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Written by Brenton Wight, researcher and LeanMachine
Copyright © Brenton Wight, LeanMachine
Doctors say there is no cure for Alzheimer’s Disease, in spite of over 80 billion dollars in research over the last few decades.
This is partly true, as there is no drug, no “magic bullet” to slow or stop this dreadful condition.
Hundreds of studies with new drugs have shown most of the time that those on a placebo did BETTER than those on the drug!
In rare cases, those on the drug did very slightly better, but any improvement was not enough to justify bringing the drug to market.
However, we CAN identify risk factors, and we CAN in most cases prevent the onset of Alzheimer’s, and we CAN in most cases reverse the disease, or at least ease the symptoms to give the patient and the carers a better quality of life.
If the intervention is soon enough, it CAN be CURED in some, but not all cases.
There is no miracle one-shot treatment, but a combination of many factors.
The time to start treatment is not when we are 60 and forget where the keys are, but from birth!
The lifetime changes we need to prevent Alzheimer’s will also prevent heart disease, diabetes, cancer and many other diseases, and give our lives vitality.
How many people are at risk?
In the USA, over 5 million Americans have Alzheimer’s disease, and around 14% of the population will eventually get Alzheimer’s, or around 45 million people.
Results in Australia are similar. Over 10% of the population over 65 have Alzheimer’s, and 30% of those over 85 have Alzheimer’s. In the decade from 2010 to 2020, deaths from Alzheimer’s has risen 20% and looks set to replace Cardiovascular disease as the Number 1 cause of death.
Many people now suffer from Early Onset Alzheimer’s, showing signs as young as 30 years of age.
In the USA, it is now the third leading cause of death, but these figures are understated. People do not actually die from Alzheimer’s – they die because the parts of the brain that control bodily functions shut down, so they die when their organs shut down.
The patient may die from pneumonia because the lungs now cannot function or some other organ fails to work and the Doctor or Coroner has to determine which organ failed.
This is a problem in every country, but some countries have very much reduced rates of Alzheimer’s, mainly due to better diets and reduced toxins.
Originally, there was no firm diagnosis without examining the brains of patients after death.
Researchers found that most patients had Amyloid Plaques in the brain, and also high levels of aluminium.
PET scans (Positron Emission Tomography) are used with a radioactive tracer (which binds to amyloid plaques) to determine the amount and location of amyloid plaques in the brain.
However, this diagnosis is still not conclusive, as many people have amyloid plaques, but no sign of any dementia even into old age, although these people have a higher risk. Often symptoms do not appear for decades after the start of amyloid plaque deposits. Other patients have no sign of Amyloid plaques but still have Alzheimer’s, so drugs developed to reduce Amyloid plaques have proven unsuccessful in prevention and treatment.
Standard blood tests for glucose level, triglycerides, kidney and liver function can help determine the risk. However, those with less than optimum blood results may die of Cardiovascular, Cancer or some other disease before Alzheimer’s sets in.
So the PET scan is used with other tests for cognitive performance to arrive at a diagnosis.
Who is at risk?
Genetics plays an important part, and so does diet, exercise, lifestyle and supplements.
Here are some risk factors, in no particular order:
- Age is the greatest risk factor. Dementia can affect about 10% of those over the age of 65, but 33% of those over 80
- Gender – Women represent over 60% of Alzheimer’s patients, but part of this may be due to their longer lifespans
- Gluten – Celiacs often have “Wheat Brain” causing disturbances, anxiety, depression and Alzheimer’s. Many dementia patients recover fully on a gluten free diet
- Prescription medications such as many sedatives, hypnotics, blood pressure, hay fever, insomnia, depression and arthritis medications are linked to higher risk of Alzheimer’s
- Anaesthetics are linked to Alzheimer’s. The more operations people have, the higher the risk
- High Blood Pressure (systolic over 140 in mid-life) doubles the risk of Alzheimer’s and increases vascular dementia by 600%, but blood pressure medications can be just as bad, so reduce it naturally without medication
- Sleep Apnea starves the brain of vital oxygen and increases risk of Alzheimer’s
- B-12 deficiency increases Alzheimer’s risk. Gastric Bypass Surgery, Celiac disease, vegan/vegetarian diets, antacids (like Nexium) and many medications all reduce availability and/or absorption of B-12
- Diabetes doubles the risk of Alzheimer’s (often called “Diabetes of the Brain” or “Type 3 Diabetes”)
- Vision problems increase Alzheimer’s risk. Opthalmologists can detect abnormal widths of blood vessels in the retina which can indicate early Alzheimer’s
- Tobacco – Smokers have double the risk for Alzheimer’s. Family and others breathing second-hand smoke also have higher risk
- Living alone after a partner’s death means we have six times the risk of Alzheimer’s, and those who divorce and live alone have three times the risk.
- Isolation is a significant risk factor for depression and dementia. Find a friend!
- Obesity is a risk. The lower the BMI (Body Mass Index) the lower the risk. Obesity raises risk by around 75%
- Family history increases the risk. See the Genetics section below, but environmental factors, diet and lifestyle choices can be passed on to children
- Education improves outcome, and lack of education increases Alzheimer’s risk. Studies suggest higher education increases “cognitive reserve” which may offset dementia symptoms
- Concussion or head trauma increases Alzheimer’s risk exponentially with the number and severity of head injuries
- Quality sleep is essential for the ability of the body to repair itself by flushing toxins from the brain
- Excessive alcohol consumption can lead to alcoholic dementia and higher risk of Alzheimer’s as well as many other health risks
- Mental activities improves the brain, physically and psychologically. Learn new things strengthens and develops new nerve cells
- Sedentary lifestyles are a large risk for the brain as well as the body. Exercise is a must for the brain and the body
- Chronic bladder disease increases risk
- Chronic Candida infections increase risk
Overcoming risk factors:
- Change the diet – see below
- Get regular, uninterrupted sleep
- Socialising, visiting friends, joining a group
- Crosswords, puzzles, new experiences, learning a musical instrument or another language
- Exercise helps control blood glucose levels, keeps excess weight down, increases oxygen and circulation, and joining a gym can also help with socialisation
- Use the many supplements available
There is a strong genetic predisposition to Alzheimer’s, but also there is a strong contribution of environment, diet and lifestyle.
Rates of Alzheimer’s disease have increased much faster than any genetic changes could have occurred.
This means that much is under our control, because even with a genetic predisposition, we can reduce risk with epigenetic (non-genetic influences on gene expression) changes.
Example: The most important genetic risk factor is the ApoE epsilon 4 allele (ApoE4), and 14% to 18% of the population has this gene.
Everyone carries two copies of the APOE gene, which makes the protein ApoE (apolipoprotein E).
There are three different types (alleles) of the APOE gene: E2, E3 and E4, and because we all have two copies of the gene, the combination determines our APOE “genotype” which can be any combination of the 2 copies: E2/E2, E2/E3, E2/E4, E3/E3, E3/E4, or E4/E4.
The majority of people have two E3 alleles (E3/E3) so this is defined as the “average risk”.
The E2 allele is the least common form, and if we have two E2 alleles (E2/E2) or one E2 and one E3 (E2/E3) we have about 40% REDUCED risk of Alzheimer’s.
The E4 allele, present in 14% to 20% of the population, increases the risk for Alzheimer’s, especially late-onset Alzheimer’s, but this does NOT mean that we will get Alzheimer’s disease if we have one or two copies of E4, as about one third of Alzheimer’s patients do not have even a single E4.
All it means is that our risk is increased, also increased is the risk of potential Alzheimer’s at a younger age.
To quantify the risk:
If we have no copies of E4, we still have around 9% risk of Alzheimer’s.
If we have a single copy of E4, our risk increases to around 30%.
If we have two copies of E4, risk is between 50% to 90% but in all cases, we CAN REDUCE the risk.
Many people are horrified to learn that they have up to a 90% risk of Alzheimer’s, but they need not be.
With some dietary, lifestyle and supplement changes, those at greatest risk can easily fall into the 10% who do NOT get Alzheimer’s.
SAD (Standard American Diet)
Genetic statistics above apply only to average people, typically Caucasians living in the Western World and consuming a typical Western diet of processed food, sugar, MSG, hydrogenated oils, chemicals, heavy metals, pesticides, insecticides and other toxic substances.
These statistics do NOT apply to those with a healthy diet of natural, organic food living in a low-toxin environment.
In fact, many people already down the cognitive decline have recovered on a healthy diet and sustained the improvement for several years, according to Dr Dale Bredesen who has been running a program for years now.
Dr Bredesen does not know how many more years it will be, but does know that patients on the program have removed the biochemical drivers which can be measured in blood tests, so so is very optimistic about their future health for many years to come.
Should we get genetic testing?
This is up to the individual. Some people would prefer not to know. Others want to know.
My father died from Alzheimer’s at about age 72 after many years in a Nursing Home, existing but without knowing who his family members were. So did my Grandmother on my Mother’s side, so I assume I may well have inherited a high genetic risk. I am now 73 as I revise this article. For me, testing is irrelevant, because I changed to a Paleo-style diet at age 63, which turned my life around.
From obese to lean, from grey hair to brown, from allergies to everything to allergies to nothing, from high blood pressure and triglycerides to normal, from poor physical strength to strong, fit and full of energy, from frequent headaches to none, from always getting sick to never getting sick.
If I had the genetic test and it was the worst result, I would only continue to do what I am doing now, using dietary and lifestyle modifications.
Have I halted Alzheimers? I hope so, but I often cannot remember some of the thousands of medical terms I have come across in my 10 years of research. Come back here in 27 years as I approach 100 and I will let you know how I have done.
Amyloid Plaques vs Tangles
Amyloid is a protein, normally found throughout the body. In Alzheimer’s, this protein divides improperly, creating beta amyloid which is toxic to brain neurons.
Amyloid is actually antimicrobial and has benefits for the body, but some people, especially those with the E4/E4 alleles cannot naturally break down these plaques, but there are dietary methods which can.
Not all Alzheimer’s patients have beta Amyloid plaques. About 10% of patients have neurofibrillary tangles which cause similar symptoms, but are also inclined to have more aggressive behavior.
Three Kinds of Alzheimer’s
Humans liberate amyloid as a protective response in the body to three different fundamental metabolic and toxic perturbations:
- Type 1: Characterized by systemic inflammation. Blood tests typically reveal high hs-CRP (high-sensitivity C-reactive protein), low albumin:globulin ratio,
and high cytokine levels such as interleukin-1 and interleukin-6. Imaging reveals temporoparietal reductions in glucose utilization.
Those at risk include people with chronic infections or inflammation from other causes, and the normal antimicrobial protective response liberates amyloids
- Type 2: Characterized by normal inflammation, but an atrophic (wasting away) profile, with reduced support from estradiol, progesterone, testosterone, insulin, and vitamin D, often with high homocysteine and insulin resistance. Imaging reveals temporoparietal reductions in glucose utilization. As NGF (Nerve Growth Factor) diminishes, amyloid production increases.
Type 2 in particular can be CAUSED by LOW cholesterol, resulting in atrophy (brain shrinkage), reduced hormone production, poor health and eventually Alzheimer’s.
All because we are taking statins that lower cholesterol, or we are not eating enough healthy fats.
We prevent our cells from doing what they are supposed to do, so we end up with a shrunken brain without the lipid (fat) content we need. A fat-free diet means atrophy of the brain.
See the Cholesterol Fraud and the Big Fat Lie sections below.
- Type 3: Different from types 1 and 2. Still β-amyloid positive and phospho-tau positive), but a younger onset (late 40s to early 60s).
Genotype ApoE is usually E3/E3 instead of E4/E4 or E3/E4 with little or no family history.
Onset usually follows a period of stress, depression, sleep loss, anesthesia, or menopause/andropause.
Memory loss is not a main symptom, instead there are cortical issues: dyscalculia (trouble with arithmetic), aphasia (trouble speaking or understanding speech – damage to the left side of the brain),
executive dysfunction (emotional or behavioural problems from frontal lobe issues).
Imaging studies often reveal extra-hippocampal disease, greater general cerebral atrophy and frontal-temporal-parietal abnormalities.
Lab results often reveal hypozincemia (low zinc) and/or a high copper:zinc ratio, and can indictate adrenal fatigue
(low pregnenolone, DHEA-S (dehydroepiandrosterone sulfate), and/or AM cortisol. Chronic infections like mycotoxins, Lyme, viral infections, HSV-1 (a herpes simplex virus) are all risk factors
Some patients have “Alzheimer’s type 1.5” where a combination of symptoms of both type 1 and 2 Alzheimer’s occurs.
Glycotoxicity (too much sugar in the brain) causes an insulin resistant brain. Combine this with AGEs (Advanced Glycation End products), and we have both inflammation from AGEs, plus atrophic withdrawal response because we are now resistant to insulin.
So we have a double condition of type 1 and type 2.
Type 3 patients often have MARCoNS (Multiple Antibiotic-Resistant Coagulase-Negative Staph), a colonisation of antibiotic-resistant staphylococcus in the nasal cavity.
Also high blood levels of TGF-beta-1 (Transforming Growth Factor beta-1), high C4A (a protein that in humans is encoded by the C4A gene), and low MSH (Melanocyte-Stimulating Hormone) is very common, typically with HLA-DR/DQ haplotypes shown by Dr Ritchie Shoemaker to be associated with CIRS.
Alzheimer’s from nose infections?
We have known for years that our healthy gut bacteria is essential to prevent almost every disease, and now research is looking at the rhinosinal microbiome, the healthy bacteria in our nose.
This is now becoming known as Inhalational Alzheimer’s.
The nose is the most direct route to the brain, and bad bacteria in the mucous lining of the airways can damage the brain.
Pathologists now believe there are unknown pathogens in the rhinencephalon, the “nose-smell” (olfacation) system.
Many Alzheimer’s patients start losing their sense of smell as one of the early signs of the disease, and this is probably why.
I am confident that my nasal bacteria is back to normal after having very bad allergies and taking antihistamines from when I was about 16 to when I was 63.
Allergies stopped when the bad diet stopped.
Dr. Susan Lynch at UCSF has found that the nose problem is not so much an unknown pathogen, but a lack of microbial diversity.
Beneficial microorganisms in the nose protect against many pathogens, and one of the best seems to be Lactobacillus sakei, used to make sake and kimchi.
This could explain why Japanese people have comparatively low rates of Alzheimer’s, although rates are rising in Japan because of the Western influence, with meat and dairy replacing rice as a staple food.
When Japanese people migrate to Western countries and adopt a Western diet, they have the same risk as anyone else.
So for the Japanese, it is not a genetic problem, but a diet problem, and this applies to everyone.
AGEs – Advanced Glycation End products
AGEs are formed when food cooked at high temperatures (over 120 degrees C) combines with sugar. AGEs are very damaging to the body, accelerating the ageing process and chronic disease.
AGEs worsen diabetes, kidney disease, Alzheimer’s, inflammation, atherosclerosis (stiffening of the arteries), cardiovascular disease and stroke.
AGEs cause glycation of LDL cholesterol, promoting oxidation, and oxidized LDL is a major factor in atherosclerosis.
AGEs form photosensitizers in the eye lens, leading to cataract development.
To reduce AGEs, never cook at high temperatures (steaming is best, always at 100 degrees C), eat plenty of raw food (salads, and small amounts of fruit), and eliminate all sugar and processed foods.
Drug companies have been trying for years to get rid of Amyloid plaques, thinking they are the cause of Alzheimer’s.
However, the body needs amyloid to protect the brain, so we need to look at what is causing the plaques instead of trying to get rid of them. Latest research shows that Amyloid plaques are antimicrobial, so can be both damaging and protecting!
Alzheimer’s – “Diabetes Type 3”
Some researchers are now labeling Alzheimer’s as “Diabetes Type 3” because sugar causes Alzheimer’s.
Sugar also causes diabetes, cardiovascular disease, obesity and many more diseases, mainly due to processed foods.
As with diabetes, where sugar causes insulin resistance, we have insulin resistance in the brain, causing degeneration.
When the brain becomes insulin resistant, it means that glucose cannot enter the brain cells, so those cells die.
However, all is not lost. If we switch to a Ketonegic diet, we can feed our brain with fat instead of sugar. More on this diet below.
Diagnosing the type of Alzheimer’s
Unlike cancer, where we can biopsy a tumour, we must look at historical, biochemical, genetic, imaging, and function information to determine the type of Alzheimer’s.
Of course this rarely happens except in research applications. The doctor simply says the patient has Alzheimer’s and may give a drug which in the long term will not make much difference.
This is a shame, because about half of all cases can be halted, and in some cases substantially improved, by reverting to the correct diet.
Even better would be to eat a correct diet from birth, reducing the risk of Alzheimer’s to near zero, as well as preventing cancer, heart disease, diabetes and other modern diseases.
Physical exercise is extremely important to keep the brain and body healthy.
Researchers are not sure why, but LeanMachine says it is obvious:
Exercise burns off the high glucose levels that cause “Diabetes of the Brain” and exercise boosts oxygen levels and circulation in the brain.
Any type of exercise is beneficial, such as:
- Walking, jogging or running
- Push-ups, chin-ups
Exercises have the added benefit of socialisation in a group, such as:
- Join a gym
- Tai-Chi or Yoga classes
- Athletics clubs
- Dancing classes
Exercising the Brain
The body has a disturbing property: Anything not used for a while gets broken down to be used somewhere else.
If we do not use a muscle for a week, the body starts breaking it down.
But if we exercise regularly, we stop muscles wasting, and we actually build up our muscles.
If we do not use parts of the brain, the body starts breaking it down.
But if we exercise our brain, we can hang on to the parts we use, and develop new pathways to replace parts we have lost. Exercises such as:
- Learning a new language
- Playing a musical instrument
- Crossword or other puzzles
- Socialising in groups or clubs
Meditation is not normally seen as exercise for the brain, but sitting in a quiet, dark room away from all daily distractions not only promotes a calming effect, but increases various brain-saving hormones.
Meditation, like dreaming, helps the brain sort out the junk memories and recent problems by concentrating on things that have made us feel good in the past.
We may have pleasant memories like sitting on a sandy beach listening to the waves rolling in on a beautiful sunny day. By concentrating on peaceful and pleasant memories, we forget problems with out hectic daily life.
The modern diet is lacking in vitamins, minerals, amino acids and other nutrients, mainly because of:
- Over-farming – growing the same food in the same ground year after year, depleting these vital elements
- Over-processing – hydrogenation, adding sugar, adding chemicals, overheating
- Toxins from farming chemicals contaminates the environment
- Water is contaminated by fluoride and chlorine
The supplements everyone over 50 should take are:
Organic Coconut Oil, taken several times a day, a tablespoon at a time.
LeanMachine considers this one of the best prevention and treatment methods available for Alzheimer’s.
This encourages the body to burn healthy fats instead of sugar, called the Ketogenic Diet which burns ketones, which is what our ancestors did in their natural low-carb diets. See the Ketogenic Diet below.
Coconut oil appears to break down the amyloid plaque buildup in the brain. Perhaps the plaques are no longer required when the brain is fed by healthy fats instead of glucose.
Coconut oil is also the absolute best for cooking, replacing any other fat, because coconut oil remains stable at high temperatures, and is full of MCT (Medium Chain Triglycerides) which go straight to the liver to be burned as fuel, and cannot be stored as fat in the body.
Coconut oil also contains Lauric Acid, which keeps our skin wrinkle-free and healthy.
– PS (Phosphatidylserene) is a component of the cerebral cortex’s neuronal membrane, and can improve memory and mood, reduce stress, improve learning and more.
It does this by controlling input and production of choline, acetylcholine, norepinephrine, dopamine and glucose.
– Vitamin B-12 because as we age, our stomach acid levels drop, preventing the high-acid conditions required for B-12 absorption from food. Even more essential for vegans and vegetarians as B-12 mainly comes from animal products.
– B-group vitamins because these are vitally important for nerves and brain health.
– ALA (Alpha Lipoic Acid) as an antioxidant to help remove heavy metals from the brain, reduce inflammation, and improve the effectiveness of votamins C and E.
– Vitamin D3 because over half the ageing population are taking statin medication (which they should NOT) and statins halt production of 7-dehydrocholesterol, the first step in the manufacture of vitamin D3. Worse, many of these seniors are in Aged Care facilities and never see the light of day, so cannot make vitamin D3 from sunlight. If they are ever taken outside, it is only early morning or late afternoon when they cannot get vitamin D3 anyway. More info in my Vitamin D3 article.
– Ginkgo Biloba is highly recommended to improve blood flow in the brain. Should not be used in conjunction with prescription blood thinners.
– TMG (Trimethylglycine) is an effective methyl donor for the facilitation of methylation processes. Supports a healthy homocysteine level, which in turn supports healthy cardiovascular function and helps prevent Alzheimer’s. Homocysteine, a damaging amino acid, with the aid of TMG, is turned into methionine, a safe and beneficial amino acid. Methylation is essential for DNA repair and production of SAMe, which helps joints, lifts mood, fights depression and protects brain cells from amyloid plaques. Read more in my TMG article.
– SAMe (S-Adenosyl Methionine) can help protect the brain and also help treat depression, anger, anxiety which are common symptoms in some Alzheimer’s patients.
– Vinpocetine has shown mixed results but mostly beneficial in limited human trials using 10mg 3 times daily.
– Vitamin E is recommended to improve the healthy fats in the brain and increase antioxidants.
– Benfotiamine with Leucine can help remove glucose and improve insulin resistance.
Many other supplements can help, including:
In addition, many supplements primarily used to treat diabetes will also help prevent Alzheimer’s.
The Cholesterol Fraud
Previous research indicated that high cholesterol was a risk factor for Alzheimer’s.
Again, this was wrong. Doctors started prescribing statin drugs for those people with high cholesterol, or those with signs of dementia with normal cholesterol.
What happened? They got Alzheimer’s WORSE and got it FASTER than patients who did NOT take statins.
Researchers only looked at total cholesterol which is a complete waste of time.
25% of the cholesterol in the body is in the brain, mainly in the myelin sheath.
Around 60% of our brain is fat, mainly in the form of cholesterol.
The myelin sheath (oligodendroglia) that surrounds and protects our neurons are 70% cholesterol, 30% protein.
Starve the brain of healthy fat, and we get Alzheimer’s. Almost guaranteed.
Reduce cholesterol and what happens? The protective myelin sheaths break down as they are starved of cholesterol, allowing the brain cells to be damaged. Damage them enough, and they die. Then we have dementia. Damage enough cells, and the brain can no longer support our basic functions, like breathing. Then we die.
This is why statin drugs are BAD.
Sure, in some cases, they can slightly reduce risk of heart attacks, but they INCREASE death from all other causes, including Alzheimer’s.
The net result is that on average, we will not live a day longer on statin medication.
Statins will give us lousy final years with muscle breakdown, osteoporosis, more sickness and dementia.
We need plenty of healthy fats like coconut oil, walnuts, avocados, fish, eggs, butter from grass-fed cows, unheated olive oil.
We must NOT consume bad fats: Canola oil, margarine, anything hydrogenated, anything heated over 120 degrees C.
Cholesterol is NOT the enemy.
We NEED cholesterol, especially HDL (High Density Lipoprotein) cholesterol which reduces inflammation, and helps clean up the body (like a garbage collector). Without HDL Cholesterol, we die within 24 hours.
We also need LDL (Low Density Lipoprotein), still incorrectly called “bad” cholesterol, as we die without it.
LDL has antimicrobial effects, so the idea that we should drive it down to zero is ludicrous. LDL is essential to transport nutrients around the body (and into the brain) as well as helping the body manufacture hormones and other important products. LDL was essential for our evolutionary ancestors millions of years ago, and we still need it.
The brain is mostly fat, and 40% of the brain is CHOLESTEROL.
Many things that were protective in our native environment are problems in our modern environment, but if we go back to our ancestral diet, problems are resolved.
Studies show time after time that people with low cholesterol die young, while people with normal to high cholesterol live longest.
These studies are ignored by the big drug companies. Because statin sales make them billions of dollars, of course they continue the Big Cholesterol Lie, one of the biggest frauds in medical history. Their own study showed increased deaths and terrible side effects so they stopped the study short at that time, supposedly to “save patient’s lives” when the opposite was true.
The dangerous cholesterol is VLDL (Very Low Density Lipoprotein) which cannot easily be tested.
Because triglycerides contain some VLDL, labs estimate VLDL value by simply taking a percentage of triglycerides.
High triglycerides are much more of a danger signal than high cholesterol, and are almost always related to obesity, poor diet of processed foods, especially dangerous fats.
The Big Fat Lie
We have been told for decades that fat is bad for us.
Forget about “low fat” or “fat free” diets.
Another big fat lie, coming from a scientist who plucked figures out of a study to suit an argument he was proposing.
When the data was analysed completely, many decades later, it showed the complete opposite.
The largest and longest study in the world was the Framingham study which showed that those who ate the most fat lived longer than those who ate the least.
Fat is not unhealthy in general, in fact it is essential for health.
The UNHEALTHY fats are man-made artificial fats (margarine, Canola oil) and other processed fats that are hydrogenated to improve shelf life and heated to extremes during manufacture, often going rancid in the process, causing oxidised VLDL (Very Low Density Lipoprotein), the REAL dangerous “food”.
What is REALLY bad is carbohydrates, and when manufacturers remove fats from food, they replace them with carbohydrates, causing most “modern” diseases including Alzheimer’s and Diabetes.
The Ketogenic Diet
For the first two million years of human life on Earth, carbohydrate consumption was very low.
Carbohydrates were uncommon, with the majority of food being nuts, seeds, eggs, fish, fruit and vegetables. Meat was eaten very rarely when an animal was killed.
These people did not burn carbohydrates for energy, they burned FAT. In particular, ketones, the basis of the ketogenic diet.
A ketogenic diet means maintaining a fasting state of ketosis. Ketones are produced when the body is in a state of ketosis.
Ketones fuel cells using a different pathway from glucose.
Glucose has to have insulin to allow glucose into cells, but as we all should know, our typical modern diet is loaded with carbohydrates, forcing the pancreas into overdrive making enough insulin.
Eventually our cells become insulin resistant, so the pancreas produces even more insulin to force glucose into the cells, creating even more insulin resistance.
We are now a full-blown diabetic, and when the pancreas starts shutting down, we need insulin injections for the rest of our life.
However, when we feed the cells with ketones, they simply enter the cell naturally, and do NOT require insulin or anything else to do so.
This is critically important for five of our modern diseases: Obesity, Cancer, Diabetes, Cardiovascular and Alzheimer’s, all caused or aggravated by high blood glucose, bad fats and inflammation.
Ketones are also signaling molecules as well.
Benefits of the ketogenic diet include:
- Helps the body express new restorative and healing genes
- Reduces inflammation (underlying cause of nearly every disease)
- Stimulates the immune system
- Aids weight loss
- Stops or slows degenerative disease
- Reduces risk of Alzheimer’s, Cancer, Cardiovascular, Diabetes and Obesity
The Anti-Alzheimer’s diet
Add these spices to every meal possible.
Of course they will spice up any meal, but also help clear the brain of problems and reduce risk of cardiovascular disease, cancer, diabetes and many more modern illnesses.
- Sage – one of the best brain-saving spices
- Cloves – one of the most potent antioxidants
- Curry – a blend of other great spices
- Ginger – reduces inflammation and improves immunity
- Turmeric – for colour, flavour and Curcumin
- Ceylon Cinnamon – Better and safer than regular cinnamon
Ketogenic Diet – Healthy fats, intermittent fasting.
Read How Cyclical Ketosis can help combat Chronic Fatigue
Avoid Trans Fats
Read Trans Fats Linked to Increased Risk for Alzheimers
Avoid Processed Foods
Only shop in the greengrocer department at the Supermarket, preferably the organic section. Buy or grow your own real food. Nothing in a bag, box, tin because toxic ingredients are sure to be added.
Forget fried foods. Steaming is the best way to cook. Never Microwave. Eat raw salads daily.
This section often updated. Please come back soon (if you remember!)
Updated 20th January 2020, Copyright © 1999-2020 Brenton Wight and BJ&HJ Wight trading as Lean Machine abn 55293601285
Reproduced from original article:
Analysis by Dr. Joseph Mercola
January 10, 2020
- Heart disease and cancer are the two top reasons people die in the U.S.; data show women who can exercise vigorously have a reduced risk of mortality from heart disease, cancer and other causes
- Women who have high cardiovascular fitness also enjoy a reduced risk of dementia, which may be related to higher levels of a protein responsible for improving mitochondrial biogenesis
- Combining intermittent fasting with the ketogenic diet plan may boost the health benefits and improve mitochondrial health. This includes not eating within three hours of going to bed to reduce free radical damage
- Lack of exercise is globally responsible for nearly 5 million deaths each year; the more you move and exercise the lower the potential rate of death. Aim to sit as little as possible during the day
Heart disease and cancer are the top two reasons people die in the U.S. The term heart disease is used to identify several types of conditions, including cardiovascular disease, coronary artery disease and heart attack. While many think of this as a man’s disease, the CDC1 reports almost as many women will die each year from it.
The most common type, coronary heart disease, affects 6.2% of women 20 and older. Many women report having no symptoms before experiencing a heart attack, but others may have symptoms of angina, nausea or fatigue. Diabetes, obesity, an unhealthy diet and lack of physical activity are all lifestyle choices that increase your risk for heart disease.
Each of these same factors increase your risk of cancer. Some of the types of cancer that more frequently affect women include breast, cervical, lung, colorectal and skin.2 Most cancers strike women after menopause, but gynecological cancers may happen at any time.
Every year 90,000 women are diagnosed with one form of gynecological cancer and 242,000 with breast cancer. The signs of gynecological cancers may be vague and mimic symptoms of other conditions, such as unexplained weight loss, constant fatigue, loss of appetite or feeling full, pain in the pelvis or a change in bowel habits.
Fitness Protects Women Against Risk of Premature Death
New data recently presented at the European Society of Cardiology3 strongly suggest that women who can exercise vigorously experience a significantly lower risk of mortality from heart disease, cancer and other causes. Although there have been multiple studies using male participants or mixed groups, the researchers proposed that information specific to women was scarce.
The study used data from 4,714 adult females who had undergone echocardiograms for known or suspected coronary artery disease. Treadmill stress tests were used with increasing intensity to measure fitness, which the researchers defined as a maximum workload of 10 metabolic equivalents (METs).
Women who were able to achieve 10 METs or more were compared to those who achieved less. A measurement of 10 METs is equivalent to walking up four flights of stairs fast without stopping or going up three flights quickly.
The researchers followed the participants for a median 4.6 years and found there were 345 deaths from cardiovascular disease, 164 from cancer and 203 from other causes. After adjusting for influencing factors, the findings revealed that women in the higher MET group had a lower risk of death from all measured causes.
By comparison, women in the lower fitness group experienced an annual rate of death nearly four times higher and the annual cancer death rate doubled. One researcher, Dr. Jesus Peteiro, noted the average age of participants was 64 years and 80% were from 50 to 75 years. He went on to comment:4
“Good exercise capacity predicted lower risk of death from cardiovascular disease, cancer, and other causes. Looking at both examinations together, women whose heart works normally during exercise are unlikely to have a cardiovascular event.
But if their exercise capacity is poor, they are still at risk of death from cancer or other causes. The best situation is to have normal heart performance during exercise and good exercise capacity.”
The women underwent imaging of their heart during the treadmill test to assess function. Those with poor function during the test were more likely to succumb to cardiovascular disease during the follow-up period, but it was not predictive of death from other causes.5 Peteiro said: “The results were the same for women over 60 and less than 60, although the group under 50 was small.”
Cardiovascular Fitness Also Reduces Risk of Dementia
Staying fit is key to reducing your potential risk for many chronic diseases, including those affecting the central nervous system. Across the world there are 47 million who are living with dementia, and this is expected to increase to 75 million by 2030. You may be able to significantly slash this risk by taking simple steps to improve your cardiovascular fitness.
A study from the University of Gothenburg in Sweden showed women with the highest cardiovascular fitness had an 88% reduced risk of dementia as compared to those with moderate fitness. Even maintaining some fitness proved to have benefit as those with the lowest level experienced a 41% greater risk of dementia than those with average fitness.
The researchers did not assess how much exercise the participants engaged in but used an ergometer cycling test during which additional resistance was added as the women continued to cycle until they were exhausted. The authors wrote:
“These results suggest that cardiovascular fitness is associated with the sparing of brain tissue in aging humans. Furthermore, these results suggest a strong biological basis for the role of aerobic fitness in maintaining and enhancing central nervous system health and cognitive functioning in older adults.”
A second way fitness may protect neurological health is by increasing levels of PGC-1alpha responsible for improving mitochondrial biogenesis. Data reveal that those with Alzheimer’s have less PGC-1alpha in their brain. Cells containing more produce less of the toxic amyloid protein associated with the development of Alzheimer’s disease.
Participants diagnosed with mild to moderate Alzheimer’s were enrolled in a four-month supervised exercise program. The results demonstrated they had fewer neuropsychiatric symptoms from the disease than the control group who did not exercise.
A progressive walking program in those with early Alzheimer’s disease led to improvements in cardiovascular fitness and functional ability. This in turn led to improved memory and increases in the size of the brain’s hippocampus.
Mitochondrial Function Linked to Reducing Risk of Disease
Your mitochondria are minute powerhouses in your cells producing a majority of the energy your body generates, as well as coordinating apoptosis, or programmed cell death, important in the prevention of malfunctioning cells that may turn into cancer.
Your brain is the most energy-dependent organ and therefore is particularly susceptible to impaired energy production. This process may then make the brain more susceptible to age-related disease.
As you age, the genes controlling mitochondrial energy generation may be turned down, and mitochondria are noted to be less dense and more fragmented. With insufficient energy and dysfunctional mitochondria, defective cells can survive and multiply.
There are several ways your mitochondria may be damaged, but much of it may result from superoxide free radicals. Although the production of superoxide is part of a normal process, when produced at higher than normal levels it damages the DNA in your mitochondria. This damage increases when you are not metabolically flexible.
That means you burn a higher percentage of carbohydrates for fuel than you do fat. The process of burning carbs leaks more electrons that combine with oxygen to form superoxide. High-carbohydrate processed foods prevent you from burning fat efficiently, which produces less oxidative stress than carbs. Your nutrition is also foundational to protecting your mitochondrial health.
Combining Nutritional Plan With Fitness Boosts Benefits
When you combine a strong nutritional plan to boost metabolic flexibility with cardiovascular fitness you build on the health benefits of both. For many years the standard dietary recommendations were three square meals a day with small snacks in between.
The most obvious risk of this eating plan is the potential of overeating. But, the less obvious risk is metabolic dysfunction, raising your risk of cancer, heart disease and dementia.
For a number of years, I have strongly advised against eating within three hours of going to bed. The authors of one study found that eating an early dinner, or skipping it entirely, changes the way the body metabolizes fat and carbohydrates. This improves fat burning and reduces hunger. The key in the study was eating the last meal of the day by the middle of the afternoon.
The only changes made to the participants’ meals was timing. The total number and types of calories remained the same. Results showed the participants were less hungry and experienced increased fat burning during the evening hours, along with improved metabolic flexibility. It appears that late night eating will boost free radical damage, negatively impacting mitochondrial function.
By taking advantage of your circadian rhythm you optimize your metabolism. During sleep your body requires less energy. Thus, if you eat right before bed, mitochondria produce excessive amounts of free radicals. In one study of 1,800 people with prostate and breast cancer, researchers found that meal timing reduced the risk of cancer.
They also found that those who awakened early had a higher risk of cancer when they ate dinner late in the evening compared to those who were more energetic at night. A very effective option is to combine intermittent fasting, extend the amount of time you go without food and follow a ketogenic diet.
Fasting upregulates autophagy and mitochondrial health, activating stem cells and stimulating mitochondrial biosynthesis. What many don’t realize is that many of these benefits happen during the refeeding phase, making what you eat foods that are essential to your optimal health.
In one study participants lost 3% of their body weight while practicing time restricted eating even though they didn’t change their nutritional choices. While they lost weight, they did not improve important disease parameters, including visceral fat, diastolic blood pressure, triglycerides, fasting glucose or fasting insulin.
When intermittent fasting is combined with a ketogenic diet it provides many of the same benefits of fasting, in addition to improvements in health such as increased muscle mass, improved insulin sensitivity, reduced inflammation, reduced risk of cancer and increased longevity.
Lack of Exercise May Be Worse Than Smoking
Exercise and nutrition are two of the best preventive strategies against many common health conditions. In one study scientists found that the lack of physical activity came with a global price tag of $67.5 billion in 2013 and that it causes more than 5 million deaths each year, while smoking kills 6 million.
Another group of researchers analyzed data on more than 120,000 people and found that cardiovascular fitness had a greater impact on risk of death than smoking, diabetes or heart disease. However, as important as cardiovascular fitness is, you’ll find you can’t out-exercise the number of hours you sit down.
The average U.S. adult will sit nine to 12 hours each day. While sitting is not inherently dangerous, the cumulative effects on your cardiovascular and musculoskeletal system can seriously impact your health and shorten your life.
In a four-year evaluation of 8,000 Americans over the age of 45, researchers found that those who moved more were healthier. There was also a correlation between death rate and the number of hours the participants spent sitting each day. The bare minimum of movement is 10 minutes for every hour of sitting. However, it is wiser to strive to sit as little as possible.
Sitting correctly requires greater muscle activation and will reduce your potential risk of lower back pain and strain. For specific instructions on how to sit right and for a list of some of the negative side effects of sitting for long periods, see “The Importance of Standing More, Sitting Less.”
Reproduced from original article:
Analysis by Dr. Joseph Mercola
January 09, 2020
- Increasing research shows that maintaining healthy levels of body fat and greater muscle mass has an effect on your brain health and may slow your rate of cognitive aging
- People with higher amounts of abdominal fat had worse fluid intelligence with age, while those with greater muscle mass were more protected against such declines
- Women who had greater muscle mass tended to have better scores in fluid intelligence during the study period
- Past research has linked midlife obesity with an increased risk of mild cognitive impairment, changes in short-term memory and executive functioning and dementia
- In addition to regular exercise to increase muscle mass, eating a ketogenic diet to maintain a healthy body weight and avoid obesity may support your brain health as you age
Staying fit as you age is about far more than aesthetics. Increasing research shows that maintaining healthy levels of body fat and greater muscle mass has an effect on your brain health and even your rate of cognitive aging. It’s known, for instance, that being obese in midlife and early late-life is associated with worse cognitive aging.1
What’s more, the amount of muscle and fat you have may be a more important factor in how your level of fluid intelligence decreases over time than your chronological age. Your chronological age, i.e., your age in years, is just a numerical measurement, but your real age is your biological age as dictated by your choices and habits, as well as your modifiable risk factors like levels of muscle and fat.
While many people tend to gain fat and lose muscle mass as they age, this can be largely combated by staying active and eating right — lifestyle choices that will influence your cognitive function significantly.
More Muscle, Less Fat Protects Your Brain
In a study by Iowa State researchers, data from 4,431 adults were examined to compare levels of lean muscle mass, abdominal fat and subcutaneous fat with changes in fluid intelligence — the ability to solve problems in new situations — over a six-year period.2,3
Those with higher amounts of abdominal fat had worse fluid intelligence with age, while those with greater muscle mass were more protected against such declines. In fact, women who had greater muscle mass tended to have better scores in fluid intelligence during the study period.
Study co-author Auriel Willette, assistant professor of food science and human nutrition at Iowa State University, said in a news release, “Chronological age doesn’t seem to be a factor in fluid intelligence decreasing over time. It appears to be biological age, which here is the amount of fat and muscle.”4
What’s more, the study revealed a link between the immune system and how changes in fat levels affect cognition. Previous research suggests a higher body mass index (BMI) leads to greater immune system activity in the blood, which in turn activates the immune system in the brain, with a negative outcome on cognitive function.5
The featured study also found that changes in white blood cells called lymphocytes and eosinophils explained the link between abdominal fat and worsening fluid intelligence in women. In men, basophils, another type of white blood cell, were linked to about half of the link between fat levels and fluid intelligence, the study found.6
“Lymphocytes, eosinophils, and basophils may link adiposity to cognitive outcomes,” the researchers explained.7 Similar research has revealed that overweight and obese individual have greater brain atrophy in middle-age, corresponding with an increase in brain age of 10 years.8
How Obesity Affects Your Brain
Obesity has multiple effects on the brain, including anatomically speaking. Obese individuals may have reduced gray matter in brain regions such as the hippocampus, prefrontal cortex and other subcortical regions. Atrophy in the hippocampus, in turn, has been linked to Alzheimer’s disease.9
Gray matter is the outer layer of the brain associated with high-level brain functions such as problem-solving, language, memory, personality, planning and judgment. Even in elderly people who are otherwise cognitively normal, obesity is associated with measureable deficits in brain volume in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus compared to individuals with a normal weight.10
Further research published in Radiology found that obesity may lead to alterations in brain structure, shrinking certain regions.11 Among men, higher total body fat percentage was linked to lower brain gray matter volume. Specifically, 5.5% greater total body fat percentage was associated with 3,162 mm3 lower gray matter volume.
Among men, 5.5% greater total body fat was also associated with 27 mm3 smaller globus pallidus volume, an association also seen in women. In women, 6.6% greater total body fat percentage was associated with 11.2 mm3 smaller globus pallidus volume.
The globus pallidus is a brain region that plays a role in supporting a range of functions, including motivation, cognition and action.12 Obesity was also associated with changes in white matter microstructure, which may be related to cognitive function.13
Cognitively speaking, there’s also a strong link between obesity and deterioration in cognitive function, as well as to other brain disorders such as dementia, anxiety and depression. Further, past research has linked midlife obesity with an increased risk of mild cognitive impairment, changes in short-term memory and executive functioning and dementia.14
Obesity-Associated Health Problems Also Harm Your Brain
Obesity’s effects on brain health are also due to its associated health problems, including heart disease, diabetes and atherosclerosis, each of which can have its own deleterious effects on your brain. For instance, as noted in Frontiers in Neuroscience:15
“Obesity-derived vascular problems, such as atherosclerosis and arteriosclerosis, which are systemic diseases, are known to affect the steady blood flow of vessels that feed the brain, thus contributing to cognitive impairment or even stroke, where large areas of the brain die due to the stop in the blood flow of a major brain artery caused by a blood clot.”
In terms of diabetes, of which obesity is a key risk factor, having this condition in midlife is associated with a 19% greater cognitive decline over 20 years compared with not having the condition.16 Even those with prediabetes had significantly greater cognitive decline than those without.
Indeed, “Epidemiological studies have linked type-2 diabetes mellitus with cognitive impairment and dementia, with insulin resistance and hyperglycemia as the probable mechanistic links,” researchers noted.17
Coming full circle, eating a highly processed, junk food diet not only increases obesity risk but also can lead to normal but elevated blood sugar levels that, in turn, can lead to impaired glucose metabolism and Type 2 diabetes. Both diabetes and higher fasting glucose levels are linked with lower total brain volume.18
Impaired glucose metabolism is then associated with neurodegeneration that impairs cognitive function. This connection begins not in old age but much earlier, such that following a healthy lifestyle in young adulthood may be protective against cognitive decline later.19
The Inflammation Connection
Obesity can trigger chronic inflammation in your body, and chronic inflammation in your brain (neuroinflammation) is known to impair neurogenesis, your brain’s ability to adapt and grow new brain cells. It’s also linked to neurodegenerative disorders such as Alzheimer’s disease (AD), and it’s been suggested that “Obesity may serve as an amplifier or initiator of the chronic inflammation observed in AD patients.”20
Further, higher levels of inflammatory markers have also been associated with lower brain volume, including “greater atrophy than expected for age.”21 Excess body fat, particularly visceral fat, is also related to the release of proteins and hormones that can cause inflammation, which in turn can damage arteries and enter your liver, affecting how your body breaks down sugars and fats.
According to a study in the Annals of Neurology, “[A]dipose-tissue derived hormones, such as adiponectin, leptin, resistin or ghrelin, could also play a role in the relation between adipose tissue and brain atrophy.”22 Further, obesity may also be associated with lower volume in brain regions that regulate food-reward circuitry,23 possibly influencing overeating.
Strength Training Is Good for Your Brain
While obesity takes a toll on your brain, increased muscle mass protects it, which is likely one reason why strength training has been found to be beneficial for your brain. In other words, your body’s physical strength may serve as a marker of your brain power.
In fact, strength training is known to trigger beneficial neurobiological processes,24 leading to positive functional brain changes, including in the frontal lobe, with corresponding improvements in executive functions. One systematic review even found that strength training led to less white matter atrophy in the brain, with researchers noting:25
“Taken together, during aging processes, a substantial decline in muscular strength, especially in lower limb muscles, occurs, and accumulating evidence suggests that lower muscular strengths are linked to poorer cognitive performance.
Hence, resistance (strength) exercises (a single bout of resistance exercise, also referred to as acute exercise) and resistance (strength) training (more than one resistance exercise session, also referred to as chronic exercise … ) seem to be promising activities to ensure the preservation of physical functioning and cognitive functions with aging.”
Regular strength training, in addition to other forms of exercise and daily activity, is an important strategy for keeping your brain sharp and may help to offset some of the cognitive decline that occurs with age.
Avoid Obesity and Protect Your Brain With a Ketogenic Diet
While obesity may accelerate neurodegeneration, regular exercise to increase your muscle mass will be protective. Further, eating a ketogenic diet will help protect your brain from free radical damage and will supply the cells with preferred fuel while also helping you to lose weight and avoid obesity.
A ketogenic diet is high in healthy fats and low in net carbohydrates (total carbs minus fiber), prompting your body to start burning fat as its primary fuel, rather than sugar. This produces ketones, which not only burn efficiently but are also a superior fuel for your brain. Ketones also generate fewer reactive oxygen species (ROS) and less free-radical damage.
One of the simple strategies you can implement is to take ketone precursors like refined MCT oils of caprylic acid (C-8). The eight-chain carbon fats are readily converted to ketones. I personally use up to 5 ounces of our Ketone Energy when I have maxed out my protein and carb intake and need a source of healthy clean fat. This keeps my ketone level around 1 to 2.0 mmol/l. Just recognize that you have to build up to a high dose of MCT oil slowly or you will have problems with loose stools.
Recent studies have also demonstrated the benefits of nutritional ketosis for brain health. In one, researchers found a ketogenic diet improved neurovascular function, in part by improving your gut microbiome.26
In a second study, the researchers concluded a ketogenic diet acted as a veritable “fountain of youth” in their animal study by significantly improving neurovascular and metabolic functions, compared to the animals eating an unrestricted diet.27 Releasing ketones into your bloodstream helps preserve brain function and protects against cognitive impairment and other neurodegenerative diseases.28
KetoFasting, the program I developed and detail in my book, “KetoFast: A Step-By-Step Guide to Timing Your Ketogenic Meals,” combines a cyclical ketogenic diet and intermittent fasting with cyclical partial fasting to optimize health and longevity.
Not only can KetoFasting help you to lose weight, but your cognition typically improves thanks to the biological cleansing and regeneration that occurs throughout your body, including your brain.
- 1, 7 Brain, Behavior, and Immunity November 2019, Volume 82, Pages 396-405
- 2, 5, 6 Science Daily December 17, 2019
- 3 Brain, Behavior, and Immunity Volume 82, November 2019, Pages 396-405
- 4 Newsweek December 20, 2019
- 8 Neurobiol Aging. 2016 Nov; 47: 63–70.
- 9, 14, 15, 17, 20 Front Neurosci. 2019; 13: 513.
- 10 Hum Brain Mapp. 2010 Mar; 31(3): 353–364.
- 11, 23 Radiology. 2019 Apr 23:181012.
- 12 Front. Neuroanat., 10 April 2017
- 13 Neuroscientist. 2013 Feb; 19(1): 8–15.
- 16 Ann Intern Med. 2014;161(11):785-793
- 18 Diabetes Care. 2011 Aug;34(8):1766-70.
- 19 Frontiers in Neuroendocrinology June 6, 2019
- 21 Neurology. 2007 Mar 27;68(13):1032-8.
- 22 Ann Neurol. 2010 Aug; 68(2): 136–144.
- 24, 25 European Review of Aging and Physical Activity volume 16, Article number: 10 (2019)
- 26 Scientific Reports, 2018; 8(6670)
- 27 Front. Aging Neurosci., 26 July 2018
- 28 Neurobiol Aging. 2012 Feb; 33(2): 425.e19–425.e27
Reproduced from original article:
Analysis by Dr. Joseph Mercola
December 20, 2019
- Chronic fatigue syndrome appears to be rooted in mitochondrial dysfunction. Your mitochondria are responsible for energy production, and as the name implies, low energy and severe fatigue are hallmarks of this condition
- Immune cells in the blood of patients diagnosed with chronic fatigue show clear signs of low energy production. The debilitating fatigue they experience is due to an inability to produce the cellular energy needed
- A ketogenic diet, high in healthy fats and low in net carbohydrates, with moderate protein, is a key dietary strategy that helps optimize mitochondrial function
- Patients with chronic fatigue also lack diversity in the gut microbiome, and the presence of certain inflammatory cytokines in their blood closely correlates with symptom severity
- Strategies that reduce inflammation, heal your gut microbiome and support mitochondrial function and energy synthesis are all beneficial for chronic fatigue patients
Chronic fatigue syndrome (CFS), which is thought to affect up to 2.5 million Americans,1 is a debilitating condition in which sufferers experience unrelenting fatigue no matter how much rest they get. Pain and chronic inflammation are other hallmarks. A number of other names are also used for this condition, including:
- Myalgic encephalopathy/myalgic encephalomyelitis (ME)
- Post-viral fatigue syndrome (PVFS)
- Chronic fatigue immune dysfunction syndrome (CFIDS)2
- Systemic exertion intolerance disease (SEID)3
The most common designation is ME/CFS and, according to the CDC, about 90% of people with ME/CFS have not yet been diagnosed.4 In the past, ME/CFS was typically brushed off as being a psychological problem, but in more recent years, researchers have discovered physiological commonalities between groups of individuals that validate their symptoms.
For example, ME/CFS patients tend to have similar changes in gut bacteria, and certain inflammatory biomarkers in your blood appear to correlate with ME/CFS symptoms.5 Most recently, researchers have found additional support for the hypothesis that ME/CFS is rooted in mitochondrial dysfunction, which makes logical sense considering your mitochondria are responsible for energy production.
These tiny powerhouses are an interconnected network that rapidly and effectively distributes energy throughout your body’s cells.6 Your mitochondria are also responsible for programmed cell death, and serve as important signaling molecules that help regulate the expression of your genes.
When your mitochondria do not work properly, low energy is a natural side effect. Knowing this, the remedy becomes clearer as well. A ketogenic diet, high in healthy fats and low in net carbohydrates, with moderate protein, is a key dietary strategy that helps optimize mitochondrial function.
What Is Chronic Fatigue Syndrome?
Until recently, the diagnosis of ME/CFS has been one of exclusion. This meant all other illnesses mimicking the symptoms of ME/CFS had to first be ruled out before doctors could suggest you were suffering from ME/CFS. Symptoms of ME/CFS can vary widely from one individual to the next.
The most common symptom is one of overwhelming exhaustion that worsens with physical or mental energy expenditure and does not get better with rest.7 It may take up to 48 hours after activity to experience the full extent of the exhaustion. Other symptoms of the condition may mimic other medical conditions, and include:8,9,10
|Muscle pain||Memory problems||Headaches|
|Sore throat||Pain in multiple joints||Difficulty sleeping|
|Tender lymph nodes||Visible muscle twitching (fasciculations)||Difficulty concentrating|
|Short attention span||Word find problems||Excessive sweating|
|Enlarged glands||Intermittent flu-like symptoms||Alcohol intolerance|
|Irritable bowl-like symptoms||Mood swings||Temperature control|
|Food intolerance||Gastrointestinal problems||Hypersensitivity to light and noise|
ME/CFS Is a Side Effect of Cellular Exhaustion
As mentioned, researchers have now identified what appears to be a root problem: exhaustion at a cellular level. This study11 was published in PLOS One at the end of October 2017. Immune cells in the blood of patients diagnosed with ME/CFS “show clear signs of low energy production,” Science Alert reports.12 This strongly suggests mitochondrial dysfunction, as the mitochondria are responsible for energy production. As noted in the featured article:13
“Researchers looked specifically at the metabolic processes of oxidative phosphorylation and glycolysis — two ways cells break apart chemical fuel to transfer energy in respiration. White blood cells taken from 52 patients with CFS and 35 controls were put through their paces under optimal and stressful conditions, testing their capacity to deal with low oxygen levels.
There appeared to be a number of key differences in their metabolic processes. But none were as dramatic as the contrast in maximum levels of respiration. By forcing the cells to boost their energy production, the researchers found those with CFS could only squeeze about another 50 percent from their cells — unlike the controls, who nearly doubled their output.”
In short, ME/CFS patients lack the ability to compensate for increased stress on a cellular level, and the debilitating fatigue they experience is due to the inability to produce the cellular energy needed to keep the body fully functional. Their mitochondria are simply unable to produce enough ATP to maintain an energy gradient across their cell membranes. As noted by the authors:
“Lower reserve capacity observed in CFS patients are indicative of the cells of patients performing closer to their capacity in normal conditions without stress than healthy controls. Lowered maximal respiration suggests that the PBMCs [peripheral blood mononuclear cells] of CFS patients are not capable of the same levels of respiration as healthy controls.”
ME/CFS Also Linked to Lack of Microbial Diversity in Gut
Another study published in the journal Microbiome evaluated the blood and stool of 48 people diagnosed with ME/CFS and compared the results to those from 39 healthy people.14,15 Here, differences were found in both stool and blood samples. Using DNA sequencing, a process of determining the precise order of nucleotides in a DNA molecule, they found a distinct lack in diversity in the gut microbiome in affected individuals.
Although these changes could not be clearly identified as either the cause or consequence of ME/CFS, researchers were heartened by the presence of these markers in 83% of the sample, and the possibility of treatment options to reduce symptoms. Quoted in the Washington Journal, professor of molecular biology and genetics at Cornell University, Maureen Hanson said:16
“Our work demonstrates that the gut bacterial microbiome in chronic fatigue syndrome patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease. Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”
Addressing Leaky Gut May Help ME/CSF Patients
The researchers theorize the inflammatory markers in the blood could be the result of a “leaky gut from intestinal problems that allow bacteria to enter the blood.”17 Indeed, other recent research18,19 has confirmed the presence of more than a dozen inflammatory cytokines in blood that closely correlate with reported symptom severity in patients suffering from ME/CFS.
This confirms a suspicion of some researchers that symptoms of fluctuating flu-like symptoms and body aches associated with ME/CFS is linked to an inflammatory response.20 It’s important to realize that there is a distinct link between leaky gut and the foods you eat. Probably the single most important factor here is the herbicide glyphosate, which is pervasive. Between 1974 and 2014, over 3.5 billion pounds of glyphosate were used in the U.S. alone.21
Worldwide in 2017, 4.4 billion pounds (2 billion kilograms) of glyphosate were being used annually.22 Glyphosate will decimate tight junctions and contribute to leaky gut. Fortunately, you can radically reduce your exposure by eating organic and avoiding processed foods, which are usually contaminated. You can also check your glyphosate level with a simple urine test, to see how badly you’ve been exposed.
Grains and lectins, even organic non-GMO, are particularly troublesome. Research shows that gluten stimulates a protein molecule in your gut called zonulin, which triggers the opening of junctures between the cells in your gut lining. In essence, it makes your gut more permeable, allowing food particles to escape into your bloodstream, causing inflammation, immune reactions and raising your risk of various autoimmune disorders.
Certain plant lectins may also contribute to leaky gut by binding to receptor sites on your intestinal mucosal cells, thereby interfering with the absorption of nutrients across your intestinal wall. As such, they act as “antinutrients” and can have a detrimental effect on your gut microbiome by shifting the balance of your bacterial flora.
Among the worst culprits are wheat germ agglutinin (WGA), found in wheat and other seeds in the grass family. In fact, according to Dr. Steven Gundry, author of “The Plant Paradox: The Hidden Dangers in ‘Healthy’ Foods That Cause Disease and Weight Gain,” gluten is a minor problem compared to WGA.
Evidence suggests lectins are strongly associated with autoimmune disorders in general, so anyone struggling with a dysfunctional immune system may want to seriously consider experimenting with a low-lectin diet. As for ME/CFS, leaky gut is not an automatic precursor. However, healing and sealing your gut and reducing the inflammatory response in your body may result in a significant reduction in chronic fatigue symptoms by supporting your immune system.
Ketogenic Diet May Speed Resolution of Chronic Fatigue
In 2015, Dr. Courtney Craig, a chiropractor and nutritionist, wrote about her personal experience with the ketogenic diet. Diagnosed with CFS in her teen years, she’s been able to control her condition using a number of integrative health strategies, including intermittent fasting and nutritional ketosis. Describing a particularly harrowing relapse, she goes on to discuss how switching to a ketogenic diet helped her rapidly recover. She writes, in part:23
“I needed a serious immune and mitochondrial reset … So, I shifted my usual paleo-diet around, and astonishingly I bounced back very quickly … I started consuming about 80 percent of my calories from healthy fats … This is something I do periodically when the fatigue rears its ugly head … It’s also advocated by doctors like … Dr. Thomas Seyfried …
I flipped a switch on my metabolism. I stopped relying so much on glucose for metabolism, and instead encouraged my liver to break down those dietary fats into ketones — a much “cleaner” energy source … The downside of burning carbohydrate as fuel, is production of cellular stress and free radicals. Ketones provide a “cleaner” energy for cells and are less damaging to cell membranes … A ketogenic diet can be initiated with a 12 to 72 hour fast.
Then the diet is maintained by consuming 75-90% of calories as fat, with the remainder coming from moderate amounts of protein and very little carbohydrate. The ketogenic diet is one that should be considered when dealing with ME/CFS … A body of research in animals and humans have highlighted some of the mechanisms by which dietary ketones promote cellular health.“
Indeed, when your body is able to burn fat for fuel, your liver creates water-soluble fats (ketones) that:
- Burn far more efficiently than carbs, thereby creating fewer reactive oxygen species and secondary free radicals that can damage your cellular and mitochondrial cell membranes, proteins and DNA
- Decrease inflammation, as they are histone deacetylase inhibitors
- Mimic the life span extending properties of calorie restriction, which includes improved glucose metabolism and reduced inflammation24
- Have a similar structure to branched-chain amino acids, thereby aiding the building muscle mass and promoting longevity
The Importance of Cyclical Ketosis
Nutritional ketosis is the metabolic state associated with an increased production of ketones in your liver; i.e., the biological reflection of being able to burn fat, and is defined as having blood ketones in the range of 0.5 to 3.0 millimoles per liter. As a general guideline, a dietary intake of 20 to 50 grams (or less) per day of net carbs (total carbohydrates minus fiber) while also keeping protein low-to-moderate is usually low enough to allow you to make the shift to nutritional ketosis.
However, once you achieve metabolic flexibility and are able to generate ketones with nutritional ketosis, it’s important to include higher carb intakes every now and then. For all its benefits, continuous ketosis actually has some downsides that are easily avoided by implementing a cyclical “feast and famine” regimen. I detail the reasons for this in my book, “Fat for Fuel.” In summary, long-term uninterrupted ketosis can trigger a rise in blood sugar by driving your insulin level too low.
This paradoxical situation can occur because the primary function of insulin is not actually to drive sugar into the cell but rather to suppress the production of glucose by your liver (hepatic gluconeogenesis).
Cycling in and out of nutritional ketosis will effectively prevent this rise in blood sugar in the absence of high glucose. So, once you are able to burn fat as fuel, having a day or two each week where you eat more net carbs and protein is important, especially when you’re doing strength training, to prevent sarcopenia.
After a day of “feasting,” you then cycle back into nutritional ketosis (the “fasting” stage) for the remainder of the week. By periodically pulsing higher carb intakes, consuming, say, 100 or 150 grams of carbs opposed to 20 to 50 grams per day, your ketone levels will dramatically increase and your blood sugar will drop.
Chronic Fatigue Patients Need Mitochondrial Support
In this 2016 interview, I discuss the importance of mitochondrial function and how it may impact your symptoms of chronic illnesses like ME/CFS. It stands to reason that a condition that triggers an inflammatory response and gut dysfunction, and that results in overwhelming fatigue, will respond favorably to treatment strategies that reduce inflammation, heal your gut microbiome and support mitochondrial function and energy synthesis.
Diet-wise, a cyclical ketogenic diet would be a foundational strategy. The following dietary recommendations will also help heal and seal your gut, lower inflammation and support healthy energy production. You can also read more about supporting your gut health in “Nourishing Your Gut Bacteria is Critical for Health and Mental Well-Being.”
|Avoid gluten and wheat products — Gliadins, a component of gluten, are a class of protein found in wheat and cereals that increase the permeability of your gut. Keep in mind that gluten can also be found in other grains, not just wheat.|
|Avoid lectins — To learn more, including which foods are best avoided due to high lectin content, please see “How to Reduce Lectins in Your Diet.”|
|Reduce your net carbs — The carbohydrate sugar, like grains, will upset the balance of microbes in your gut. Sugar is the food source for bacteria that can prompt damage to your intestinal walls, while fiber is the food source for bacteria that build your intestinal membranes.
Your net carbs are the total grams of carbohydrates you’ve eaten in a day, minus the grams of fiber you’ve eaten. The difference is your net carbs. Seek to reduce your net carbs to 50 grams per 1,000 calories of food you eat each day.
|Increase your fiber intake — The fiber you eat from whole foods is the nutrient source for bacteria in your gut that helps maintain and build the membrane cells in your intestinal walls. This helps to seal the “gaps” between the cells and reduces any leakage of waste products and bacteria into your blood stream. Focus on eating whole food vegetables, nuts and seeds (with the exception of lectin-rich varieties).|
|Eat fermented foods — Fermented foods are a great source of natural probiotics to feed healthy microbes in your gut. Olives, pickles, kimchi, cheese from grass fed cows, homemade yogurt and sauerkraut are just a few of the foods you may not have considered. Your best bet is to make your own. In this video, Julie and I demonstrate how to make your own fermented vegetables at home.
|Supplement with nutrients important for cellular energy synthesis such as ubiquinol, the reduced form of CoQ10, and D-ribose, a core building block of adenosine triphosphate or ATP. Also eat foods rich in glutathione precursors, sulfur and selenium to encourage glutathione production. Glutathione is one of your body’s most important antioxidants and a natural detoxification agent.|
|Intermittently fast, making sure your last meal is taken at least three hours before bedtime. The rationale for avoiding late night eating is directly tied to the way your body produces energy.|
Other Strategies to Help Reduce Chronic Fatigue Symptoms
There is no known cure for ME/CFS, but there are strategies that can help alleviate symptoms,25 over and beyond the dietary recommendations already mentioned. My full metabolic mitochondrial therapy program is described in my book, “Fat for Fuel.” Cold thermogenesis, photobiology, detoxification, exercise and avoiding electromagnetic fields are all strategies that will help improve mitochondrial health and function.
When it comes to exercise, work out according to your ability, with a focus on increasing the amount of exercise you can handle. Research shows that a combination of aerobic activity and strength training can improve pain and fatigue symptoms. Gentle exercise such as yoga can also be an excellent part of your program, and yoga benefits your mind as well as your body.
You may also want to address your mental outlook. In addition to talk therapy, I would recommend trying The Emotional Freedom Techniques (EFT) to help normalize your bioenergetic circuitry. Emotionally traumatic events can leave “energy blockages” for many years, which then interfere with your overall health, including immune function. There are many different techniques that can be used, but EFT is my favorite, and it’s easy to learn and apply.
- 1 CDC, July 22, 2019
- 2 National CFIDS Foundation, July 2, 2019
- 3 National Academy of Sciences February 10, 2015 Press Release
- 4, 7, 8 CDC, July 12, 2018
- 5 Science Daily June 27, 2016
- 6 Molecular Expressions, Mitochondria
- 9 CDC, November 19, 2019
- 10 Stanford Medicine, October 28, 2014
- 11 PLOS One October 24, 2017
- 12, 13 Science Alert November 7, 2017
- 14 Microbiome 2016; 4(1)
- 15, 16, 17 Washington Post June 30, 2016
- 18 PNAS June 28, 2017
- 19, 20 Science Alert, August 1, 2017
- 21 EcoWatch, January 10, 2017
- 22 Healing Earth, Zach Bush Interview August 4, 2017
- 23 Health Rising April 6, 2015
- 24 IUMB Life April 3, 2017, DOI: 10.1002/iub.1627
- 25 CDC, November 19, 2019, Treatment of ME/CFS
Reproduced from original article:
December 05, 2019
- Seasonal affective disorder (SAD) is a form of depression that occurs seasonally, typically ramping up in the fall and winter months and disappearing come spring
- Helpful treatments include optimizing your vitamin D and omega-3 levels, light therapy (including blue light exposure in the morning, but not later in the day), optimizing your sleep, the Emotional Freedom Techniques and exercise
- Your health and mood are intricately tied to exposure to sunlight. For example, your serotonin levels (the hormone typically associated with elevating your mood) rise when you’re exposed to bright light. Your melatonin level also rises and falls (inversely) with light and darkness
- Vitamin D deficiency is very common, and should be a top consideration when you’re looking for a solution to flagging mood and energy — especially if it occurs during fall and winter months
- While light therapy can take up to four weeks before you notice improvement, it was shown to be more effective than antidepressants for moderate to severe depression in a 2015 study
The loss of daylight hours during winter is a common cause of seasonal affective disorder (SAD), a type of depression that hits seasonally and lifts as spring and summer rolls back around.
The fact that SAD occurs when the days begin to darken and sunlight is at a minimum is not a coincidence. Your health and mood are intricately tied to exposure to sunlight. For example, your serotonin levels (the hormone typically associated with elevating your mood) rise when you’re exposed to bright light.
Your melatonin level also rises and falls — inversely — with light and darkness. When it’s dark, your melatonin levels increase, which is why you may feel tired when the sun starts to set, and in the heart of winter, this may be at as early as 3 p.m. if you live far from the equator. Light and darkness also control your biological clock, or circadian rhythm, which impacts hormones that regulate your appetite and metabolism.
As explained in the paper, “Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches,” published in the journal Depression Research and Treatment in 2015:1
“… SAD is a recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months. A subsyndromal type of SAD, or S-SAD, is commonly known as ‘winter blues.’ Less often, SAD causes depression in the spring or early summer.
Symptoms center on sad mood and low energy. Those most at risk are female, are younger, live far from the equator, and have family histories of depression, bipolar disorder, or SAD … Typical treatment includes antidepressant medications, light therapy, vitamin D, and counselling.”
Considering the many health risks associated with antidepressants, and the fact that their efficacy is right on par with placebos, my recommendation is to avoid them if at all possible.
Aside from light therapy and vitamin D, other drug-free treatment options include optimizing your omega-3 level, exercise, the Emotional Freedom Techniques (EFT) and normalizing your circadian rhythm, all of which will be reviewed here.
The Role of Vitamin D
People with SAD tend to have lower serotonin and higher melatonin levels, which can account for the fatigue, tiredness and depressed mood typically associated with this condition. According to the Depression Research and Treatment paper:3
“A systematic review and meta-analysis concluded that low levels of vitamin D are associated with depression … During the winter months of November through February, those living about 33 degrees north or 30 degrees south of the equator are not able to synthesize vitamin D.
Many people with SAD and S-SAD have insufficient or deficient levels of vitamin D, and although no further studies have confirmed the findings, research investigating this association suggests that taking 100,000 IU daily may improve their symptoms.
Taking vitamin D before winter darkness sets in may help prevent symptoms of depression. Adverse reactions or intoxication is rare but could occur from doses of more than 50,000 IU per day.”
Vitamin D deficiency is very common, and should be a top consideration when you’re looking for a solution to flagging mood and energy — especially if it occurs during fall and winter months.
Ideally, you’ll want to get your vitamin D level tested twice a year, in summer and winter, when your levels are highest and lowest. This will help you fine-tune your dosage over time. While regular sun exposure is the best way to optimize your vitamin D level, this isn’t possible in many areas during the winter, thus necessitating the use of oral supplements instead.
GrassrootsHealth has a helpful calculator that can help estimate the dose required to reach healthy vitamin D levels based upon your measured starting point. The optimal level you’re looking for is between 60 and 80 ng/ml, and for all-around health, you’ll want to maintain this level year-round.
Omega-3 Fats Are Important Too
Another nutrient that can be helpful is marine-based omega-3. As noted in a 2009 review4 of three studies looking at the impact of omega-3 supplementation on patients with unipolar depression, childhood major depression and bipolar depression:
“Twelve bipolar outpatients with depressive symptoms were treated with 1.5-2.0 g/day of EPA for up to 6 months. In the adult unipolar depression study, highly significant benefits were found by week 3 of EPA treatment compared with placebo.
In the child study, an analysis … showed highly significant effects of omega-3 on each of the three rating scales. In the bipolar depression study, 8 of the 10 patients who completed at least one month of follow-up achieved a 50% or greater reduction in Hamilton depression scores within one month.”
In another study5 published that same year, people with lower blood levels of omega-3s were found to be more likely to have symptoms of depression and a more negative outlook while those with higher blood levels demonstrated the opposite emotional states.
A more recent review,6 published in 2015, pointed out that “Cell signaling and structure of the cell membrane are changed by omega-3-fatty acids, which demonstrates that an omega-3-fatty acid can act as an antidepressant.”
Importantly, this paper also points to research showing that the ratio of omega-3 to omega-6 is an important factor that can influence your depression risk. People with severe symptoms of depression have been found to have low concentrations of omega-3 in conjunction with considerably higher concentrations of omega-6.
You can learn more about the importance of this ratio in “Getting Your Omega-3 to Omega-6 ratio Right Is Essential For Optimal Health.” The key, really, to normalizing this ratio is to increase your omega-3 intake while simultaneously lowering your omega-6 consumption. This means you’ll need to ditch processed and fried foods, as they’re typically loaded with omega-6-rich vegetable oils.
Get Tested Today
GrassrootsHealth, which is conducting consumer-sponsored research into both vitamin D and omega-3, is one of your most cost-effective alternatives when it comes to testing.
Their vitamin D testing kit enrolls you into the GrassrootsHealth D*Action project, where your anonymized data will help researchers to provide accurate data about the vitamin D status in the population, the level at which disease prevention is obtained, and guidance on dosing to achieve optimal levels.
Their vitamin D, magnesium and omega-3 test kit is another option that will allow you to check the status of several vital nutrients at once. Each kit contains instructions for how to collect your blood sample. You then mail in your sample and fill out a quick online health questionnaire through GrassrootsHealth. A link to your test results will be emailed to you about a week after your blood samples have been received.
Light Therapy Is More Effective Than Antidepressants
Light therapy,7 using full-spectrum nonfluorescent lighting that has blue light to artificially mimic sunlight, is among the most effective treatment options for SAD. You want to avoid fluorescents as they emit large amounts of dirty electricity. Ideally, have the light exposure in the morning, well after sunrise. As noted in the Depression Research and Treatment paper:8
“Knowing the difference decreased daylight can make in triggering SAD and S-SAD, approaches seeking to replace the diminished sunshine using bright artificial light, particularly in the morning, have consistently showed promise …
Light boxes can be purchased that emit full spectrum light similar in composition to sunlight. Symptoms of SAD and S-SAD may be relieved by sitting in front of a light box first thing in the morning, from the early fall until spring …
Typically, light boxes filter out ultraviolet rays and require 20–60 minutes of exposure to 10,000 lux of cool-white… light daily during fall and winter.
This is about 20 times as great as ordinary indoor lighting … Light therapy should not be used in conjunction with photosensitizing medications such as lithium, melatonin, phenothiazine antipsychotics, and certain antibiotics.”
While light therapy can take up to four weeks before you notice an improvement, it was shown to be more effective than antidepressants for moderate to severe depression in a 2015 study.9,10 In it, the researchers evaluated the effectiveness of light therapy, alone and in conjunction with the antidepressant fluoxetine (sold under the brand name Prozac).
The eight-week trial included 122 adults between the ages of 19 and 60, who were diagnosed with moderate to severe depression. The participants were divided into four groups, receiving:
- 30 minutes of light therapy per day upon waking, using a 10,000 lux Carex brand day-light device, classic model, plus a placebo pill
- Prozac (20 mg/day) plus a deactivated ion generator serving as a placebo light device
- Light therapy plus Prozac
- Placebo light device plus placebo pill (control group)
In conclusion, the study found that the combination of light therapy and Prozac was the most effective — but light therapy-only came in at a close second, followed by placebo. In other words, the drug treatment was the least effective of all, including placebo.
The mean changes in the Montgomery-Åsberg Depression Rating Scale from baseline to the eight-week end point was 16.9 for the combination therapy (active light- and drug therapy), and 13.4 for light therapy alone.
Blue Light During Daytime Hours May Improve Your Mood
In addition to the bright white light used in light therapy, blue light has also been shown to be useful. According to a 2010 study,11 blue light appears to play a key role in your brain’s ability to process emotions, and its results suggest that spending more time in blue-enriched light could help prevent SAD.
Blue light is prevalent in outdoor light, so your body absorbs the most during the summer and much less in the winter. Because of this, the researchers suggested that adding blue light to indoor lighting, as opposed to the standard yellow lights typically used, may help boost mood and productivity year-round, and especially during the winter.
Keep in mind, however, that blue light after sunset or before sunrise should be avoided, as it can disrupt your circadian rhythm. In fact, one of the reasons for insomnia and poor sleep is related to excessive exposure to blue light-emitting technologies such as TV and computer screens, especially in the evening.
The blue light depresses melatonin production, thereby preventing you from feeling sleepy. So, to be clear, you only want to expose yourself to blue light in the morning, and possibly afternoon, but not in the evening.
In “How the Cycles of Light and Darkness Affect Your Health and Well-Being,” researcher Dan Pardi explains the peculiar effect blue light has on your brain, which sheds further light on why it’s so important to expose yourself to blue light during daytime hours only, and why you need to avoid it at night:
“[R]ods and cones in the eye… are specialized cells that can transduce a photo signal into a nerve signal… In the mid-90s, a different type of cell was discovered… [called] intrinsically photosensitive Retinal Ganglion Cells (ipRGC).
It does the same thing as rods and cones: it transduced light to a nerve signal. But instead of the signal going to your visual cortex, it goes to your master clock. Those cells are most responsive to blue light. If you can block blue light, you can actually create something called circadian darkness or virtual darkness.
What that means is that you can see, but your brain doesn’t think that it’s daytime; your brain thinks that it’s in darkness. That is actually a practical solution for living with artificial light in our modern world…
With more awareness, future digital devices will adjust lighting in the evening to automatically dim and emit amber/red light [instead of blue]. This is much better for healthy circadian rhythms and sleep quality.”
As you can tell by Pardi’s explanation above, the blue light issue is closely related to your sleep quality and circadian rhythm maintenance, and this too is an important component of mental health.
Historically, humans went to sleep shortly after sunset and woke up when the sun rose. Straying too far from this biological pattern will disrupt delicate hormonal cycles in your body, which can affect both your mood and your health. Indeed, the link between depression and lack of sleep is well established, and sleep disturbance is one of the telltale signs of depression.12
Sleep therapy has also been shown to significantly improve depression. While there are individual differences, as a general rule, you’ll want to aim for about eight hours of sleep per night.
For many, this will require going to bed earlier, which can be difficult if you’ve been watching TV or using electronics beforehand, as the blue light from the screen suppresses your melatonin production.
So, an important part of the solution is to avoid screen-time for a couple of hours before bed. Alternatives to not watching TV or using electronics is to install a blue light modulating software such as Iris,13 or using blue-blocking glasses.
Just make sure you don’t wear blue blocking glasses during the daytime, which is when you need the blue light exposure. Also, make sure the glasses filter out light between 460 to 490 nanometers (nm), which is the range of blue light that most effectively reduces melatonin. You can easily tell this by looking at a blue light and if it doesn’t disappear with the glasses, it is not blocking that frequency.
Exercise Helps Prevent Depression
Like sleep, exercise can impact your risk of depression. Even a minimal amount of exercise may be enough to combat depression in some people — as little as one hour a week could prevent 12% of future cases of depression, according to one study.14
Participants were followed for 11 years in this study, during which time it was revealed that people who engaged in regular leisure-time exercise for one hour a week, regardless of intensity, were less likely to become depressed. On the flipside, those who didn’t exercise were 44% more likely to become depressed compared to those who did so for at least one to two hours a week.
Exercise benefits your brain and mood via multiple mechanisms, including creating new, excitable neurons along with new neurons designed to release the GABA neurotransmitter, which inhibits excessive neuronal firing, helping to induce a natural state of calm15 — similar to the way anti-anxiety drugs work, except that the mood-boosting benefits of exercise occur both immediately after a workout and on in the long term.
Exercise also boosts levels of potent brain chemicals like serotonin, dopamine and norepinephrine, which may help buffer some of the effects of stress. What’s more, anandamide levels are known to increase during and following exercise.16 Anandamide is a neurotransmitter and endocannabinoid produced in your brain that temporarily blocks feelings of pain and depression. It can also be activated with CBD products.
Tap for Symptoms of Depression
Last but not least, EFT, a form of psychological acupressure, is a noninvasive way that can help treat symptoms of depression, whether related to seasonal light differences or not.
Some people avoid energy psychology, believing it’s an alternative form of New Age spirituality. Nothing could be further from the truth. It is merely an advanced tool that can effectively address some of the psychological short circuiting that occurs in emotional illnesses.
It is not associated with any religion or spiritual outlook at all, but merely an effective resource you can use with whatever spiritual belief you have. In the video above, EFT practitioner Julie Schiffman demonstrates how you can use EFT to relieve your symptoms.
It’s the Season To Be Glad, Not SAD
Since SAD is triggered by the loss of light, it makes sense that light therapy is among the most effective treatments. Vitamin D and/or omega-3 deficiency, as well as lack of sleep and exercise, can also play a significant role, so addressing these basic lifestyle factors could also be what you need to avoid the winter blues.
In closing, it may be worth noting that it’s natural for your body to want to slow down somewhat in the wintertime. While this can be difficult when your work and personal life dictate otherwise, allowing yourself to slow down a bit and surrender to the overwinter process may ultimately help you to respect your body’s circadian rhythm, and recharge.
That said, this doesn’t mean you should plant yourself on the couch for the winter and not venture outdoors. On the contrary, staying active and spending time outdoors during the day are among the best “cures” for SAD.
- 1 Depression Research and Treatment 2015; 2015: 178564
- 2 Depression Research and Treatment 2015; 2015: 178564, 2. An explanation of Seasonal Affective Disorder
- 3 Depression Research and Treatment 2015; 2015: 178564, 3.3 Vitamin D
- 4 CNS Neurosci Ther. 2009 Summer;15(2):128-33
- 5 Psychother Psychosom 2009;78:125–127
- 6 Integrative Medicine Research 2015 Sep; 4(3): 132–141, 2. Omega-3 fatty acids and depression
- 7 Live Science February 12, 2019
- 8 Depression Research and Treatment 2015; 2015: 178564, 3.2 Light therapy
- 9 JAMA Psychiatry November 18, 2015. doi:10.1001/jamapsychiatry.2015.2235
- 10 Reuters November 19, 2015
- 11 Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19549-54
- 12 Dialogues Clin Neurosci. 2008 Dec; 10(4): 473–481
- 13 Iris Blue Blocking Software
- 14 American Journal of Psychiatry October 3, 2017, DOI: 10.1176/appi.ajp.2017.16111223
- 15 The Journal of Neuroscience May 1, 2013; 33(18):7770-7
- 16 Transl Psychiatry. 2014 Jul 8;4:e408.
Reproduced from original article:
November 26, 2019
- Ali and Orooba Hamideh’s disabled 9-year-old son, Ameer, lost his vaccine exemption after the passage of New York’s Senate Bill S2994A in June 2019, which removed all non-medical exemptions to school vaccination requirements
- Ameer was born prematurely and suffered a stroke at birth. He was diagnosed with cerebral palsy at age 3, and has a rare seizure disorder called Lennox Gastaut syndrome
- Ameer’s seizures began after his first round of vaccines at 5 months of age. His parents, who attributed the seizures to the complications at his birth, dutifully followed the recommended vaccine schedule. It wasn’t until he got a flu shot at the age of 2 that they started asking questions
- After getting a medical exemption from his neurologist, Ameer was again denied school access after the New York Department of Health denied the exemption, stating his seizure condition was not a contraindication to vaccination
- The Hamideh family sued the school, and November 12, 2019, the Erie County Supreme Court judge presiding over the case issued a temporary restraining order to allow Ameer to attend his classes at the CHC Learning Center for the duration of the court proceedings. The case is still ongoing
The global vaccine market was valued at $35.8 billion in 2018, and it’s predicted to nearly double by 2024.1,2 One major reason for this exponential growth has to do with the fact that more vaccines are being mandated as a condition for school attendance, while vaccine exemptions are being eliminated.3
After a U.S. Supreme Court ruling in 2011, vaccine manufacturers are also the only corporations selling products in the U.S. that cannot be sued, even when there is evidence the company could have made a product safer.4,5
After Congress amended the 1986 National Childhood Vaccine Injury Act at the end of 1987, doctors and medical workers who administer federally recommended vaccines that injure or kill children can’t be sued either.6 In 2016, Congress expanded vaccine manufacturer liability protection to include federally recommended vaccines that injure or kill pregnant women or their unborn infants in the womb.7
This blanket protection from liability is part and parcel of what makes vaccines so profitable — and potentially hazardous.
Making matters worse, state legislatures in California8 and New York9 have passed laws that remove the legal right for doctors to exercise professional judgment and conscience when granting children a medical exemption to vaccination.10,11,12
A recent case highlighted by The Highwire demonstrates just how difficult it has become to obtain a vaccine exemption — even when a child’s life is clearly at high risk for suffering harm from vaccination — and the disastrous ramifications it can have for families whose children are denied school access simply because they’re not willing to roll the dice when it comes to protecting their child from harm.
Vaccination Laws Sacrifice the Vulnerable
In the video above, Del Bigtree, CEO of the Informed Consent Action Network (ICAN), a nonprofit he founded in 2017, interviews Ali and Orooba Hamideh, who live in New York. Their disabled 9-year-old son, Ameer, lost his vaccine exemption after the passage of New York’s Senate bill S2994A13 in June 2019, which removed all non-medical exemptions to school vaccination requirements.14
Weeks later, the New York health department issued a new rule that denied New York physicians the legal right to grant a child a medical exemption to vaccination unless the reasons given strictly conform to vaccine contraindications approved by public health officials at the U.S. Centers for Disease Control (CDC).15,16
Ameer was born prematurely and suffered a stroke at birth. He was diagnosed with cerebral palsy at age 3, thought to be the result of the brain damage he suffered from his stroke. Ameer also has a rare seizure disorder called Lennox Gastaut syndrome (LGS17).
His seizures began after his first round of vaccines at 5 months of age. His parents, who attributed the seizures to the complications at his birth, dutifully followed the recommended vaccine schedule. It wasn’t until he got a flu shot at the age of 2 that they started asking questions.
As with previous vaccines, his seizures and other symptoms worsened directly after the shot. After researching the matter, and finding others whose stories mirrored their own, they decided to not give Ameer any more vaccines.
They opted to file a religious vaccine exemption for Ameer, simply because it was easier, but the new law meant Ameer could no longer attend school, and he ended up missing months of education and therapy over the summer while his parents turned to Ameer’s neurologist, who has treated him for nine years. She issued a medical exemption, stating:
“Patient carries a diagnosis of Lennox Gastaut with refractory seizures. Patient has a history of hospitalization following immunizations in the past for seizure activity triggered by those immunizations.”
Seizure Disorder Not a Valid Contraindication to Vaccination
With the medical exemption in place, Ameer was allowed back to school. But then, September 12, 2019, the Hamidehs received a copy of a letter from the New York Department of Health sent to Ameer’s school, recommending his medical exemption should be denied. Dr. Elizabeth Rausch-Phung, director of the New York Bureau of Immunization, wrote:
“I have reviewed the documentation submitted by Sarah Finnegan, MD with regard to the medical exemption request for the student in your school …
Lennox Gastaut with refractory seizures is not a valid contraindication to this student receiving MMR, varicella, polio, or Tdap vaccines pursuant to Public Health Law (PHL) 2164 and the accompanying regulations at 10 NYCRR Subpart 66-1. Therefore, I recommend against accepting this medical exemption.”
Ameer was again kicked out, for while the health department didn’t forbid the school to accept the exemption, the school refused to go against the health department’s recommendation, saying it would be “foolish” of them to do so.
“You feel awful,” Ali says. “You have no choice over your child. No choice at all.” Seizure disorders are serious medical conditions, and Ameer’s parents fear that any additional vaccines could cause uncontrolled seizure activity leading to his death.
Since the family started him on a ketogenic diet and CBD oil, Ameer has gone from 20 to 30 seizures a day to none. He’s making progress that simply isn’t worth risking. Yet, as noted by Bigtree, New York state essentially delivered a potential death sentence to this child — all because he’s missing his fifth Tdap booster.
Justice for Ameer — For Now
In desperation, Ali vented his frustration on Facebook, asking for help. The story went viral, being shared more than 100,000 times, eventually making headlines on local news.
As noted by Bigtree, one of the official justifications for removing non-medical vaccine exemptions and mandating certain vaccines is to protect immunocompromised children who cannot be vaccinated.
Yet here we have a child whose history clearly shows he is at grave risk for vaccine damage, whose neurologist agrees vaccination could compromise his health and worsen his already serious condition, and he’s somehow not worthy of that same protection.
Ameer, by the way, is not an isolated case — 26,000 children in New York lost their rights to public education with the passing of S2994A.18
In The Highwire video above, the Hamidehs mention they would take legal action if the school did not allow Ameer back in. Since the airing of that episode, Ameer’s case has been brought to court, resulting in a temporary legal victory.
November 12, 2019, the Erie County Supreme Court judge presiding over the case issued a temporary restraining order to allow Ameer to attend his classes at the CHC Learning Center for the duration of the court proceedings.19 But first, Ali had to present to the court a signed affidavit from the neurologist, confirming the signature on the medical exemption wasn’t a fraudulent one.
This request was so out of the ordinary and the neurologist was so surprised and confused by the request that she initially refused. Fortunately, by the time Ali and his attorney reached the court house, she’d emailed them the signed affidavit. No school representative from the school or state education department attended the hearing. The case goes back to court in December. As reported in an ICAN press release:20
“Because of Ameer’s previous severe reaction to the DTaP vaccine — most recently a grand mal seizure that sent him, uncontrollably screaming, to the hospital — his parents Ali and Orooba Hamideh followed the advice of Ameer’s physician to not give him an additional dose.
ICAN took up the family’s cause and turned its team of attorneys to the case, which pointed out — among other things — New York state law allows any doctor to provide a valid medical exemption, and does not provide the Department of Health the authority to overrule that exemption.
‘This is so satisfying because of what it means for the Hamideh family,’ says Del Bigtree … ‘The State thought they could steamroll the Hamideh family. Their bureaucratic decision regarding Ameer’s medical treatment, made without ever even talking to his doctor, could have seriously injured him.’”
‘Nothing Is Working the Way It’s Supposed To’
At the end of the November 12, 2019, video update above, Bigtree says:
“I will tell you my experience today, in watching how the courts were dealing with this issue, and watching the hoops having to be jumped through that lawyers don’t normally see in any other case … — doctors being forced to sign [an affidavit confirming] their own signature — this is just a bizarre world we are living in right now.
And it’s extremely distressing that in almost every department of our government … nothing is acting or working the way it’s supposed to work. This is not how our system is designed. This vaccine issue is putting everything on tilt. There’s something really wrong here.”
As for how it will all end, only time will tell, but for now, Ameer is allowed to receive the therapy and education he needs and deserves. But what about the tens of thousands of other children in New York and around the nation who have been ruthlessly stripped of their right to a public education?
Some families are making plans to move out of the state because their children are already vaccine injured or have brain and immune system disorders that do not qualify for medical exemptions under narrow federal vaccine use guidelines.
Others say they will quit their jobs and move in order to avoid having to vaccinate their unvaccinated children. One such couple, featured in an August 29, 2019, article21 on Syracuse.com, stopped vaccinating their children after their eldest son developed autoimmune encephalitis after getting the HPV vaccine and was hospitalized for 31 days.
Like the Hamidehs and so many others, this family does not consider themselves “anti-vaxxers” but “ex-vaxxers.” They’ve “been there, done that,” and realized the risks were real and very serious, and weren’t worth taking.
Approved Vaccine Contraindications Are Almost Nonexistent
The fact that a serious seizure disorder isn’t a valid contraindication for vaccination should set off warning bells, especially since febrile seizures is a possible side effect of most vaccines.
Ameer’s case clearly demonstrates just how dangerously narrow the vaccine contraindications really are, and how it’s nearly impossible to get a medical exemption under the CDC Advisory Committee on Immunization Practices’ (ACIP) rules.
Vaccine contraindications are the health conditions ACIP agrees are valid reasons for not getting vaccinated. The problem is, under ACIP guidelines, there’s virtually no health condition or vaccine reaction history that is an absolute contraindication to vaccination, and this is what your doctor has been taught to believe as well.22
For example, ACIP tells doctors that pregnancy or severe immunodeficiency are contraindications to getting live virus vaccines like MMR and varicella zoster — but inactivated vaccines are not an absolute contraindication for either of these groups.23
This is a very important point, because we’re often told that ACIP-recommended vaccines must be mandated for children in order to protect pregnant women and the severely immune compromised24,25 who cannot be vaccinated. Yet clearly, this is not true.
According to the CDC’s ACIP, there are only two types of vaccine reactions that are absolute contraindications to getting revaccinated and thus warrant a medical exemption:26
- A life-threatening allergic anaphylactic reaction that occurs within minutes of vaccination.
- Development of encephalopathy, such as prolonged seizures, coma and other brain dysfunction, within seven days of receiving pertussis-containing vaccines — but only if the doctor believes the encephalopathy is “not attributable to another cause.”
Vaccine Precautions, Another Short List
The CDC also publishes a very short list of health conditions that warrant “precaution,” as they “might increase the risk of a serious adverse reaction, cause diagnostic confusion, or might compromise the ability of the vaccine to produce immunity.”27
Only one CDC-approved universal precaution applies to all vaccines: Having a “moderate or severe acute illness with or without fever.” But this is not a total contraindication, which means a doctor could still decide to vaccinate an acutely and severely ill patient, as it’s up to his or her discretion what “moderate or severe acute illness” is.
The CDC also recommends that hospitalized patients should be vaccinated as long as they’re “not acutely, moderately or severely ill” — as if hospitals are filled with people who are only mildly ill from chronic conditions.
The core message the CDC sends to doctors is that 99% of the U.S. population are candidates for vaccination 100% of the time.28 It’s not surprising then that most doctors, pharmacists and other vaccine providers — who cannot be sued if a vaccine injures or kills — simply ignore any listed precautions.
What Role Have Conflicts of Interest Played?
At the end of the day, what all of this means is that most vaccine damaged children have no chance of getting approved for a medical exemption, and are forced to play Russian Roulette with their lives if they want a public education. It really shouldn’t be this way.
It’s wrong. And it’s so clearly wrong that it’s not hard to understand why people like the Hamidehs conclude that it’s really all about making a profit at any cost, even if the cost is the life of a child. Indeed, evidence of financial conflicts of interest are all around.
A U.S. House Committee on Oversight and Government Reform investigation published in 2000 found serious conflicts of interest between the pharmaceutical industry and voting members of two of the most important federal vaccine advisory committees in the U.S:29,30
- The ACIP, which reviews and votes on the quality of scientific evidence used to make national vaccine policy
- The FDA Vaccines and Related Biological Products Advisory Committee, which reviews and votes on the quality of scientific evidence used to license new vaccines
Yet, to this day, government-appointed members of both ACIP and FDA vaccine advisory committees can receive conflict of interest waivers by the U.S. Department of Health and Human Services, which allows them to vote on the licensing of vaccines and make national vaccine policy that is turned into public health law.31,32,33,34
We Are Not All the Same
Emerging science reveals we are not all the same and do not respond the same way to infectious diseases or vaccines. Responses to infectious diseases and the risk for complications can vary depending upon genes, environment, age and health at the time of infection.35,36
That is why malnourished, vitamin-deficient children living in poverty, for example, are at higher risk for complications from measles and other infections.37,38,39
Your risk of having a vaccine reaction can also range from zero to 100%. It again depends on genetic influences, your epigenetic history, microbiome, environmental factors, your age and current state of health, the type and number of vaccines you get, and how much time has elapsed between them if you’re getting more than one.40,41,42,43
Research has also confirmed that vaccinated individuals can still get infected with and transmit infections like measles, pertussis and influenza to other people, sometimes without showing any symptoms at all.44,45,46
With that evidence, the vaccine acquired herd immunity argument really falls apart, yet like so many other medical myths, it keeps being repeated long after its been disproven.
- 1 Vivoxa Market Analytics, Global Vaccines Market/Market Size, Growth, Analysis and Forecast 2019-2024, March 2019
- 2 Market and Markets. Vaccines Market worth $66.45 billion by 2027, at a CAGR of 6.7%.
- 3 National Vaccine Information Center. State Law and Vaccine Requirements. 2019.
- 4 Fisher BL, Williams K, Wrangham TK. July 11, 2014.
- 5 BusinessWire February 23, 2011
- 6 NVIC. May 2018
- 7 Business Wire December 8, 2016
- 8 NVIC Newsletter August 5, 2015
- 9 The Vaccine Reaction June 14, 2019
- 10 Associated Press September 10, 2019
- 11 YouTube, ABC10 (Sacramento) September 9, 2019
- 12 Lohud August 18, 2019
- 13 New York Senate Bill S2994A
- 14 Politico June 13, 2019
- 15 Associated Press. Aug. 17, 2019.
- 16, 26, 27 CDC.gov, Vaccine Recommendations and Guidelines of the ACIP: Contraindications and Precautions. Aug. 20, 2019.
- 17 Rarediseases.org LGS
- 18 Syracuse.com August 19, 2019
- 19 The Highwire November 12, 2019
- 20 PR Newswire, ICAN, November 12, 2019
- 21 Syracuse.com August 28, 2019
- 22 CDC. Vaccine Recommendations and Guidelines of the ACIP: Contraindications and Precautions. Aug. 20, 2019.
- 23 General Principles and Table. 4-1: Contraindications and precautions to commonly used vaccines. Aug. 20, 2019.
- 24 Alliance for Human Research Protection (AHRP). May 16, 2015. Immunocompromised children: what are the infectious risks from the unvaccinated?
- 25 The Vaccine Reaction May 21, 2017. Quit Using Immunocompromised People to Push Your Agenda
- 28 NVIC. Sept. 17, 2019.
- 29 U.S. House of Representatives, Committee on Government Reform Majority Staff Report June 15, 2000
- 30 ICIS Aug. 23, 2000
- 31 Bionity. Advisory Committee on Immunization Practices.
- 32 CDC.gov. Advisory Committee on Immunization Practices Policies and Procedures December 2018, Pg. 1
- 33 Public Availability of Advisory Committee Members’ Financial Interest Information and Waivers. March 2014.
- 34 Vaccine 2018; 36(49): 7439-7444.
- 35 British Medical Bulletin 1999; 55(2): 401-413 (PDF)
- 36 Annu Rev Genomics Hum Genet 2013; 14: 215-243.
- 37 Bulletin of the World Health Organization 2000; 78: 1207-1221.
- 38 Nutr Rev 2008; 66(9): 487-505.
- 39 N Engl J Med 1990; 323: 160-164.
- 40 Evaluating Biological Mechanisms of Adverse Events: Increased Susceptibility
- 41 Expert Opin Biol Ther 2010; 8(11): 1659-1667.
- 42 Braz J Med Biol Res 2012; 45(5): 376-385.
- 43 Complex Child E-Magazine June 2009 (PDF)
- 44 NVIC Newsletter May 25, 2019.
- 45 NVIC Newsletter Sept. 12, 2018.
- 46 Epidemiol Infect 2019; 147.
Reproduced from original article:
- Type 1 diabetes is an autoimmune disease in which your immune system attacks and destroys the pancreatic cells that produce insulin, which is why it’s also referred to as insulin-dependent diabetes
- Type 1 diabetics require a steady supply of insulin for their survival, as their bodies produce little or no insulin at all
- As prices of insulin have skyrocketed, many Type 1 diabetics are now risking their lives by rationing insulin
- The price of insulin tripled between 2002 and 2013, and has doubled again since then. The three dominant makers of insulin, Eli Lilly, Sanofi and Novo Nordisk, all sell their insulin for approximately the same prices, and have raised them in lockstep, raising suspicions of price fixing
- Your lifestyle will have an impact on your blood sugar control. Ways to help manage your glucose levels include limiting your net carb intake, timing your meals appropriately, eating nutritious foods and exercising regularly
Conventional medicine still has Type 2 diabetes misidentified as a blood sugar problem. In reality, the condition is rooted in insulin resistance and faulty leptin signaling, caused by chronically elevated insulin and leptin levels. In other words, it’s a diet-derived condition that can be reversed using a cyclical ketogenic diet and fasting.
This is why the medical community’s approach to Type 2 diabetes treatment, which typically involves the administration of insulin, is fatally flawed and professionally irresponsible. Treating Type 2 diabetes with insulin is actually one of the worst things you can do, as it simply accelerates dying from the disease.
Type 1 diabetics, on the other hand, do require a steady supply of insulin for their survival, as their bodies produce little or no insulin at all. Previously called juvenile diabetes, there are actually more adults with Type 1 diabetes than there are children with the condition, with an estimated 1 million to 1.5 million Type 1 diabetics in the U.S. alone.
Type 1 diabetes is an autoimmune disease in which your immune system attacks and destroys your pancreatic cells that produce insulin, which is why it’s also referred to as insulin-dependent diabetes. Tragically, as prices of insulin have skyrocketed, many Type 1 diabetics are now risking their lives by rationing their insulin use.1
Skyrocketing Costs Force Type 1 Diabetics to Risk Their Lives
In a recent article,2 The Washington Post tells the story of Alec Raeshawn Smith, who was diagnosed with Type 1 diabetes in 2015, just shy of his 24th birthday. Two years later, his health insurance coverage under his mother’s policy expired, leaving him with two expensive options: Get his own insurance, which would cost about $450 per month with a $7,000 deductible, or pay for his diabetic supplies out of pocket. The Washington Post continues:
“What Alec soon learned was just how much his insulin would end up costing… The price of insulin — once modest — has skyrocketed in recent years, making the lifesaving medication a significant, even burdensome, expense, especially for the uninsured and underinsured.
The costs are so heavy that they have driven some patients to ration their supplies of the drug in a dangerous gamble with life-threatening consequences. At the time Alec discussed skipping insurance coverage, he told his mother, ‘It can’t be that bad.’ Within a month of going off her policy, he would be dead …
As Nicole [Alec’s mother] cleaned out his cluttered blue car, littered with old prescription receipts, she started to cobble together just how much his insulin and blood sugar testing supplies cost without insurance or discounts. The total, by her count, was nearly $1,300 per month …
That $1,300 was almost $200 more than Alec’s biweekly paycheck. Nicole now believes that Alec was rationing his insulin because of the cost … ‘We realized that he had been taking less insulin and less often than he should, trying to make it stretch until he got his next paycheck.’ He was found dead three days before payday.”
Price Gouging Insulin Should Be a Crime
As noted in the featured article,3 the three researchers (Frederick Banting, Charles Best and James Collip4) who in 1921 discovered insulin — thereby transforming diabetic treatment and offering hope for a more or less normal life for Type 1 diabetics, who were previously doomed to die young — sold their patent to the University of Toronto for $1 each.
According to historian Michael Bliss,5 these researchers were trying to provide a great humanitarian gift to the world. In the hands of drug companies, however, insulin has become a guaranteed profit center totally isolated from the inventors’ benevolent intentions for the use of their discovery.
The price of insulin tripled between 2002 and 2013,6,7 and has doubled again since.8 At present, the three dominant makers of insulin, Eli Lilly, Sanofi and Novo Nordisk — which control 96% of the insulin market9 — all sell their insulin for approximately the same prices, and have raised them in lockstep, raising suspicions of price fixing.10
Drug makers also continue fine-tuning their formulas to prevent low blood sugar episodes, and while that’s good, it also ensures the drug patents don’t expire, preventing generics from being introduced.11
“For decades, manufacturers improved formulas, first using animal parts, then producing human insulin using bacteria and recombinant DNA. The 1990s saw the advent of insulin analogs, synthetic drugs made to better mimic the body’s own insulin production,” The Washington Post writes.12
“Today, critics argue that the price of insulin has far outpaced any innovations … In 1996, when Eli Lilly debuted its Humalog brand of insulin, the list price of a 10-milliliter vial was $21. The price of the same vial is now $275. Those costs can be compounded by the multiple vials that diabetics may require to survive each month.”
Price Hikes Threaten Insulin-Dependent Americans’ Lives
The Washington Post13 cites IBM Watson Health data showing Sanofi’s Lantus brand went from $35 per vial when introduced in 2001 to about $270 today, and Novolog, by Novo Nordisk, which started out at $40 per vial when released in 2001, now sells for around $289.
According to a 2016 JAMA study,14,15 the nondiscounted price for Lantus in the U.S. in 2015 was as high as $372.75, and the discounted price $186.38. Meanwhile, that same drug sold for $67 in Canada, $60.90 in Germany and $46.60 in France.
Even more telling is a 2018 study16 showing the estimated cost of manufacturing a 12-month supply of analog insulin is between $78 and $133 per patient, and $48 to $71 per patient per year for biosimilars. Why are patients having to pay as much as $24,000 a year for insulin that costs less than $133 to manufacture?
In response to growing outcry and lawsuits over insulin prices, Eli Lilly introduced Lispro, a less expensive generic version of its insulin Humalog, in May 2019.17,18 Lispro is said to sell at about half of the list price of Humalog.
According to a company statement,19 “The people who are most likely to benefit from Insulin Lispro Injection are Medicare Part D beneficiaries, people with high-deductible health plans and the uninsured who use Humalog.”
Lack of Competition, Payment Incentives Drive Prices
Why the dramatic increase in insulin prices? A November 2018 congressional caucus report,20,21 “Insulin: A Lifesaving Drug Too Often Out of Reach,” sought to identify the reasons behind these literally life threatening price hikes. As noted in this report:22
“Every day 7.5 million Americans rely on insulin [my note: over 6 million of these are Type 2 diabetics and should not be taking insulin] to manage their blood sugar levels and prevent debilitating, even deadly complications.
This lifesaving drug, however, has become increasingly unaffordable. Its average price has nearly doubled since 2012, putting an enormous financial burden on millions of patients.
For more than a year, Representatives Diana DeGette (D-CO) and Tom Reed (R-NY), the co- chairs of the Congressional Diabetes Caucus, have conducted a bipartisan inquiry to uncover the sources of this dramatic price increase.
This culminating report provides an overview of the insulin supply chain, discusses the drivers behind rising insulin prices, and recommends policy solutions to lower costs …
Many of the complicating reasons will be detailed further in this inquiry, including the myriad steps that insulin takes from manufacturer to patient, the perverse payment incentives and methodologies, the lack of transparency in pricing and outdated patent regulations, among other things.
These market failures have allowed a handful of players along the insulin distribution pipeline from manufacturers to health insurers to capitalize on their strategic positions, driving up the price of insulin and minimizing competition.
Congress should pursue a handful of legislative actions to increase price transparency, promote competition among insulin makers, and encourage the use of value-based contracts. Congress should also consider working on targeted patent reforms to prevent anti-competitive practices and streamline the drug approval process at the Food and Drug Administration for biosimilar insulins.”
While 1 in 4 patients gambles with their lives by rationing their insulin supplies by what they can afford,23 others have taken to illegally importing insulin from other countries where prices are more reasonable.
The Washington Post24 recounts testimony from one father who told senators a 90-day supply of insulin for his son costs $1,489.46 through insurance with a high deductible. He’s resorted to buying insulin from a Canadian pharmacy, from which he can get the same amount of insulin for $350 including shipping.
According to the article, while this is technically illegal, “the Food and Drug Administration generally doesn’t prosecute individuals if it’s a short-term supply for personal use.”25 Many others have turned to GoFundMe to raise donations for their insulin purchases.
Why Rationing Your Insulin Is a Dangerous Gamble
For Type 1 diabetics, whose bodies can’t make insulin, getting a steady supply is crucial for their health. Taking lower doses, or skipping doses, can be immediately life threatening and in the long term can result in even more costly health problems. As noted in the featured article:26
“Poor glycemic control can lead to blindness, kidney failure, amputation, heart disease and stroke. In the short term, patients who stop taking enough insulin can lapse into diabetic ketoacidosis, a condition where blood sugars get too high and the body’s blood becomes acidic. It can become fatal in just hours or a few days.”
While not an ideal solution, The Washington Post points out an alternative solution: older versions of insulins, available at Walmart for approximately $25 per vial.
While there’s some evidence showing these older formulas, which came out in the 1980s, are more likely to trigger dangerously low blood sugar and are typically thought to be safer for Type 2 diabetics than Type 1 diabetics, the doctors interviewed by The Washington Post agree it’s better than nothing.
Similarly, in the information sheet, “Diabetes Meds on a Budget,”27 Beverly Thomassian, a registered nurse and president of Diabetes Education Services, points out:
“The older insulins are regular and NPH. They are available as Humulin R and N (Eli Lilly) and Novolin R and N (Novo Nordisk). These biosynthetic insulins take longer to start working and the NPH peaks at 4 – 10 hours.
ReliOn Brand — Walmart sells Novolin insulin Regular, NPH and 70/30 (biphasic insulin) under the ReliOn label at discounted prices … Newer insulins are referred to as analogues. The amino sequence of these insulins has been slightly rearranged through genetic engineering to make them more rapidly available or take longer to absorb …
Given these pricing disparities, please consider reading this article28 published in Diabetes Care, 2009 — that describes the effective use of NPH and Reg to manage Type 2 diabetes.
The authors research shows that for type 2s, NPH and Regular insulins are as effective as the newer analogues in getting glucose to goal. The main drawbacks are well known; the peak of NPH slightly increases risk of hypoglycemia and patients will get better post prandial glucose control by taking regular insulin 30 minutes before meal (vs at meals with the analogs).”
Insulin Makers Sued
As mentioned, the surprisingly similar price hikes by all three makers of insulin have raised suspicions that the companies are in collusion. It wouldn’t be the first time. In February 2010, Mexico fined Eli Lilly and three Mexican drug companies $1.7 million each for colluding to eliminate competition by agreeing to take turns in placing winning bids for insulin, thereby artificially raising prices.29
In January 2017, a class action lawsuit30 was filed against Sanofi, Novo Nordisk and Eli Lilly in Massachusetts federal court, claiming the companies are in violation of the Racketeer Influenced and Corrupt Organizations Act.31 The New York Times reported:32
“The lawsuit … accuses the companies of exploiting the country’s opaque drug-pricing system in a way that benefits themselves and the intermediaries known as pharmacy benefit managers.
It cites several examples of patients with diabetes who, unable to afford their insulin treatments, which can cost up to $900 a month, have resorted to injecting themselves with expired insulin or starving themselves to control their blood sugar.
Some patients, the lawsuit said, intentionally allowed themselves to slip into diabetic ketoacidosis — a blood syndrome that can be fatal — to get insulin from hospital emergency rooms.”
In October 2018, the attorney general of Minnesota, Lori Swanson, also filed a lawsuit against the three insulin makers, charging them with deceptive and misleading price increases.33 As reported by The Hill:34
“The lawsuit alleges that there is a deceptive difference between the sticker price of these insulins and the actual price that insurers pay after negotiators known as pharmacy benefit managers (PBMs) get discounts.
The attorney general says drug companies are raising the sticker price ever higher so that they can give larger discounts to the PBMs, which helps them secure more favorable coverage of their products relative to their competitors in insurance plans.
The problem, Swanson says, is that the spiking sticker prices hurt people who don’t have insurance or who have high deductibles they have to pay before insurance kicks in.
‘The lawsuit alleges that the list prices the drug companies set are so far from their net prices that they are not an accurate approximation of the true cost of insulin and are deceptive and misleading,’ the attorney general’s office says.”
Biohackers Make Their Own Insulin
Aside from rationing, extended fasting, insulin sharing, using expired insulin, setting up GoFundMe campaigns or illegally importing insulin from other countries, some Type 1 diabetics are taking insulin production into their own hands.
In a recent Elemental Medium article,35 Dana Smith talks about the Open Insulin Project, “a biohacker collective that is trying to produce the lifesaving drug and provide it to people with diabetes for free, or close to it.” She writes:
“The group was founded in 2015 by Anthony Di Franco, a computer scientist with Type 1 diabetes, and a longtime member of the California hacker scene … He and his collaborators think one solution to the pricing crisis lies in enabling patients and hospitals to create insulin themselves.
The group works out of Counter Culture Labs in the trendy Temescal neighborhood of Oakland … ‘If we can make this stuff in our janky lab on a $10,000 a year budget, there’s no way it should cost this much,’ says Thornton Thompson, a molecular biologist who is part of Open Insulin.
‘One of the big goals of the project is just to demonstrate that.’ Scientists make insulin by inserting a gene that codes for the insulin protein into either yeast or bacteria. These organisms become mini bio-factories and start to spit out the protein, which can then be harvested, purified, and bottled.
Scientists at Genentech were the first to synthesize insulin this way back in 1979 from the bacterium E. coli, and drug manufacturers have been using the method ever since. Open Insulin’s goal is to develop a similar way to generate insulin that doesn’t infringe on any patents and can be made publicly available.”
The Open Insulin Project
To produce insulin, the group uses yeast rather than E. coli. A French biochemist named Yann Huon de Kermadec joined the Open Insulin Project about a year-and-a-half ago. He took charge of the manufacturing process and obtained the appropriate insulin gene, which is then inserted into the DNA of the yeast, thereby producing a small amount of insulin protein.
They’ve not yet been able to extract high-enough amounts to move on to the purification stage, so at present they’re still working on increasing the yield. “If they succeed, they will go through the final steps of purifying and testing the protein. Once they’re confident that what they’ve produced really is pure insulin, Di Franco will serve as the group’s first guinea pig,” Smith writes.
According to Open Insulin, 10 liters of yeast culture are enough to make insulin for 10,000 individuals, with a startup cost as low as $1 per person. Indeed, as noted earlier, insulin manufacturing is pretty darn inexpensive — at most around $133 per person per year for an analog, and as low as $48 per person per year for a biosimilar.
Once a well-working insulin has been developed, the group hopes to make the recipe open-source, allowing hospitals and other patient groups make it for themselves. Thompson told Smith:
“What we’re interested in medium- and long-term is to try to organize networks of production and distribution centers that work by a fundamentally different model. We want to partner with hospitals, free health care clinics, patient organizations, diabetes groups. What if you could set up a small-scale production center in the back of a hospital?”
Di Franco adds, “Economically, I think it’s much better to do it in this decentralized way. A very small investment from each patient could fulfill the patient’s needs and make insulin very close to free for everyone who needs it with this kind of technology.”
As you’d expect, others are less than excited about such a prospect, not because it would create much-needed competition, but because of safety concerns. For example, Dr. Eric Topol, chair of innovative medicine and executive vice president at the Scripps Research Institute, told Smith:
“There are so many things that could go wrong in the process: the sterilization, the efficacy, the safety. It’s like Murphy’s law, here. These are potent drugs that can have serious side effects. I just don’t see that that is a safe or practical route.”
Millions of Americans Get Their Medications Outside the US
At present, there are no easy solutions for insulin-dependent diabetics. What’s clear is that it shouldn’t cost thousands of dollars a month for an essential drug required to keep these people alive.
If you’re in this boat, consider talking to your doctor about the possibility of using the older biosynthetics, Humulin R and N, or Novolin R and N, available for about $25 at Walmart. It may not be ideal (you can read about some of the concerns in this Insulin In Nation article36) but it’s probably still better than nothing. Even better, however, especially for Type 1 diabetics, is getting your insulin from overseas — or even just next door, north or south of the U.S. border.
Research published in 2015 shows that 952,000 Californians cross into Mexico every year for lower-priced health care, including prescription drugs.37 From the northern border, a random survey of Americans showed that 8% of respondents or someone they knew had imported their medications from Canada.
In numbers, that adds up to 19 million individuals — with estimates that the numbers are probably much higher — crossing into Canada just to be able to afford medications they may very well not be able to live without.38 But is this legal? And if it is, how do you do it? And if you’re not near the southern or northern U.S. borders, is there anywhere else to go? According to the FDA:
“In most circumstances it is illegal for individuals to import drugs or devices into the U.S. for personal use because … [they] have not been approved for use or sale in the U.S. … The FDA cannot ensure the safety and effectiveness of medicine purchased over the internet from foreign sources, storefront businesses that offer to buy foreign medicine for you, or during trips outside the U.S.”
The FDA does make exceptions for certain medications under specific situations, but even so, the amounts can’t be for more than a three-month supply. That said, Kaiser Health Network39 reports that personal use purchases for drugs not considered a risk by the FDA — such as insulin — in 90-day supplies are not being prosecuted.
And just how much are Americans saving by crossing the border? Kaiser Health gave an example of a woman vacationing in Canada who visited a local pharmacy for an emergency insulin refill for her daughter: The pack of insulin pens, which cost $700 in the U.S., was a mere $65.
The same box costs $73 in Germany; $57 in Israel; $51 in Greece; $61 in Rome and $40 in Taiwan. It’s no wonder millions of Americans are getting prescriptions by mail order overseas! Yet, even though they’re not prosecuting people for it, the FDA is clamping down on mail orders by going after them at international mail facilities.
According to online journalism group Tarbell,40 the FDA intercepted 10,731 prescription drug packages in 2017; by May 2018, they’d confiscated 19,318. Their goal is to intercept 100,000 a year.
So, what can you as a consumer do, if you can’t afford the outrageous — bordering on criminal — pricing and you’re not brave enough to test the system and try to take a vacation out of the country or order by mail? One way to begin could be to study the FDA’s personal importation guidelines to see if there is some way you can qualify for an exception so you can get your insulin from out of the country legally.
Guidelines for Insulin-Dependent Diabetics
Also remember that your lifestyle will have an impact on your blood sugar control. Ways to help manage your glucose levels include the following. Just be sure to consult your physician before making any drastic changes to your lifestyle habits and dietary plan, to avoid wild blood sugar fluctuations.
- Limiting your net carb intake (total carbs minus fiber) — When you eat high-carb foods, your body converts the starches and sugars into glucose, which will enter your bloodstream and increase your blood glucose levels. Make sure you monitor your carbohydrate intake to avoid hyperglycemia.
- Timing your meals appropriately — Meal timing is crucial to the treatment and management of Type 1 diabetes, since it may affect the efficiency of your insulin intake. The best time to eat your meal depends on the type of insulin that you’re taking. For example, regular insulin should be taken 30 minutes before a meal.41
- Eating only nutritious foods — Avoid eating foods that contain sugar, preservatives, trans fat, refined flour and other unhealthy ingredients. Rather, fill your plate with wholesome foods rich in vitamins and minerals. You should also consume foods that are high in healthy fats and probiotics, since these may help you gain better control of your blood glucose levels.
- Exercising regularly — Following an active lifestyle will help regulate your blood sugar levels, as it allows your body to use insulin more efficiently, and can help you avoid long-term complications associated with Type 1 diabetes, such as heart disease.42
- 1, 11 Click2Houston.com March 13, 2019
- 2, 3, 10, 12, 13, 23, 24, 25, 26 Washington Post January 7, 2019
- 4, 31, 35 Elemental Medium May 30, 2019
- 5 Washington Post October 31, 2016
- 6, 14 JAMA 2016;316(8):858-871
- 7 JAMA 2016;316(8):858-871 (Full Study PDF)
- 8, 21 Congressional Caucus on Diabetes November 1, 2018
- 9, 16 BMJ Global Health 2018; 3(5)
- 15 JAMA 2016;316(8):858-871 (Full Study PDF) page 859
- 17, 19 Eli Lilly May 22, 2019
- 18 CNN May 22, 2019
- 20, 22 Congressional Caucus on Diabetes, Insulin: A Lifesaving Drug Too Often Out of Reach (PDF)
- 27 Diabetes Meds on a Budget Beverly Tomassian, Diabetes Education Services (PDF)
- 28 Diabetes Care 2009 Nov; 32(suppl 2): S253-S259
- 29 Reuters February 23, 2010
- 30 US District Court District of Massachusetts, Class Action Complaint No. 1:17-cv-10158, January 30, 2017 (PDF)
- 32 New York Times January 30, 2017
- 33 STAT News October 16, 2018
- 34 The Hill October 16, 2018
- 36 Insulin In Nation September 16, 2016
- 37 USITC Trends in U.S. Health, August 2015
- 38 CMAJ 2017 Jun 19; 189(24): E817–E818.
- 39 Kaiser Health Network February 12, 2019
- 40 Tarbell June 14, 2018
- 41 MedicineNet, Type 1 Diabetes Diet
- 42 Endocrine Web Type 1 Diabetes and Exercise
Reproduced from original article:
Analysis by Dr. Joseph Mercola Fact Checked – October 13, 2019
Note: Video not available on this site.
To view video, please go to original article above.
- In “Cancer and the New Biology of Water,” Dr. Thomas Cowan explains why cancer is not a problem of oncogenes but rather a problem involving the cytoplasm — the structured water — of the cell
- Mitochondrial defects are an integral part of the breakdown of the structure in the water, which then triggers the formation of cancer
- Lifestyle strategies that will help restructure the water in your cells, thereby helping prevent cancer include eating a ketogenic diet and exposing your body to sunlight and near-infrared light such as near-infrared sauna
- Other strategies include grounding to the earth by walking barefoot, posing yourself to the biofields of other biological entities, such as the touch of other humans and animals, and hyperbaric oxygen therapy
- Mistletoe therapy stimulates your fever response. It’s an immunostimulating medicine that also works like a chemo drug
Dr. Thomas Cowan is a practicing physician, founding board member and vice president of the Weston A. Price Foundation.
I’ve previously interviewed Cowan on a number of different topics, including the link between vaccines and autoimmune disease, the use of low-dose naltrexone for autoimmune disease and novel treatments for heart disease. Here, we discuss his latest book, “Cancer and the New Biology of Water.”
“I wrote a series of three books. The first one on the heart, the second one on vaccines and autoimmunity and then this one on cancer. As I got into it, I realized it was all about water,” Cowan says.
“The first book was basically two premises: One is that the heart doesn’t pump the blood. The reason for the movement of the blood in your body is not because there’s a propulsion by the heart [but] because of the dynamics of water …
Then I got into the vaccine book and what childhood illness means. That took me deeper into what cells are made of. Somehow it hit me that the whole problem of cancer is a cytoplasmic, i.e., water problem.
It became like the culmination of this series of writing and thinking about human biology, biology in general, and how wrong we have the whole thing, basically.”
Cancer and the Biology of Water
In 1971, President Nixon declared war on cancer. As noted by Cowan, we had just discovered the oncogene at that time, which was thought to be the reason for why people had cancer.
In the decades since, vast sums of money have been spent on cancer research. Were oncogenes the correct target, the war on cancer should have been won by now, yet we’re no closer to a cure today than we were back then. Cowan cites research by the Australian government, which concluded that improvement in cancer statistics as a result of chemotherapy is 2.3%.
“That’s an abysmal return on a $500 billion investment … Probably the costliest endeavor humans have ever undertaken, except maybe war,” Cowan says. “What’s the problem? The problem I submitted in the book is that cancer is not a problem of oncogenes. It isn’t even a problem of the DNA. It isn’t even a problem of the nucleus …
There have been a number of studies over the years where they transplant the nucleus from a healthy cell into another healthy cell and the progeny are normal, as you would expect.
But then they take the nucleus out of a cancer cell, where these oncogenes [are], the DNA that supposedly cause cancer, and put that into a healthy cytoplasm, the progeny are normal. When they take a normal nucleus and put it into the cytoplasm of a cancer cell, it turns the progeny cancerous.
That simple experiment tells you exactly where in the cell the problem of cancer lies, which is in the cytoplasm. The cell has two parts. Basically, it’s a lipid biomembrane that has a nucleus and a cytoplasm. The cytoplasm is basically structured water or a gel.
Now we know that the cytoplasm is the site of cancer. The events in the nucleus are a consequence of degeneration of the cytoplasm, not the other way around.
When these researchers did this, and identified clearly that the site of the cancer problem is in the cytoplasm, they postulated that something in healthy cytoplasm must be able to heal the mutations of the DNA in the nucleus, which there’s no evidence for.”
The Cytoplasm’s Role in Cancer
Cowan argues that the real problem in cancer lies in the structured water of the cell, i.e., the cytoplasm. Similarly, Thomas Seyfried, Ph.D., whom I’ve interviewed on this topic as well, believes the studies Cowan mentioned above reveal the problem is rooted in the mitochondria, which also reside in the cytoplasm.
Mitochondrial dysfunction is certainly one aspect, Cowan admits, but more specifically, he believes mitochondrial defects are an integral part of the breakdown of the structure in the water, which then triggers the formation of cancer.
“When you look at what the function of the mitochondria is — which is essentially to produce adenosine triphosphate (ATP) — and you see what the role of ATP is and how integral ATP is to the structuring of the water in the cytoplasm, then you begin to see the connections between the mitochondrial dysfunction … [and the] deterioration of the cytoplasmic water that leads to cancer.”
Oftentimes, cancer can be palpated (provided the tumor is large enough). The tumor turns into a palpable lump because the density of the cells is too high, Cowan says. The cells are essentially clumped together, and they’ve lost their normal spatial orientation.
All cells have a certain spatial orientation because there’s an electrical charge around the cell. When two cells start coming together, the charge repels them apart. This allows all the cells to remain at an appropriate distance from each other. This distance varies depending on the cells and organs in question, but all tissues have a spatial orientation that allows the tissue to remain healthy and normal.
Structured Water Is Responsible for Cellular Charge
Conventional medicine says that the charge around each cell comes from the distribution of sodium and potassium across the cell membrane. However, Cowan points out that experiments by cell physiologist and biochemist Gilbert Ling, performed more than three decades ago, showed that for the sodium-potassium pump to be responsible for the creation of this charge, the cell would need about 30 times the energy at its disposal.
So, according to Cowan, this belief, while being a cornerstone of modern biology, is little more than a myth. Something else causes the charge, but what? Cowan answers that question with the following explanation:
“It comes about because in the cytoplasm is a mesh network of water, which, by some genius of nature, is so constituted that it, by itself, it traps potassium and excludes sodium … The proper healthy grid, mesh or structuring of the water, in itself, is the pump. No energy needed, just like the heart.
The whole idea of a stupid pump pushing is ridiculous. It’s done by the miracle of water. The charge distribution, the spatial orientation of a cell, is because of the structuring of the water. That’s one.
The second thing is the other hallmark of cancer cells: They all have an abnormal number of chromosomes. It’s called aneuploidy, as opposed to a diploid cell, which means humans have 46 chromosomes. If you get an abnormal number, that’s an abnormal cell we call cancer.
How does that happen? It happens because of events in the cytoplasm, which pulls the two chromosomes apart and makes new copies of mitosis. It doesn’t happen properly because the milieu in the cytoplasm, that structured water, is disturbed.
Therefore, you get all these errors of mitosis, and the energy used for mitosis is deficient. That’s because of the mitochondrial problem. You get errors in chromosome replication called aneuploidy. When you get an aneuploid cell that has an abnormal spatial orientation, that’s called a cancer cell.”
How to Restructure the Water in Your Cells
Once you understand the importance and influence of the cytoplasm, the structured water inside your cells, in the development of cancer, the next question becomes: How do you restructure that water? A significant portion of Cowan’s book covers this important topic.
To illustrate how structured water is made, he compares it to Jell-O. Jell-O is made by mixing gelatin proteins with water and then adding heat. The heat unfolds the proteins, exposing their hydrophilic surfaces, which then grab onto the water.
As the mixture cools, it forms a gel, “which is basically identical to the state that the cytoplasm is in,” Cowan says. To structure the water in your cells and basically mimic this Jell-O making procedure, you can:
- Eat a cyclical ketogenic diet — When fats are metabolized in your mitochondria, they create deuterium depleted water (DDW), which is hydrogen-rich. The more hydrogen you get, the more ATP your cells generate, which in turn allows your cells to create more structured water
- Regularly expose much of your skin to sunlight
- Regularly expose your skin to near-infrared light, such as a near-infrared sauna or a heat lamp bulb. Not only does it restructure water, but it also detoxifies your cells by creating sweating, which purifies the cytoplasm
- Expose yourself to the biofields of other biological entities, such as the touch of other humans and animals
Now, ATP is instrumental for protein unfolding — which is an integral part of the process of creating structured water — and if you have an ATP deficiency, “as happens when you have mitochondrial disease, it’s like trying to make Jell-O without heat,” Cowan says.
“You get clumps of dysfunctional proteins with water that can’t be structured. That’s what you see with cancer cells … If you want to have properly structured water, which then creates healthy cell division and healthy spatial orientation in the cells, you need sunlight, earth and human touch — the biofields of other biological entities, especially those who wish you well, so to speak, like your dog.”
Another alternative is hyperbaric oxygen therapy, although this is not something most people will be able to do at home. By providing more oxygen to the tissues at increased partial pressure, the oxygen is pushed into the mitochondria, allowing them to generate more ATP, which in turn allows your cells to create more structured water.
In his book, Cowan also discusses mistletoe therapy, which he recommends almost universally for his cancer patients. He expounds on the benefits of this therapy as follows:
“Cancer is growing and parasitizing you, sucking your nutrients, just like the mistletoe sucks the nutrients from the oak tree. But there’s a central difference, which is the mistletoe has learned to cooperate with the oak tree, and so each do better together than they would do alone, whereas in cancer, the tumor has parasitized you and you do worse.
What we need is a situation where we bring back that cooperation … This is not a survival of the fittest … That’s not how it works in nature. Nature is a cooperative venture … Mistletoe tells you to see it like that. Now, that’s the metaphor.
[Mistletoe] stimulates fever response, so it is an immunostimulating medicine. It stimulates white blood cells. It stimulates all these aspects of immune response. It stops cells from growing, so it works like a chemo drug, as well … We want the simulation, the purification, the detoxification that happens with fever therapy. Mistletoe does that.”
The idea that fever is a healing aid goes back to a cancer treatment developed in the 1890s by William Coley, a bone surgeon. The treatment, which involves giving isolated proteins from the erysipelas bacteria at a specific dose to induce a fever, is known as “Coley’s toxin.”1
“Around 1989, for I don’t know what reason, I get in the mail a book from Coley’s granddaughter about 2,000 cases he treated and the results — about 60% of them, stage 4. All different kinds of cancer were cured by Coley’s toxins. It’s very well documented.
It was the main adjunct of cancer therapy in the United States for a couple of decades. It was used up until the ’60s. Many, many papers written about it, peer-reviewed journals. There’s no doubt that it was more effective than any adjunctive therapy for cancer we have today.
In a sense though, it’s a blueprint. When you talk about hyperthermia, the problem is it doesn’t work as well as Coley’s toxins. I think the reason for that is [hyperthermia] doesn’t turn on your innate cellular immune system. It’s just heating up your cells.
I’m not saying that something good doesn’t happen from heating up your cells, but it’s not the same. Coley’s was a way of internally generating the temperature, and so is mistletoe, although mistletoe isn’t as dramatic as Coley’s toxins …
[Today, Coley’s toxin] is not available anywhere. It’s very sad. There should be a way of stimulating fever. I had occasion to use it a little bit years ago. You could basically generate any temperature you want. It’s pretty rigorous therapy. You get shakes and chills and not everyone wants to do that. But if you do that, you have a dramatic detoxification-purification response …
None of these strategies are a magic bullet. The point I’m trying to make is that healthy cytoplasm, which is basically a structured water gel, that’s the key focus … All those [factors discussed earlier] contribute to the quality of the gels that you’re going to produce. That’s what good health is.”
Cowan’s book ends with the story of Sleeping Beauty. “It’s what we tell children to teach them how the world works,” he says. Sleeping Beauty, a princess, is bewitched by an evil witch, which in fairytales always illustrates the materialistic side of life.
“When you’re bewitched by materialism … you fall into chaos and disrepair has happened in the story. Something has to come along to wake you up, not to a new way of seeing, as they say in the story, but to your true nature.
That’s where we’re at now. We’re living out the story of Sleeping Beauty. We’re bewitched by materialism and we can’t see our true nature. That’s become a real problem. [Getting out of that matrix involves] an interesting combination of all these techniques that we’re talking about …
Cyclical ketosis, sunlight, walking in the ocean, infrared saunas … fever therapy, bringing back therapies like Coley’s toxins. There’s another side too, which is to change our minds … Somehow, we have to change our mind and … see the world as it is.
I often tell people and patients, ‘If you see the world from a materialistic point of view and you realize that the matter we’re talking about is made of atoms, which are, themselves, 99% space, just empty, so how does that work? It’s an illusion.’ Once we see that we’re essentially crystallized energy, then you start to wake up.
The most hopeful thing I think I can tell people is that once you begin to open your mind, there’s more out there than was taught in school or that your doctors tell you. Somehow the world seems to feed you information or give you clues as to where to go next.
You don’t need me to tell you what to do or where to go next. Somehow it just happens. I don’t know if you would agree, but in my life, once you open yourself to this possibility, to me, it’s like the spiritual world comes in to offer a hand. The next thing you know, you meet this person. Next thing you know, you [learn] things that you didn’t know before.
You just keep opening your mind. If we keep doing that, we can build a different world. You don’t have to do anything. You just have to stop not doing things, believing that there’s nothing there.”
To learn more, be sure to pick up a copy of Cowan’s book, “Cancer and the New Biology of Water.” I definitely recommend it and all the resources in there. It’s a great read. Cowan tells a good story, which makes his books easy to digest. “I hope that it catalyzes some institution, some person — somebody — to say, ‘We’ve got to do things differently because this isn’t working,” Cowan says.
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- Functional genetics looks at the single nucleotide polymorphisms (SNPs, pronounced “snips”) of genes
- When you have SNPs (genetic variants or defects on the genes), enzymes may not be working effectively, or the gene may be upregulated or downregulated
- While traditional genetics often looks for potential disease states, functional genetics looks for potential impairment of function and helps find the best nutritional intervention to bring your body back into balance
- People with genetic weaknesses that hamper detoxification who are exposed to high amounts of environmental toxins can be struggling with health due to their limited ability to detoxify
- NutriGenetic Research Institute is devoted to functional genomic testing, training health professionals to help people understand the results and how to apply it to improve their health
Functional genomics is a gene testing modality with enormous value that many are completely unaware of. Bob Miller1 is a certified traditional naturopath specializing in genetic-specific nutrition. He’s the founder of the NutriGenetic Research Institute,2 devoted to testing and helping people understand the results of their functional genetic testing and how to apply it to improve their health.
“As a traditional naturopath, we’re not licensed medical doctors, so we don’t diagnose, treat or prescribe,” Miller explains. “We look at the functional approach of, ‘How is the terrain off in the body?’ … [W]hen the body is toxic or inflamed, that’s when pathogens have a better opportunity to thrive.
Many years ago, I learned about how homocysteine has pathways that clear it that may be impaired by genetic variants. I became very fascinated by it. I started looking at the enzymes that clear it, and then the genetics behind it.
My whole naturopathic and holistic practice is [now] dedicated to helping clients measure their functional genomics, which is quite a bit different than traditional genetics that looks for disease patterns, and trying to find out how we can make interventions to bring the body back into balance …
Our goal is to be able to make a contribution to functional practitioners, so they can do their job a lot better and improve the lives of those who are suffering with some of those things that nobody can seem to figure out …
To sum up what we’re finding is that those with genetic weakness in detox pathways are exposed to environmental factors we weren’t dealing with 50 to 75 years ago; their ability to detox is overwhelmed. I think this is a whole new paradigm that we have to look at in wellness.
Those who don’t have a specific disease, so to speak, but are just totally overwhelmed by all of the epigenetic factors, such as pesticides, electromagnetic fields (EMFs) … excess iron … plastics … mold … [and] sometimes even oversupplementation with things like folate and glutamine … that no matter what they try, it doesn’t work …
That’s why we need to move to personalized care, based upon the individual. Fortunately, we now have tools to do that.”
What Is Functional Genetics?
Certain genes are known to predispose you to, or raise your risk of, certain diseases. That’s not what we’re talking about here. Functional genetics looks at the single nucleotide polymorphisms (SNPs, pronounced “snips”) of genes related to function.
You’ve probably seen representations of the DNA ladder. On the end of each rung is a molecule from each of your parents. These molecules can either make your DNA optimal or, if you have a SNP, meaning a defect, that gene will not work at optimal efficiency. Miller explains:
“To make this simple, we eat fats, carbohydrates and proteins. We drink water, breathe air and are exposed to sunlight. What an absolute miracle it is that all of that turns into us: our blood, our skin, our nails, our organs and our thought processes. All of that is one enzymatic process after another.
So, an enzyme takes substance A; pulls in what we call cofactors and makes substance B. That continually happens throughout your body — one process after another. It’s your genetic makeup that [provides] the instructions on how to make these enzymes.
When we have genetic variants, SNPs, on the genes, sometimes those enzymes either aren’t as effective … or might be upregulated or downregulated. Therefore, that substance A to substance B [conversion] may not occur as it should.
Now, people get all excited about whether they have genetic variants or not, but there’s something else just as important. That’s the cofactor. Remember, substance A plus cofactors turns into substance B. You could have absolutely perfect genetics, that enzyme is made perfectly, but if you’re missing the cofactors, that A to B [conversion] is not going to work …
Where people really get hit hard is when they’ve got genetic weakness and cofactor weakness. Then there’s a third piece. Sometimes there are things that interfere. For example, lead, mercury and other things may suppress that enzymatic function …
Now, interestingly, we have all kinds of backups. One pathway may not be working, but another one might kick in. But what we’re observing … is that those who are struggling usually have multiple pathways blocked. Plus, they get multiple epigenetic exposures … When you get those epigenetic and genetic factors going together, that’s when things really start going awry.”
The Relationship Between mTOR Pathway and Autophagy
Autophagy means “self-eating” and refers to your body’s process of eliminating damaged and defective cellular parts that are targeted for lysosome, which then digests them. The mammalian target of rapamycin (mTOR) is a molecular signaling pathway responsible for either growth or repair, depending on whether it is stimulated or inhibited.
I’ve often stated that to upregulate maintenance and repair (which will boost longevity and reduce your risk for cancer), you need to suppress the mTOR pathway. One of the most efficient ways to do this is to limit your protein intake, but it’s not the only way. Autophagy and mTOR are two processes that work together, but are inverse to each other. Miller likens mTOR to a construction crew, whereas autophagy refers to the cleanup crew.
“One of the ways you can tell if your autophagy is not working is when you get those age spots, sun spots, liver spots, whatever you’d like to call them,” Miller says. “That’s when the old cell is not cleared away and it becomes oxidized, it becomes senescent. It actually becomes a free radical-giving reactive oxygen species.
Now, we need a balance between [mTOR and autophagy]. We need a time to build and we need a time to clean. One of the things our research institute [found] in some of our studies on those with chronic Lyme disease [is] that we are being exposed to more epigenetic environmental factors that stimulate mTOR … ”
Factors That Activate mTOR Versus Those That Support Autophagy
Examples of environmental factors that activate mTOR include:
|Xenoestrogens (chemicals in plastic)||EMFs|
|Excess iron||Excess folic acid, folate or methyl folate|
|Excess glutamate||Amino acids such as leucine, isoleucine and valine|
When mTOR is activated, it inhibits autophagy and, according to Miller, many of the health challenges people face these days appear to be related to excess mTOR activation.
This is also one way by which a cyclical ketogenic diet helps improve your health, as it inhibits mTOR and activates autophagy. When mTOR is chronically activated, it will not only inhibit autophagy but also impair apoptosis (cell death), and if that’s impaired, your risk for cancer will significantly increase as well.
“We have identified the genes that are involved with autophagy,” Miller says. “They’re called Unc-51 like autophagy activating kinase 1 (ULK1), serine/threonine-protein kinase (ULK2), 5’ AMP-activated protein kinase (AMPK) and AuTophaGy related 1 (ATG1).
Those all stimulate autophagy. We’re finding that when people have a lot of genetic variants, especially when they inherit it from both parents, this is where their autophagy’s weakened. They’re 45 years old and covered with age spots. They can’t detox.
Ketogenic diet, intermittent fasting and nutrients [such as] lithium and berberine support autophagy. Resveratrol and curcumin slow down mTOR.
When you put the three together — the caloric restriction mimetics (CRM) [editor’s note: supplements that mimic the antiaging effects of calorie restriction] … along with the keto diet, along with some form of intermittent fasting — you’re able to bring balance to mTOR and autophagy.”
If Ketogenic Diet or Intermittent Fasting Fails for You, This Could Be Why
While intermittent fasting is an excellent strategy for a majority of people, it doesn’t work as expected for everyone. As explained by Miller, members of his research team have discovered having a functional heme pathway is extremely important when you’re on a ketogenic diet and/or intermittently fasting.
Heme protein is created through an eight-step process beginning with succinyl coenzyme A (succinyl CoA), glycine and amino acids. Heme protein in turn is a component of hemoglobin, but it’s also involved in the making of nitric oxide, catalase, superoxide dismutase (SOD) and sulfite oxidase (SUOX), which is your sulfide to sulfate conversion.
“It’s involved in so many processes that I didn’t even realize until we started to research,” Miller says. “This [heme] pathway may be impaired by … glyphosate [which impacts glycine] … lead … and genetic variants in the heme pathway.
If any of those happen, you don’t make adequate heme, so you’re going to be a very poor detoxer. Now, what’s interesting … [is that] if porphyrins [glycoproteins responsible for pore formation in cell membranes] are not transferred one to another, they will block the gamma-aminobutyric acid (GABA) receptor sites. GABA is the ‘Don’t worry. Be happy. Sleep. Relax’ [neurotransmitter]. Clearly, there are problems with anxiety in the world today.
If this heme pathway gets disturbed, people oftentimes crave carbohydrates. If they try to go keto, it doesn’t work. If they try to do intermittent fasting, it doesn’t work … It’s a small amount of people, but for some individuals who just crave carbohydrates, they’ll get hangry if they don’t have their carbohydrates. They’re actually feeding that heme pathway.
If someone’s ever tried keto and is like, ‘This just does not work for me,’ there’s a potential that the heme pathway could be impaired. You have to keep those carbohydrates coming in on a regular basis to feed it, or else you feel horrible. I remember in the past people telling me, ‘Whenever I try to eat healthy, I feel horrible. When I eat junk, I feel better.’
I used to think, ‘Yeah. I’m not sure I buy that.’ But now that you understand this heme pathway and how carbohydrates and simple sugars can feed it, it starts to make sense that that is a potential scenario for some people.”
Even if You’re Anemic, You May Be Overabsorbing Iron
As mentioned earlier, iron stimulates mTOR. Clearly, iron is crucial for optimal health. Without sufficient amounts of iron, you cannot make sufficient amounts of hemoglobin, which carries oxygen through your body. However, in excess, iron is incredibly destructive.
“Here’s one of the interesting things we found through our research. There are many people who have genetic predisposition to overabsorbing iron, yet they’re told all their life they’re anemic. It just seems like such a dichotomy; how can you be anemic if you’re overabsorbing iron?
One of the things that we … find in many who are struggling and can’t get answers anywhere else is that they overabsorb iron. There’s an enzyme called ferroportin, [which] is what takes iron out of the cells. SNPs there, or genetic defects, inhibit the removal of the iron. Through something called the Fenton reaction … iron may combine with hydrogen peroxide to make hydroxyl radicals.
This can then go on to make another nasty free radical called peroxynitrite. Consequently, the person is anemic because they are measuring what’s in the blood, but the iron can be in excess and inside the cells, causing massive inflammation.
As that iron bangs around inside the cell, it creates fatigue, because the mitochondria are having a hard time making energy. These are the people who if someone gives them iron, many times, they feel considerably worse, because they’ve just fed the fire.
In our consulting, one of the things we probably do the most is identifying the Fenton reaction going on and taking remedial action to, for example, help turn the hydrogen peroxide into water through an enzyme called catalase; supporting enzymes and antioxidants called glutathione and thioredoxin that turn the hydrogen peroxide into water, [and] using homeopathics to make the iron behave itself.”
Hydrogen water can be helpful here, Miller notes, because it helps decrease the excess hydroxyl radicals. “Quite simply, H2O2 plus iron equals hydroxyl free radical (OH-), which is one of the most highly reactive and damaging free radicals,” Miller explains.
I’ve previously interviewed Tyler LeBaron, one of the leading experts on molecular hydrogen, and he believes the benefits may be related more to the upregulation of antioxidant pathways, such as the nuclear factor erythroid 2-related factor 2 (Nrf2). Either way, whatever the mechanism, it seems clear hydrogen water has the ability to neutralize free radicals.
Situations in Which NAC or Methyl Folate May Backfire
I’ve previously written about the benefits of N-acetyl cysteine (NAC), the rate-limiting factor for glutathione, which is a master antioxidant made by your body. However, in order for this to work, you must have the required enzymes. What’s more, if you have an iron problem, the cysteine you take can combine with the iron to create hydroxyl radicals — essentially worsening your situation.
“It goes back to the fact that we’ve got to get away from the cookie cutter, ‘Oh, you’re inflamed. Take NAC.’ NAC can be the perfect thing for you, or it can make you worse, depending on your genomic make up,” Miller says.
Miller has developed a hierarchical pyramid of different variables and his approach to treating them. Interestingly, many who superficially look at functional genomics think that the methylation defect is one of the most important. It is important, but according to Miller there are many others that supersede it in terms of importance.
“[Methylation] is about how we take folic acid or folate from our diet and turn it into methyl folate, which is a very important molecule. For a woman who’s pregnant, you’ve got to have it for a good pregnancy. We’re not saying it’s not a good thing … Now, one of the interesting things about methyl folate is you need it for pregnancy because it supports mTOR.
If someone’s already in mTOR dominance and they take methyl folate, they’re going to get more anxious and more inflamed. I’ve talked to so many people who’ve said, ‘Oh, yeah. I have MTHFR. Somebody put me on methyl B12, methyl folate. I felt great for two weeks, and then I crashed.’
The reason they may have crashed is because they started to stimulate mTOR, weakening their autophagy even more, driving more inflammation … As we dug deeper, we realized that methyl folate is important, but it has to be done at the right time. That’s why I developed my pyramid.
At the very bottom we have things we have to address first, such as, is iron becoming a free radical? Is hydrogen peroxide not being cleared? Is there nitric oxide synthase (NOS) uncoupling? — where rather than making nitric oxide, we make more peroxynitrite.
And then we look at how we’re making antioxidants. How’s our glutathione pathways? How’s our superoxide dismutase? How are we making NADPH? … For the most part, I believe that when people are massively inflamed, you need to address that first.
If someone is massively inflamed, if their iron is creating hydroxyl radicals, if they have weakness in their antioxidants … and you throw methyl folate in there … there’s a very good chance it will make the situation worse.
By and large, if someone’s massively inflamed, I’d like to think about methyl folate six to eight months down the road, two to three days a week. We tend to think, ‘If a little’s good for us, a lot must be good for us.’ I’m now thinking need to be pulsing things.”
I totally agree pulsing is a key component that should not be overlooked, whether you’re taking supplements, fasting or doing a ketogenic diet. It’s important to go through cycles of buildup and tear-down.
For example, during a partial fast, you’re stimulating autophagy through caloric restriction. At that time, you would not want to take anything that stimulates mTOR (such as methyl folate or any of the other items listed above), as by stimulating mTOR you effectively interrupt the autophagy process.
Mast Cells Could Be Wreaking Havoc With Your Health
Glutathione rapidly loses electrons, making it useless unless recharged by nicotinamide adenine dinucleotide phosphate hydrogen (NADPH). As explained by Miller, the “NADPH steal,” a term he coined, may also be at play in many of the health issues people face today.
It’s becoming more widely known that you can have excess mast cells. Miller estimates about 80 percent of his clients have excess mast cell activation triggering histamine reactions. One of the signs of this is redness of the face due to heat intolerance. Sensitivity to touch is another, as are frequent, red, raised rashes.
Mast cells are white blood cells that come to the rescue when there’s a pathogen or a foreign invader that needs to be eliminated. While overfiring mast cells can cause problems, they’re not inherently bad, and strategies that inhibit them can backfire. Instead, Miller recommends determining why your mast cells are overactive.
His team presented research at the International Lyme and Associated Diseases Society’s 19th Annual Conference in November last year, identifying epigenetic factors that stimulate mast cells. He explains the relationships between mast cells, NADPH, NOX and glutathione:
“In simple terms, glutathione … has one chance to give a free radical an electron. Once it does that, it becomes oxidized. Then we need to donate that electron back. There’s this substance called NADPH that donates that electron back.3 It takes that oxidized glutathione and turns it back into reduced. That’s a good thing.
Now, NADPH has a dual role. There’s also an enzyme called NOX (NADPH oxidase). Its only purpose is to take this NADPH and turn it into a free radical … Now, they’ve done studies on animals. When they knock out that NOX enzyme, the animal dies from infection because it doesn’t have the ability to kill the pathogen.
Again, NOX and free radicals are not bad. But there are multiple factors that are now overstimulating NOX. One of them is sulfite. Sulfite needs to turn into sulfates. If we have deficiency of heme, we may not turn sulfites in sulfates … If sulfites don’t turn into sulfates, the sulfites may tell the NOX enzyme, ‘You need to make inflammation.’
Dopamine stimulates it [NOX], so stress will cause it. Glutamate stimulates it. Iron stimulates the NOX enzyme, and so does excessive mTOR … The NADPH steal is when NADPH gets stolen away from recycling glutathione, recycling thriodoxine, making nitric oxide, and potentially making excess mast cells.
There are a lot of people struggling with excess mast cells firing. They’re really sick. They don’t know what to do … Mold will also stimulate mast cells …
To sum it up, NADPH is critical for recycling your antioxidants. I believe the nicotinamide adenine dinucleotide (NAD+) and the NADPH are some of the most important things we can have adequate levels of for longevity and good health. We’re using up a lot of it because we’re exposed to so many toxic substances. Then, if another set of substances are stealing it to stimulate NOX to make mast cells, then we’ve just doubled the problem.”
Molecular hydrogen serves a role here as well, as studies have shown molecular hydrogen is an effective inhibitor of NOX,4 and can increase your concentration of NADPH. Curcumin also inhibits NOX, as does luteolin, apigenin and olive leaf. Aldosterone, on the other hand, stimulates NOX, Miller says.
This interview is quite loaded with information, not all of which has been covered in this article. For even more side notes and fascinating tangents, I recommend listening to the interview in its entirety.
Health practitioners interested in learning more about functional genomic analysis and how to apply it in your own practice, see the NutriGenetic Research Institute’s website, where you can sign up for their 30-hour, 14-module online certification course to become a nutritional genetic consultant.
Webinars for health practitioners are held every other Thursday. They also hold an annual conference in Hershey, Pennsylvania. The next one is scheduled for November 2019. In September, they’re also holding a seminar on environmental toxicity, detoxification and methylation mapping.
Patients interested in more information are directed to the yourgenomicresource.com which includes a listing of doctors who have completed the training and are qualified to provide nutritional guidance based on your SNPs. Up until last year, Miller could guide patients based on the genetic data provided by companies such as 23andMe. Now, he has developed his own DNA testing, which is capable of identifying some 300,000 SNPs.
Importantly, NutriGenetic Research Institute will never sell your private DNA or health data to anyone, which is one of the reasons why 23andMe is so inexpensive — they make their money by selling your DNA results to drug companies.
“I have pledged to everyone in writing that this data will never be sold to anyone. The other thing people can do, if they’re still worried, you can just change your name. Just come up with a fake name. It doesn’t matter. We don’t care. You just have to remember what it is,” Miller says.
“The [DNA] data from Brooks at Rutgers gets loaded into my software, which is in Chambersburg, Pennsylvania — a huge database. Then it crunches the data and gives a report, including the pyramid …
If you’re sick, you’ve been everywhere and you’re not getting better, this is certainly an option … Our whole goal is to help people get well. And to make a little bit of a dent in functional medicine — to help functional practitioners have tools that they can help, because functional medicine doctors see the tough cases. We want to give them some tools so that they can do a better job …
One of my favorite sayings is, ‘Genetics is never a diagnosis, but it tells you where to start looking.’ It’s like shining a light. ‘Think about looking here. Investigate whether this is a problem.’ Sometimes the SNPs show a problem, sometimes they don’t, but it can really give you clues to look where you may never have thought to look before.”
- A recent case report of 100 patients diagnosed with cognitive decline using the ReCODE protocol show both subjective and objective improvements in all participants
- The ReCODE protocol, which involves identifying the drivers of cognitive decline (such as pathogens, toxins and metabolic changes), then targeting those in a personalized program that includes dietary and lifestyle changes, allows your brain to create and maintain synapses again, thereby treating the root of the problem
- A hallmark of neurodegenerative diseases such as Alzheimer’s is that proteins are aggregated and are typically misfolded
- By inducing ketosis, improving insulin sensitivity and supporting the mitochondria, you can often regain the ability to refold or proteolyze misfolded proteins
- Electromagnetic field exposures, such as that from cellphones and Wi-Fi, may play an important role in Alzheimer’s, as it triggers high amounts of oxidative stress and damage to proteins and DNA
Alzheimer’s disease, which is the most common form of dementia, eventually leads to the inability to carry out even the most basic of bodily functions, such as swallowing or walking. It is ultimately fatal, as conventional treatment options are few and universally ineffective.
Like autism among children, Alzheimer’s among seniors has reached epidemic proportions, with no slowdown in sight. On the contrary, evidence suggests the trend is worsening.
At present, Alzheimer’s affects an estimated 5.8 million Americans,1 and projections suggest the disease will affect 1 in 4 Americans within the next two decades. By 2050, Alzheimer’s diagnoses are projected to triple.2,3
And, while the U.S. Centers for Disease Control and Prevention lists the disease as the sixth leading cause of death in the U.S.,4,5 statistics published in the journal Neurology in 2014 revealed Alzheimer’s is vastly underreported on death certificates. In reality, the disease likely killed 503,400 American seniors in 2010,6 making it the third leading cause of death, right behind heart disease and cancer.7
The good news is that contrary to conventional claims, there are ways to prevent and even treat this tragic disease — not by drugs, but by diet and other lifestyle changes.
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,” has identified a number of molecular mechanisms at work in Alzheimer’s, and created a novel program called ReCODE to treat and reverse it.8
100-patient case report sheds light on treatment options
Bredesen’s most recent publication is a case report9,10 of 100 patients using the ReCODE protocol. He has previously published three case reports, each involving just 10 patients. This 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.
“By all the criteria, these people showed improvement, subjective and objective,” Bredesen says. This is no small thing, as there is no conventional treatment that can reverse Alzheimer’s. There have been many drug trials to date, but all have failed to reverse the disease. As noted by Bredesen:
“There are a couple of medications, Aricept, Namenda … but these have a very, very modest impact. The most important thing is their improvement is not sustained. They don’t change the outcome of the disease. You get a little bump in improvement, then you go right back to declining.
The most important part of the [ReCODE] protocol … is that the improvement is sustained. You’re actually going after the root cause of what is causing the cognitive decline. That’s a big difference.”
Alzheimer’s is a protective response to inflammation
If one were to summarize Bredesen’s approach in one sentence, it would be “to improve the ratio between synaptoblastic and synaptoclastic activity, which is the brain’s ability to create new synapses versus destroying them.” In other words, the treatment allows your brain to create and maintain synapses again. Bredesen explains:
“The molecular biology of this disease shows that what we call Alzheimer’s disease is actually a protective response. It’s essentially a scorched-earth retreat.
You’re pulling back and saying, ‘We’re not going to let this insult kill us, so we’re going to scorch the earth so it (whether it’s bacteria or something else) cannot take advantage … of what’s there.’ You’re literally downsizing [your synapses]. As long as those insults are going on, you will be downsized.”
Beta-amyloid is a protein that is highly correlated with Alzheimer’s. However, all attempts at removing it have failed to improve the condition. Clearly, beta-amyloid in and of itself is not the primary cause, so simply getting rid of it is not the answer.
In Bredesen’s paper, he discusses the role of beta-amyloid as an antimicrobial peptide (AMP). Importantly, AMPs are critically important for host immunity. They target organisms such as bacteria, mycobacteria, viruses, fungi and protozoa. He explains:
“Here is the trick. It turns out amyloid beta is really part of the innate immune system. Its antimicrobial effect was first discovered and published by professor Robert Moir and professor Rudy Tanzi at Harvard.
This thing actually has, again, a protective response. Not only is it an AMP, but it also binds some toxins. For example, mercury, other divalent metals like iron and things like that. [Amyloid beta] has multiple effects. It is part of your response to insult.
When you take that into account, you realize it’s fine to remove amyloid, but please don’t do it before you remove all the insults. We’ve seen numerous people now who have had the amyloid reduced and gotten worse because the ongoing insults are still there.”
Most recently, the drug company Biogen halted its Phase II clinical trial for aducanumab, a drug designed to remove beta-amyloid, and this is the typical story for these kinds of drugs. And then a major trial of yet another approach to amyloid removal, the BACE inhibitor CNP520, was halted because the drug was associated with increased cognitive decline and brain atrophy.11
The protein refolding process is impaired in Alzheimer’s
About one-third of the proteins your body makes on any given day are misfolded. Thankfully, your body has a mechanism by which those 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.
In fact, heat-shock proteins are a corollary of autophagy, the process by which your body cleans out damaged organelles. This relates to Alzheimer’s, because the refolding process is one of several factors that need to work in order for your brain to function. As noted by Bredesen:
“In all of these different neurodegenerative diseases, whether you’re talking about Alzheimer’s, Huntington’s, Lou Gehrig’s disease, Parkinson’s disease or Lewy body, they all feature proteins that are aggregated and that are typically misfolded. They are not degraded appropriately.
You lose not only the ability to fold but the ability to degrade these proteins. That is a critical piece. In fact, just recently, an article came out on a common neurodegenerative condition, newly described, which is called LATE, which is limbic-predominant, age-related TDP-43 encephalopathy.
In other words, this is a little bit like Alzheimer’s … [LATE] features TDP-43, which is a protein that is involved in numerous things, including protein folding … We lose that [protein-folding] ability as we start to downsize [synapses], as you don’t have an appropriate energy, you don’t have the appropriate trophic support.
You don’t have the appropriate hormonal and nutritional support … When we target ketosis, when we target insulin sensitivity, when we target mitochondrial support, that typically allows you to generate the appropriate ability to refold misfolded proteins …
You can induce the heat-shock response … by doing this combination of sauna and then [going] into the cold and then back to the sauna and then back to the cold …
You are recurrently activating this critical response [by doing that]. There’s no question it is going to be important, especially in ALS, but likely in all of the neurodegenerative conditions.”
The link between protein folding and cell death
As noted by Bredesen, there are three kinds of autophagy: macro-autophagy, micro-autophagy and chaperone-mediated autophagy. Each offers a slightly different way to repair, remove or recycle damaged organelles within the cell.
Specific proteins, for example, can be targeted for chaperone-mediated autophagy. Bredesen recounts findings of research he did to ascertain the linkage between protein folding and programmed cell death (apoptosis, where the entire cell is killed off and removed):
“If you fail to reform these [misfolded proteins], you literally activate an entire system that initially stops producing more protein. It’s basically saying, ‘We’re not keeping up with this. We’re going to shut this down.’ It attempts to refold. Then it attempts to destroy the proteins if it can’t refold them.
Then ultimately, if it cannot … keep up … it literally activates programmed cell death through specific caspases … This is something where you want to intervene upstream; understand why this is happening. And then if you’re unable to keep up with this, now, at least increase your heat-shock proteins so that you can refold. In this case, you prevent the induction of programmed cell death.”
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.
The case for cyclical fasting
While autophagy is clearly of critical importance, you don’t want to be in continuous autophagy. You also need to cycle through the rebuilding phase. One of the ways in which you can control this is through cyclical fasting. Bredesen typically recommends an intermittent fasting approach.
“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.”
Test your ketones
So, to recap, while dementia patients with excess weight tend to respond favorably to cyclical fasting, at least initially, underweight patients may experience cognitive decline, as they’re simply too underweight to produce ketones in response to the fasting. For those who are underweight, Bredesen recommends using a ketone supplement such as medium-chain triglycerides (MCT) oil.
If that doesn’t bring you into the desired ketone level (1.5 to 4.0 mmol), or if it’s adversely affecting your low-density lipoprotein (LDL) particle number, he might recommend exogenous ketones — either ketone esters or salts. “We’d like to look at your LDL particle number and use that to titrate, to make sure that your LDL particle number is not too high,” he says.
To test your ketones, I recommend KetoCoachX.12 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.
Energy demands are not met in neurodegenerative diseases
Nutritional ketosis, in which your body produces endogenous ketones (water-soluble fats), is important for all neurodegenerative diseases, but it’s not a complete cure-all. Bredesen explains:
“What we’ve come to realize from the research over the years is that neurodegenerative diseases, whether Alzheimer’s … macular degeneration … Lewy body, Parkinson’s or ALS, they all have one thing in common. They are related to specific subdomains of the nervous system.
Each of these has a unique requirement for nutrients, hormones, trophic factors, et cetera … In each case, there is a mismatch between the supply and the demand. For most of your life, you’re keeping up with that demand. With all of these diseases, you have a repeated or a chronic mismatch between the support and the requirement.
In Parkinson’s disease, it’s quite clear. You can create Parkinson’s disease simply by inhibiting mitochondrial Complex I. That specific subdomain of motor modulation, which is what Parkinson’s is all about, is the thing that is the most sensitive to reductions in mitochondrial Complex I support.
Therefore, when people have this, you need to bring the supply back in line with the demand. A critical way to do that is to supply the appropriate ketosis — the appropriate energy.
Now, if the person is continuing to be exposed to whatever chemicals are inhibiting Complex I — and it’s typically … mold-related biotoxins or organic toxins such as paraquat or glyphosate — as long as these are ongoing, you’re going to get very temporary relief.
The goal here is both to get rid of what is inhibiting Complex I and to flood the system, to help the system by giving appropriate support for the energetics … With Alzheimer’s, we’re really talking about a mismatch in trophic support. You’ve got this ongoing need as you’re making neuroplasticity.”
Why late-night eating is ill advised
Although I am not ApoE4-positive, I prefer fasting for 16 hours a day, essentially narrowing my eating window to just four to six hours. I also make sure to eat my last meal three to six hours before bedtime. One of the reasons for this advice is because avoiding late-night eating will increase your nicotinamide adenine dinucleotide (NAD+) levels, which are important for a variety of bodily functions.
Importantly, it will also reduce nicotinamide adenine dinucleotide phosphate (NADPH), which is essentially the true cellular battery of your cell and has the reductive potential to recharge your antioxidants. The largest consumer of NADPH is the creation of fatty acids.
If you’re eating close to bedtime, then you’re not going to be able to use the NADPH to burn those calories as energy. Instead, they must be stored some way. To store them, you have to create fat, so you’re basically radically lowering your NADPH levels when you eat late at night because they are being consumed to store your extra calories by creating fat.
Bredesen’s protocol includes this strategy as well. He calls his approach “KetoFlex 12/3,” because it generates mild ketosis and is flexible diet-wise. It can be done whether you’re a vegetarian or not. The 12/3 stands for a 12-hour minimum fast each day, and eating the last meal three hours before bedtime.
“Sirtuin-1 (SIRT1) was identified as a critical molecule, both for longevity and has been studied extensively for its effects on longevity, but also for its effects on Alzheimer’s disease …
ApoE4 actually enters the nucleus and downregulates the production of this critical molecule, so you can see one of its many effects on Alzheimer’s disease. Well, when SIRT1 is made, it is actually made in an autoinhibitory fashion. It’s just like having a gun in a holster. It’s not active … NAD activates the SIRT1.
So does resveratrol. This is why people take resveratrol [or] nicotinamide riboside. These are both activating this program, which is moving you from … more of a pro-inflammatory approach to a longevity approach — a change in your metabolic pattern. That includes activating things like autophagy and also having an anti-Alzheimer’s and a pro-longevity effect …
[Q]uercetin also has an interesting impact on senescent cells … I think that that’s going to turn out to be an important way to impact a number of age-related conditions, including neurodegeneration.”
The drawback, and the reason you cannot rely on supplements alone, is that the bioabsorption of these polyphenols, like quercetin for example, is quite low. Oftentimes, you cannot absorb enough to get the full benefits.
Limit electromagnetic field exposures
There’s also convincing evidence showing electromagnetic field exposures (EMFs) such as that from cellphones and Wi-Fi play an important role. Bredesen agrees, and recommends his patients limit such exposures. In summary, EMFs activate your voltage-gated calcium channels, allowing the release of excess nitric oxide and superoxide in the cell, resulting in the creation of peroxynitrite.
Peroxynitrite causes similar damage to your DNA as ionizing radiation. It also damages your stem cells, mitochondria, proteins and cell membranes. Poly-ADP ribose polymerase helps repair DNA damage by extracting an adenosine diphosphate (ADP) molecule from NAD. Approximately 100 to 150 NAD are required to repair a single DNA break.
While this process works quite well, problems arise when continuous DNA damage requiring continuous PARP activation occurs, as this ends up decimating your NAD+ level. Bredesen adds:
“This is a critical area. The big problem we’ve had with this so far is that we can measure your NF-κB activation; we can measure your status of hormones, nutrients, magnesium, on and on and on. Typically, with our approach, we measure 150 different variables.
There is no simple way to measure the effect of EMF on a given person’s nervous system. I look forward to the day when we can do a test and say, ‘Aha. This person has 27.2 on their effects on their voltage-gated calcium channels because of EMFs.’ Because then we’ll really be able to alter that.
For now, the best we can say is — just as we go after biotoxins and chemotoxins — [EMF] is a physical toxin. The best we can say is, ‘Minimize that to the extent you can.’ You can certainly measure the exposure. We just don’t have a good way yet to measure its effect on your brain.”
There’s no decline in sight for Alzheimer’s, at least in the foreseeable future, so it would behoove most people to just assume you’re headed for it and take action now, regardless of your age, to prevent it. When it comes to Alzheimer’s, prevention is surely far easier than trying to treat it once it has set in. As noted by Bredesen:
“This is all about prevention and early reversal. Those are the people where we see virtually 100% response. This is why I think there needs to be a global effort to decrease the burden of dementia. We’re just now starting a clinical trial. We’ve been trying to get institutional review board (IRB) approval for years …
It has finally been approved, so we’re starting a trial with Dr. Ann Hathaway, Dr. Deborah Gordon and Dr. Kat Toups, who are all seeing patients. We’re very excited to see what the trial will show with this approach. Because certainly, anecdotally, we’re hearing it all the time.
As you mentioned, we just published a paper a few months ago on 100 patients who showed documented improvement … I’m convinced we could, today, if everyone got an appropriate prevention, make this a very rare disease.”
Bredesen’s case report13 is open access, so you can download and read the full study. To learn more about Bredesen’s ReCODE protocol, see our previous interview, featured in “ReCODE: The reversal of cognitive decline.” In it, he reviews the various subtypes of Alzheimer’s, based on metabolic profiling, the influence of genetics, recommended screening tests and much more.
His book, “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline,” also provides the details, and would be a valuable reference in anyone’s health library.
You can also learn more about Bredesen and his work by following him on Facebook, Twitter or visit his website, drbredesen.com. Last but not least, keep an eye out for his latest book, “The First Survivors of Alzheimer’s.” This book, scheduled to come out toward the end of 2019, will feature first-person accounts from patients diagnosed with Alzheimer’s who beat the odds and improved.
- 1, 5 Alz.org, 2019 Disease Facts and Figures
- 2 CNN June 8, 2015
- 3 Nature 2014: 20; 415-418
- 4, 7 CDC.gov Leading causes of death in the US
- 6 Neurology March 5, 2014; 82(12)
- 8 AHNP Precision Health ReCODE, The Bredesen Protocol
- 9, 13 Journal of Alzheimers Disease & Parkinsonism 2018; 8(5): 450
- 10 Rezilir Health LLC, 100 Case reports for the reversal of cognitive decline
- 11 Alzforum July 12, 2019
- 12 KetoCoachX.com