attack by 218% in men, while women with high levels were 5.53 times more likely to have a fatal heart attack.

As discussed in "Why Hard Water Decreases Heart Attacks," magnesium insufficiency has also been implicated in heart attacks, so you want to make sure you're getting enough magnesium from your diet and/or supplements. In "Could You Have a Heart Attack and Not Know It?" I also review some of the underlying issues that cause heart attacks, and additional steps you can take to lower your risk.



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Alzheimer’s disease, a condition characterized by an accumulation of beta-amyloid plaques and neurofibrillary tangles in the brain, affects an estimated 5 million Americans; this number is expected to reach 14 million by 2060.1 With no known cure, researchers are scrambling to find treatments, often with a misguided focus on drugs designed to remove excess beta-amyloid in the brain.

Drug development for Alzheimer’s has so far been a dismal failure, with 300 failed trials to date.2 Despite the history of letdowns, the latest failed drug trial is still making waves in the research community because there were high hopes that it would provide a breakthrough treatment for people with gene mutations known to cause Alzheimer’s.

Now, with the experimental drugs failing to lead to improvements, researchers are asking if the focus on drugs to target and neutralize beta-amyloid in the brain is all wrong, and if other potential targets should become the focus of future research.3

Two Experimental Drugs Fail to Improve Alzheimer’s

The study, which was a collaboration between Washington University in St. Louis, drug companies Eli Lilly and Roche, the National Institutes of Health and others, involved 194 participants, of which 52 took Roche’s drug gantenerumab and 52 took Eli Lilly’s solanezumab.

The drugs were intended to remove beta-amyloid from the brain, and while the researchers are still evaluating this outcome, they failed to achieve the primary outcome of the study, which was slowed cognitive decline, as measured by tests on thinking and memory.

The study, Dominantly Inherited Alzheimer Network-Trials Unit (DIAN-TU), involved people with an inherited form of early-onset Alzheimer’s known as dominantly inherited Alzheimer’s disease or autosomal dominant Alzheimer’s disease, which account for less than 1% of Alzheimer’s cases.4

While in most cases Alzheimer’s symptoms begin after the age of 60, and risk increases with increasing age, people with this early-onset Alzheimer’s may begin to experience memory decline in their 30s, 40s or 50s. However, the brain changes that occur are similar in both those with inherited Alzheimer’s and the more common sporadic Alzheimer’s, so a treatment that works in one will likely work in the other.

According to a Washington University School of Medicine in St. Louis news release, a silent phase of Alzheimer’s occurs up to 20 years before symptoms develop. Study participants were expected to develop symptoms within 15 years of enrolling in the study or had very mild symptoms at the beginning of the study. Most also had early signs of the disease in their brains. Researchers explained:5

“People who inherit the mutation are all but guaranteed to develop symptoms at about the same age their parents did. While devastating for families, such mutations allow researchers to identify people in the early stages of the disease before their behavior and memory begin to change.”

The news that the drugs had failed came after an average of five years of follow-up and was a shock even to the researchers. “It was really crushing,” lead study author Dr. Randall Bateman of Washington University St. Louis told The New York Times.6 However, should it have been so shocking, considering both drugs have failed previously?

Experimental Drugs Have Failed in the Past

Researchers with the featured study are still wondering whether the experimental drugs could work at different doses or if they would work better if they were started even earlier. However, past studies suggest the drugs are useless for Alzheimer’s.

In one study of solanezumab, published in The New England Journal of Medicine in 2018, patients with mild dementia due to Alzheimer’s disease received solanezumab or placebo intravenously every four weeks for 76 weeks.7 The drug did not significantly affect cognitive decline, and the researchers even suggested this could be because the target is all wrong:8

“ … [S]olanezumab was designed to increase the clearance of soluble Aβ [amyloid-beta] from the brain, predicated on the Aβ hypothesis of Alzheimer’s disease — that the disease results from the overproduction of or reduced clearance of Aβ (or both).

Although the amyloid hypothesis is based on considerable genetic and biomarker data, if amyloid is not the cause of the disease, solanezumab would not be expected to slow disease progression.”

A study comparing gantenerumab at different doses with placebo came up with similarly disappointing results. A futility analysis was conducted when 50% of the patients had completed two years of treatment, and it found no differences between the drug or placebo, prompting researchers to stop the study early.9

A subsequent study that significantly increased the dose of the drug found it did reduce amyloid-beta plaques in Alzheimer’s patients,10 but how this translates to affecting cognitive decline remains to be seen.

Beta-Amyloid Is a Symptom of Alzheimer’s — Not the Cause

The reason why beta-amyloid drugs continue to fail to improve Alzheimer’s disease is because beta-amyloid is a symptom of Alzheimer’s — not the cause.

Alzheimer’s has many causes, as discussed eloquently by Dr. Dale Bredesen, professor of molecular and medical pharmacology at the University of California, Los Angeles School of Medicine, and author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.”11

Bredesen’s ReCODE protocol evaluates 150 factors — including biochemistry, genetics and historical imaging — known to contribute to Alzheimer’s disease. This identifies your disease subtype or combination of subtypes so an effective treatment protocol can be devised.

For instance, Bredesen states that type 1 Alzheimer’s is “inflammatory” or “hot,” and patients present predominantly inflammatory symptoms. Type 2 is atrophic or “cold,” with patients presenting an atrophic response. In type 3, or toxic “vile” Alzheimer’s, patients have toxic exposures.

There’s also a mixed type, type 1.5, which is referred to as “sweet” and is a subtype that involves both inflammation and atrophy processes, due to insulin resistance and glucose-induced inflammation. An algorithm is used to determine a percentage for each subtype based on the variables evaluated, and an individualized treatment protocol is created.

ReCODE Protocol Leads to Improvement in 100 Patients

Bredesen’s most recent publication is a case report of 100 patients using the ReCODE protocol.12,13 He has previously published three case reports, each involving just 10 patients. The fourth case report contains 100 patients treated at 15 different clinics across the U.S., all of which have documented pre- and post-cognitive testing.

Not only did all show improvement in symptoms, some of them also showed improvement in their quantitative electroencephalographs (EEGs). Others who underwent magnetic resonance imaging (MRI) with volumetrics also showed objective improvement.

The results are impressive, to put it mildly. Here’s an example of just one patient’s outcome — a 73-year-old woman with cognitive decline who could not remember recent conversations, mixed up the names of people and pets and forgot the names of books she had read. Her significant other described her memory as “disastrous,” but this changed remarkably for the better:14

“She was treated with the programmatic approach described previously, and over 12 months, her on-line cognitive assessment improved from the 9th percentile to the 97th percentile. Her significant other noted that her memory had improved from “disastrous” to “just plain lousy” and finally to “normal.” She remains on the therapeutic program, and has sustained her improvement.”

Understanding Ketosis and Autophagy for Alzheimer’s

A hallmark of neurodegenerative diseases such as Alzheimer’s is that proteins are aggregated and typically misfolded. By inducing ketosis, improving insulin sensitivity and supporting the mitochondria, you can often regain the ability to refold or proteolyze misfolded proteins.

Likewise, researchers wrote in the International Journal of Neuropsychopharmacology, “Research teams have reported some success in ameliorating the severity of symptoms in neurodegenerative diseases, most notably in patients with mild cognitive impairment or early Alzheimer’s disease [via diet-induced ketosis and/or ingestion of ketone bodies] … ”15

Bredesen's ReCODE protocol makes use of nutritional ketosis, in which your body produces endogenous ketones (water-soluble fats), but that’s not all. Your body has a mechanism by which misfolded proteins are refolded. Heat-shock proteins play a central role in this process, and if the misfolding is too severe, the heat-shock proteins help remove them altogether.

Heat-shock proteins are a corollary of autophagy, the process by which your body cleans out damaged organelles, which relates to Alzheimer’s because the refolding process is one of several factors that need to work in order for your brain to function. In Medicinal Research Reviews, researchers explained:16

“There are few more neurodegenerative diseases, like amyotrophic lateral sclerosis (ALS), Alzheimer's, and other dementias that have been investigated for their autophagy interconnection in the last two decades …

Autophagy also clears the aggregates formed by Alzheimer's and dementia associated proteins tau, β‐secretase, and presenilin 1 for neuronal cells and provide cytoprotection against proteotoxicity caused by these mutant proteins aggregates.

The autophagy pathway participates in amyloid‐beta (Aβ) protein secretion and further clearance of accumulated aggregates of this protein in Alzheimer's disease.”

Intermittent Fasting for Alzheimer’s

Unfortunately, a vast majority of people do not have well-functioning autophagy, for the simple reason that they’re insulin-resistant. If you’re insulin-resistant, you cannot increase your adenosine 5’ monophosphate-activated protein kinase (AMPK) level, which prevents the inhibition of mammalian target of rapamycin (mTOR), and mTOR inhibition is one of the primary drivers of autophagy.

Ultimately, Bredesen typically recommends an intermittent fasting approach, which helps your body to cycle through autophagy and the rebuilding phase:

“You want to use appropriate fasting and an appropriate diet to activate this autophagy,” Bredesen says. “We recommend … 12 to 14 hours [of fasting] if you are apolipoprotein E4-negative (ApoE4-negative) … If you are ApoE4-positive, you’d want to go longer — 14 to 16 hours. There’s nothing wrong with doing a longer fast …

The reason we suggest longer for the ApoE4-positives [is because] if you are ApoE4-positive, you are better at absorbing fat. It tends to take longer to enter autophagy …

Typically, we recommend it about once a week. But again, a longer fast once a month is a good idea. It depends a lot on your body mass index (BMI). What we found is people who have higher BMIs respond better to this fasting early on. They’re able to generate the ketones.

If you lose both the carbohydrates and the ketones, you end up [feeling] completely out of energy … We are very careful when people are down below 20 on their BMI, especially the ones 18 or below. We want to be very careful to make sure to cycle them [in and out of ketosis] once or twice a week …

These are the ones where, often, exogenous ketones can be very helpful early on … Measure your ketones. It’s simple to do. We want to get you into, ultimately, the 1.5 to 4.0 millimolar [range for] betahydroxybutyrate. That is the goal.”

To test your ketones, I recommend KetoCoachX.17 It’s one of the least expensive testing devices on the market right now. Another good one is KetoMojo. KetoCoach, however, is less expensive, the strips are individually packed and the device is about half as thick as KetoMojo’s, making it easier to travel with.

While drug trials for Alzheimer’s continue to fail, Bredesen’s latest book, “The First Survivors of Alzheimer’s,” contains exciting first-person accounts from patients diagnosed with Alzheimer’s who beat the odds and improved. You can learn more about Bredesen and his work by visiting his website, drbredesen.com.



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