ALZHEIMER'S DISEASE 

Story at-a-glance

• Between 1999 and 2014, the death rate from Alzheimer’s increased by 55 percent, killing more than 93,500 Americans in 2014, according to a review of death certificates
• Research published in 2014 found Alzheimer’s deaths were severely underreported on death certificates. Researchers estimate the annual death toll from Alzheimer’s actually exceeds half a million
• Many lifestyle and environmental factors contribute to the rise in Alzheimer’s, including inappropriate diet, inactivity, insulin resistance, prion infection, lack of sun exposure and overexposure to toxic chemicals and non-native electromagnetic fields.
• By Dr. Mercola

Alzheimer’s disease, which is the most serious 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 5.4 million Americans.1

Projections suggest the disease will affect 1 in 4 Americans within the next two decades, and by 2050, Alzheimer’s diagnoses are projected to triple.2,3 Shocking statistics published in the journal Neurology in 2014 revealed Alzheimer’s killed more than 503,000 American seniors in 2010, making it the third leading cause of death, right behind heart disease and cancer.4

Now, data published in the U.S. Centers for Disease Control and Prevention’s (CDC) Morbidity and Mortality Weekly Report reveals that between 1999 and 2014, the death rate from Alzheimer’s increased by 55 percent,5,6,7,8 — a rather radical increase in a mere 15 years.

The CDC report also noted the number of people dying from the disease at home, opposed to in a care facility, has increased from 14 to 25 percent. This means many Alzheimer’s caretakers are unpaid family members and friends — a task known to be taxing from both an emotional and financial perspective. While these statistics sound dire enough, the reality may be even worse than that.

Alzheimer’s Deaths Are Likely Severely Underreported

The CDC report used data collected from U.S. death certificates. However, the 2014 Neurology study revealed Alzheimer’s deaths are grossly underreported on death certificates. In 2010, death certificates showed there were less than 84,000 deaths from Alzheimer’s. Meanwhile, by ascertaining the cause of death based on evaluation of donated organs from the diseased, the actual death toll attributable to dementia came out to 503,400.

If such a trend of underreporting Alzheimer’s disease as a cause of death holds true, the increase in Alzheimer’s deaths over the past 15 years may in fact be far greater than 55 percent.

Indeed, the CDC claims Alzheimer’s is the sixth leading cause of death, while the results from the 2014 study ranked it third. According to the CDC, Alzheimer’s killed 93,541 Americans in 2014 — a far cry from the estimated annual death toll of 503,400, reported in the Neurology study. Whatever the case may be, what’s clear is that severe, lethal dementia is rapidly rising, and the medical establishment is no closer to solving the riddle of causation than they were 30 years ago.

What’s Causing Alzheimer’s Disease?

It’s often said that the underlying causes of Alzheimer’s disease are unknown, but there’s no shortage of theories. Based on the available science, here are several of the most prominent or likely culprits that can raise your risk of Alzheimer’s disease:

Insulin resistance Mounting research suggests Alzheimer’s disease is intricately connected to insulin resistance; even mild elevation of blood sugar is associated with an elevated risk for dementia.9 Diabetes and heart disease10 are also known to elevate your risk, and both are rooted in insulin resistance. Neurologist David Perlmutter warns anything that promotes insulin resistance, like a processed food diet, will also raise your risk of Alzheimer’s. Recent research has strengthened the link between insulin resistance and dementia even further, particularly among those with existing heart disease.11,12,13 Studies have also confirmed that the greater an individual’s insulin resistance, the less sugar they have in key parts of their brain, and these areas typically correspond to the areas affected by Alzheimer’s.14,15

Vitamin D deficiency The Scotland Dementia Research Centre also noted there’s a very clear link between vitamin D deficiency and dementia.16 Indeed, studies have shown vitamin D plays a critical role in brain health, immune function, gene expression and inflammation — all of which influence Alzheimer’s. A wide variety of brain tissue contains vitamin D receptors, and when they’re activated by vitamin D, it facilitates nerve growth in your brain. Researchers also believe optimal vitamin D levels boost levels of important brain chemicals, and protect brain cells by increasing the effectiveness of glial cells in nursing damaged neurons back to health. Considering an estimated 95 percent of seniors are at risk of vitamin D deficiency or insufficiency, vitamin D may be a very important factor for successful prevention among the general population. Research also shows people living in northern latitudes have higher rates of death from Alzheimer’s than those living in sunnier areas,17 suggesting a link between sun exposure, vitamin D and brain health. In a 2014 study,18 considered to be the most robust study of its kind at the time, those who were severely deficient in vitamin D had a 125 percent higher risk of developing some form of dementia compared to those with normal levels. The findings also suggest there’s a threshold level of circulating vitamin D, below which your risk for dementia increases. This threshold was found to be right around 20 nanograms per milliliter (ng/ml) or 50 nanomoles per liter (nmol/L) for Europeans. Higher levels are associated with better brain health in general, and based on a broader view of the available science, 20 ng/ml is still far too low. The bulk of the research suggests a healthy range is between 40 to 60 ng/ml.

Lack of sun exposure While vitamin D deficiency is directly attributable to lack of sensible sun exposure, vitamin D production is not the only way sun exposure can influence your dementia risk. Evidence suggests sunlight is a beneficial electromagnetic frequency (EMF) that is in fact essential and vital for your health in its own right. About 40 percent of the rays in sunlight is infrared. The red and near-infrared frequencies interact with cytochrome c oxidase (CCO) — one of the proteins in the inner mitochondrial membrane and a member of the electron transport chain. CCO is a chromophore, a molecule that attracts and absorbs light. In short, sunlight improves the generation of energy (ATP). The optimal wavelength for stimulating CCO lies in two regions, red at 630 to 660 nanometers (nm) and near-infrared at 810 to 850 nm. I’ve recently interviewed two different experts on photobiomodulation, a term describing the use of near-infrared light as a treatment for Alzheimer’s. To learn more about this fascinating field, please see my interviews with Michael Hamblin, Ph.D., and Dr. Lew Lim. Both have published papers on using photobiomodulation to improve Alzheimer’s disease. Photobiomodulation also improves oxygenation to your cells by releasing nitric oxide, and is a vasodilator that helps relax your blood vessels, lower your blood pressure and improve vascular health. Additionally, delivering red (660 nm) and near infrared light (830 nm) to the mitochondria promotes synthesizing of gene transcription factors that trigger cellular repair, and this is as true in the brain as anywhere else in your body.

Prion infection In addition to viruses, bacteria and fungi, an infectious protein called TDP-43, which behaves like infectious proteins known as prions — responsible for the brain destruction that occurs in Mad Cow and Chronic Wasting Diseases — has been linked to Alzheimer’s. Research presented at the 2014 Alzheimer's Association International Conference revealed Alzheimer's patients with TDP-43 were 10 times more likely to have been cognitively impaired at death than those without.19 Due to its similarities with mad cow disease, investigators have raised the possibility that Alzheimer’s disease may be linked to eating meat from animals raised in concentrated animal feeding operations (CAFOs).

Environmental Toxins  Experts at the Edinburgh University's Alzheimer Scotland Dementia Research Centre have compiled a list of top environmental risk factors thought to be contributing to the epidemic, based on a systematic review of the scientific literature.20,21,22,23 As much as one-third of your dementia risk is thought to be linked to environmental factors such as air pollution, pesticide exposure and living close to power lines. The risk factor with the most robust body of research behind it is air pollution. In fact, they couldn’t find a single study that didn’t show a link between exposure to air pollution and dementia. Particulate matter, nitric oxides, ozone and carbon monoxide have all been linked to an increased risk. Living close to power lines also has “limited yet robust” evidence suggesting it may influence your susceptibility to dementia.

Non-native or artificial electromagnetic fields (EMF) Non-native EMFs contribute to Alzheimer’s by poisoning your mitochondria, and this is not limited to living in close proximity to power lines. It also includes electromagnetic interference from the electric grid and microwave radiation from your cellphone, cellphone towers and Wi-Fi. This is a very deep and important topic that I plan to greatly expand on later this year. Based on what I’ve found so far, I’m convinced enough now to never put my cellphone on my body unless it is in airplane mode, and will not hold my cellphone unless it is on a selfie stick.

Inactivity / lack of exercise Exercise has been shown to protect your brain from Alzheimer's and other dementias, and also improves quality of life if you’ve already been diagnosed.24 In one study,25 patients diagnosed with mild to moderate Alzheimer’s who participated in a four-month-long supervised exercise program had significantly fewer neuropsychiatric symptoms associated with the disease (especially mental speed and attention) than the inactive control group. Other studies26 have shown aerobic exercise helps reduce tau levels in the brain. (Brain lesions known as tau tangles form when the protein tau collapses into twisted strands that end up killing your brain cells.) Cognitive function and memory27 can also be improved through regular exercise, and this effect is in part related to the effect exercise has on neurogenesis and the regrowth of brain cells. By targeting a gene pathway called brain-derived neurotrophic factor (BDNF), exercise actually promotes brain cell growth and connectivity. In one yearlong study, seniors who exercised grew and expanded their brain’s memory center by as much as 2 percent per year, where typically that center shrinks with age. Evidence also suggests exercise can trigger a change in the way the amyloid precursor protein is metabolized,28 thus slowing the onset and progression of Alzheimer's. By increasing levels of the protein PGC-1alpha (which Alzheimer’s patients have less of), brain cells produce less of the toxic amyloid protein associated with Alzheimer's.29

Hypertension and heart disease Arterial stiffness (atherosclerosis) is associated with a hallmark process of Alzheimer’s, namely the buildup of beta-amyloid plaque in your brain. The American Heart Association (AHA) warns there’s a strong association between hypertension and brain diseases such as vascular cognitive impairment (loss of brain function caused by impaired blood flow to your brain) and dementia.30 Moreover, in one clinical trial,31 test subjects who consumed high-fructose corn syrup developed higher risk factors for cardiovascular disease in two weeks, demonstrating just how influential your diet can be on your heart and brain health in the long term.

Genetic predisposition Several genes that predispose you to Alzheimer’s have also been identified.32 The most common gene associated with late onset Alzheimer’s is the apolipoprotein E (APOE) gene. The APOE e2 form is thought to reduce your risk while the APOE e4 form increases it. That said, some people never develop the disease even though they’ve inherited the APOE e4 gene from both their mother and father (giving them a double set), so while genetics can affect your risk, it is NOT a direct or inevitable cause. Your risk for early onset familial Alzheimer’s can also be ascertained through genetic testing.33 In this case, by looking for mutation in the genes for presenilin 1 and presenilin 2. People with one or more genetic predispositions are at particularly high risk of developing Alzheimer’s at a very young age. At just 31 years of age, Rebecca Doig is thought to be one of the youngest Alzheimer’s cases presently known.

Early Alzheimer’s Prevention Is Required to Stem the Tide of Dementia

There is no known cure and no effective conventional treatments for Alzheimer’s, making prevention an overarching priority. Regardless of your age, now is the time to really start looking at which of these possible causes might be influencing your risk. If you’re finding this information now and are in your 20s or 30s, consider yourself blessed with foresight.

You still have time to address most if not all of these possible factors. But don’t dawdle too long. Early onset of Alzheimer’s is also on the rise. Already, nearly 5 percent of Americans with the disease are younger than 65. The video above features the story of Amy Norton, who was diagnosed with Alzheimer’s at the age of 43. As noted by the American Alzheimer’s Association:34

“Many people with early onset are in their 40s and 50s. They have families, careers or are even caregivers themselves when Alzheimer's disease strikes. In the United States, it is estimated that approximately 200,000 people have early onset.”

The good news is that lifestyle choices such as diet, exercise and sleep can have a significant impact on your risk. As previously noted by Dr. Richard Lipton of the Albert Einstein College of Medicine — where they study healthy aging — lifestyle changes “look more promising than the drug studies so far” when it comes to addressing Alzheimer’s.35

Cyclical Ketogenic Diet Can Help Reduce Risk of Alzheimer’s

In recent years, I’ve become deeply interested in and familiar with the medical literature detailing the influence of mitochondrial function on health. It’s become quite clear to me — and to many other experts in the field — that mitochondrial dysfunction is at the heart of virtually all chronic disease, including heart disease, cancer and Alzheimer’s.

Mitochondria are tiny organelles found in most of your cells, responsible for production of energy in the form of adenosine triphosphate (ATP). Your mitochondria have a series of proteins in the electron transport chain, in which they pass electrons from the metabolic products of the food you eat to combine it with oxygen from the air you breathe and ultimately form water. This is called aerobic respiration.

The more mitochondria you have and the healthier they are, the more energy your body can generate and the lower your risk of chronic disease. Disturbingly, research suggests 50 percent of people under the age of 40 have early onset mitochondrial dysfunction. It’s no wonder then that diseases historically known to affect the very old are now affecting people in middle age or even younger. Dementia is certainly one of those.

The good news is there are many ways to optimize your mitochondrial function, and this is the focus of my new book, “Fat for Fuel,” which details my metabolic mitochondrial therapy (MMT) program in full — starting with what you eat every day. Mounting evidence suggests the ability to burn fat for fuel is a crucial component of good metabolic health and mitochondrial function, and to do that, you simply cannot subsist on a standard American diet of processed food.

You need a diet that powers your brain and body with healthy fats. When your body burns fat as its primary fuel, ketones are created, which burn efficiently, are a superior fuel for your brain, and generate fewer reactive oxygen species and less free radical damage. A ketone called beta-hydroxybutyrate is also a major epigenetic player, stimulating beneficial changes in DNA expression, thereby reducing inflammation and increasing detoxification and antioxidant production.

MMT Is Part of the Answer

As a general guideline, until you are able to burn fat as your primary fuel, it is best to restrict your intake of net carbs (total carbs minus fiber) to about 20 to 50 grams per day while also keeping protein low enough to allow you to make the shift to nutritional ketosis — the metabolic state associated with an increased production of ketones in your liver. This is the biological reflection of being able to burn fat for fuel.

Nutritional ketosis is defined as blood ketones that stay in the range of 0.5 to 8.0 millimoles per liter (mmol/L). I explain the ins and outs of implementing this kind of diet, and its many health benefits, in the book. In it, I also explain why cycling through stages of feast and famine, opposed to continuously remaining in nutritional ketosis, is so important.

By periodically pulsing higher carb intakes, your ketone levels will dramatically increase and your blood sugar will drop. The pulsing will also prevent the loss of muscle that can occur when you remain in nutritional ketosis for extended periods of time.

A fascinating paper that demonstrates the power of lifestyle modifications for the prevention and treatment of Alzheimer’s is that of Dr. Dale Bredesen, a UCLA researcher who, by leveraging 36 different healthy lifestyle parameters — several of which are included in my MMT program — was able to reverse Alzheimer’s in 9 out of 10 patients. This included the use of:

Exercise	Ketogenic diet	Optimizing vitamin D	Optimizing hormones
Increasing sleep	Meditation	Detoxification	Eliminating gluten and processed food

His work was published in the journal Aging in 2014. You can download the full-text case paper online, which details the full program.36According to Bredesen, “The results … suggest that, at least early in the course, cognitive decline may be driven in large part by metabolic processes.”

Lifestyle Strategies That Reduce Your Risk of Alzheimer’s Disease

While genetics can raise your risk of Alzheimer’s, even genetic predisposition does not mean dementia is your inevitable fate. On the other hand, you may have no genetic predisposition for dementia and still lose your mind. It’s important to remember that your genetic expression is predicated on epigenetic factors such as your diet, exercise, sleep and environmental exposures. You can, to a great degree, influence your genetic fate, no matter what you start out with.

When it comes to preventing Alzheimer’s, enhancing your mitochondrial function, which I detail in my book, “Fat for Fuel,” is paramount. MMT, I believe, helps you build a solid base for health and general disease prevention. In addition to that, the following strategies (some of which are part of MMT) are particularly important for the prevention of Alzheimer’s:

Address your diet: Eat real food, ideally organic, and avoid processed foods, especially refined carbohydrates and vegetable oils Contrary to popular belief, the ideal fuel for your brain is not glucose but ketones. Ketones are what your body produces when it converts fat into energy. Healthy fats to add to your diet include avocados, butter, organic pastured egg yolks, coconuts and coconut oil, grass fed meats, raw nuts and animal-based omega-3. High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer's disease, thereby slowing down its progression and lowering your risk of developing the disorder. Avoid all trans fats or hydrogenated fats. This includes margarine, vegetable oils and various butter-like spreads. Keep your added sugar levels to a minimum and your total fructose below 25 grams per day, or as low as 15 grams per day if you already have insulin/leptin resistance or any related disorders. Most will also benefit from a gluten-free diet, as gluten makes your gut more permeable, which allows proteins to get into your bloodstream where they sensitize your immune system and promote inflammation and autoimmunity, both of which play a role in the development of Alzheimer’s.

Optimize your gut flora To do this, avoid processed foods, antibiotics and antibacterial products, fluoridated and chlorinated water, and be sure to eat traditionally fermented and cultured foods, along with a high-quality probiotic if needed. Dr. Steven Gundry does an excellent job of expanding on this in his new book “The Plant Paradox.” I will be interviewing him later this year, but his innovative approach has great potential to help your health.

Intermittently fast Intermittent fasting is a powerful tool to jump-start your body into remembering how to burn fat and repair the insulin/leptin resistance that is a primary contributing factor for Alzheimer’s.

If you enjoy black coffee, keep the habit While I would not encourage you to drink coffee if you’re not already a coffee drinker, if you enjoy it, there’s good news. Caffeine triggers the release of BDNF that activates brain stem cells to convert into new neurons, thereby improving your brain health. High-quality coffee also has many beneficial polyphenols that can improve brain function. In one study, people with mild cognitive impairment whose blood levels of caffeine were higher (due to coffee consumption) were less likely to progress to full-blown dementia compared to those who did not drink coffee.37 In another study, older women whose coffee consumption was above average had a lower risk of dementia.38 Just make sure your coffee is organic, as coffee tends to be heavily sprayed with pesticides. For more details on making your coffee habit as healthy as possible, please see my previous article, “Black Coffee in the Morning May Provide Valuable Health Benefits.”

Move regularly and consistently throughout the day The following lecture by physical therapist Teresa Liu-Ambrose, Ph.D., details the impact of exercise on dementia prevention and treatment.

Optimize your magnesium levels Preliminary research strongly suggests a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Magnesium threonate appears particularly useful as it has the ability to cross your blood brain barrier.

Get sensible sun exposure to optimize your vitamin D and reap other photobiomodulation benefits Sufficient vitamin D is imperative for proper functioning of your immune system to combat inflammation associated with Alzheimer's. If you are unable to get sufficient amounts of sun exposure, make sure to take daily supplemental vitamin D3 to make your blood level at least 40 to 60 ng/ml. This is typically about 8,000 units of vitamin D for most adults. That said, please do remember that sun exposure is also important for reasons unrelated to vitamin D. The near-infrared light in sunlight actually helps boost cognition and reduces symptoms of Alzheimer’s via a process known as photobiomodulation.

Avoid and eliminate mercury from your body Dental amalgam fillings are one of the major sources of heavy metal toxicity; however, you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.

Avoid and eliminate aluminum from your body Common sources of aluminum include antiperspirants, nonstick cookware and vaccine adjuvants. For tips on how to detox aluminum, please see my article, “First Case Study to Show Direct Link between Alzheimer’s and Aluminum Toxicity.” There is some suggestion that certain mineral waters high in silicic acid may help your body eliminate aluminum. Later this year I will be interviewing Wendy Meyers, an expert on detoxification and minerals, about some simple strategies you can use to address this.

Avoid flu vaccinations Most flu vaccines contain both mercury and aluminum.

Avoid statins and anticholinergic drugs Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence and certain narcotic pain relievers. Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10, vitamin K2 and neurotransmitter precursors and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.

Limit your exposure to non-native electromagnetic fields (cellphones, Wi-Fi routers and modems) The primary pathology behind cellphone damage is not related specifically to brain tumors, or even to cancer. The real danger lies in damage from the reactive nitrogen species peroxynitrites.39 Increased peroxynitrites from cellphone exposure will damage your mitochondria, and your brain is the most mitochondrial-dense organ in your body. Increased peroxynitrite generation has also been associated with increased levels of systemic inflammation by triggering cytokine storms, autonomic hormonal dysfunction and mitochondrial dysfunction. Peroxynitrite is an unstable structural ion produced in your body after nitric oxide is exposed to superoxide, and this complex chemical process begins with exposure to low-frequency microwave radiation from your cellphone, Wi-Fi and cellphone towers.40,41

Get plenty of restorative sleep Sleep is necessary for maintaining metabolic homeostasis in your brain. Wakefulness is associated with mitochondrial stress; without sufficient sleep, neuron degeneration sets in. While sleep problems are common in Alzheimer’s patients, poor sleep may also be contributing to the disease by driving the buildup of amyloid plaques in your brain. While you sleep, your brain flushes out waste materials, and if you don’t sleep well, this natural detoxification and clean-out process will be severely hampered.

Challenge your mind daily Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of dementia and Alzheimer's. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer's disease.

McDonald’s to outsource more human jobs to machines

admin | Jun 26, 2017 | Comments 0

A decision this week by McDonald’s to replace thousands of human employees in its workforce with self-serve ordering kiosks in the coming months portends bad times ahead for entry-level workers and others who are stuck in low-skilled jobs.

As reported by Zero Hedge, industry analysts estimate that the fast food giant will add around 2,500 electronic ordering kiosks by the end of this year, and add 3,000 more by the end of 2018. Mobile ordering is also on the way, coming to 14,000 locations around the U.S. by year’s end.

The ordering kiosks will replace human cashiers, and you can be certain that those jobs are never coming back. (RELATED: Is this YOU? 1 in 4 Americans completely BROKE and in no position to help themselves when SHTF)

The example set by McDonald’s will no doubt be replicated throughout the fast food and restaurant industry, and why not? Getting rid of human workers solves many problems — poor employee attitudes toward customers, chronic tardiness, sick days, theft, and, most importantly, rising pay, thanks to far-Left “progressives” who think low-skilled burger-flipping and fry-making ought to pay as much as a skilled technical job.

Lowering labor costs is especially important in the fast food industry because the profit margins are so slim as it is. This will help restaurant owners immensely with their bottom lines, but it will take hundreds of thousands of jobs (eventually) permanently out of circulation.

But there are many more jobs that are going to disappear — replaced by electronic kiosks, robots and other machines.

As Robotics.news reported in late May, one new alarming report estimated that the loss of retail jobs in the coming years will surpass 7 million:

A report by investment advisory firm Cornerstone Capital Group revealed that nearly half of all retail workers in the U.S. face job insecurity as use of automation technology continues to rise across the country. According to the report, around 16 million people in the U.S. work in the retail industry. This equates to about one in 10 American employees, the 56-page report showed.

Another factor harming retail jobs: Disappearing retail outlets, thanks to a dramatic rise in online shopping (and all of the other employee problems and costs mentioned above). BankRate reports that 21 retailers are closing thousands of brick-and-mortar stores in 2017, including Macy’s, Payless Shoe Source, Radio Shack, mall mainstay J.C. Penney and others.

And while President Donald J. Trump has promised to bring back millions of jobs to the U.S. that have been lost to globalist outsourcing for two decades, the truth is he’s fighting the political establishment and market headwinds like automation and store closures.

So much lost opportunity will lead to mass civil unrest as, almost overnight, millions of people become unemployable because they did not have a robot-proof or electronics-proof skill. Needless to say, then, it is vital that you assess your own skill set today and work to make yourself valuable and marketable to current and future employers.

Here are some jobs that should be safe for the foreseeable future:

— Reporter/writer/correspondent

— Astronomers

— Paramedic/EMS/Medical personnel

— Miners

— Occupational therapists

— Robotics programmer/technician/developer/builder

— Solar technology expert

— Construction/road repair/infrastructure builder

— Computer programmer/app developer

Having these skills will also make you more valuable, even in a collapse situation:

— Gardener/farmer

— Healthcare provider

— Construction/builder

— Firearms expert

— Rancher/animal husbandry

— “Handyman/woman”

Some people have tried to predict what sort of jobs will be phased out, maintained or created in the future. Figuring out which jobs are going to go the way of “human alarm clocks” in the 1800s and which ones will be created in the future (human designers?) is difficult, but it’s a good idea to get started thinking about it now, while major job changes are on the way.

J.D. Heyes is a senior writer for NaturalNews.com and NewsTarget.com, as well as editor of The National Sentinel.

Sources:

ZeroHedge.com

Robotics.news

MarketPlace.org

AgencyCentral.co.uk

Originally posted: http://www.naturalnews.com/2017-06-25-mcdonalds-to-outsource-human-jobs-to-machines.html

THE BLACK CODE /  THE AFRICAN PLEDGE

 

Mitochondrial Eve In 1987, A world wide survey of human mitochondrial DNA (mtDNA) was published by Cann, Stoneking, and Wilson in Nature magazine. Its main point was that "all mitochondrial DNAs stem from one woman" and that she probably lived around 200,000 years ago in Africa. When the media picked up from Wilson, one of the authors of the paper, that they had found the "Mitochondrial Eve" or "African Eve", the story became a sensation. Have scientists found "the mother of us all"? Most people know about the nuclei of cells and that the genetic inheritance from both parents are found in the nucleus. Humans have 46 chromosomes which they inherit from both their parents. Parts of both the DNA from the mother and father are put together in a recombination process that allows the children to have traits from both their mother and their Father. However, there is DNA located in other parts of the cell. In the cytoplasm, organelles called mitochondria, which provide energy for the cell in the form of ATP, also have DNA. This DNA, however, does not seem to come from both parents. Instead, it comes only from the mother and not from the Father (There seems to be some rare exceptions to the rule that only the mother contributes the mitochondrial DNA. See the mitochondrial Clock Update: Is maternal mitochondrial inheritance still thought to be true?). Initially, it was thought that for humans, most of the sperm remained outside of the egg. Only the head with the nuclear DNA and the centrosome, were thought to enter the egg. But that view has changed. Now it has been determined that the whole sperm enters the egg. However, virtually all of the sperm is broken down by enzymes. Only the chromosomes found in the head of the sperm in crystalline form are preserved and used in the recombination process to produce the final version of the new egg cell DNA. The sperm mitochondria and its DNA are broken down by enzymes made for that purpose. See the mitochondrial Clock Update: for details. However, the end result is still the same. The mitochondria and its DNA from the sperm are not used. Only the mitochondria from the egg are used for the newly developing person. So, our mitochondrial DNA is essentially identical to that of our mother. Mitochondrial DNA is transfered from mother to daughter, generation after generation. The mitochondrial DNA in the son, which he got from his mother, is a dead end street, since his mitochondrial DNA will not be used in his children. Nuclear DNA changes a lot since it undergoes recombination in every generation. However, the mitochondrial DNA gets transfered from generation to generation without any recombination. Only the normal mutation rate that occurs when DNA is replicated allows the mitochondrial DNA to change. This is why the world wide survey was able to determine that all people are related via some original mother which they called the "mitochondrial Eve". They produced ancestral trees that depended on the slow mutation rate of mitochondrial DNA to estimate how the whole human population came from a single woman. After the initial discovery of the "mitochondrial Eve", Wilson felt uneasy about using the term "Eve" because it caused many to think that she was the only woman living at that time, much like what is written in Genesis of the Bible concerning Adam and Eve in the Garden of Eden. Also, the usual evolutionary time-scale for man did not allow such a short time as 200,000 years. Rather, it is believed that man has been around for a much longer period of time. Java man is thought to be 800,000 years old. Homo erectus specimens are found all throughout the world. Over forty specimens of Asian Homo erectus which have been found in China, have been dated 220,000 to 500,000 years of age. Lucy, and the earliest remains of specimens that are thought to be of the first to stand upright, are thought to be at least 1 to 4 million years of age. So, because the presence of man is thought to have been around for a much longer period of time than just 200,000 years, it was concluded that the mitochondrial Eve must not have been the first human female nor would she have been the only female alive at the time. Evolutionists have come to believe that Eve must have been one of many women of her time, in a genetic bottleneck. A time when there were a tiny population of people alive. It is not known why the human population would became so depleted in a bottleneck. Some suggests that environmental pressures could have brought the human population almost to extinction. It has even been suggested, that the ability to speak languages was a reason why only one group survived over all others. All sorts of reasons have been offered to explain why bottlenecks would exist: a continuous plaque, asteroid impact, or a climate change are just a few of the many ideas. Many suggest that Eve must have had some vast superiority because her offspring are thought to have conquered the whole world without any evidence of any interbreeding. Others state that selection had nothing to do with the takeover of the human population. They inject that it was a purely statistical process. Paleoanthropologists Attack the Mitochondrial Eve Story The story of the mitochondrial Eve is not what paleoanthropologists wanted to hear. They did believe that man came from Africa, but they believed it happened one million years ago. If Eve had lived a million years ago, most of the paleoanthropologists would have accepted the idea with open arms because the mitochondrial Eve data would have fit into the data they had. Now it seemed that there were several waves of humans that left Africa. Each wave seems to have taken over the world. Eve must have lived in Africa, 200,000 years ago, and then her descendants started migrating out of Africa, maybe 100,000 years ago to take over all the earth and all the older man types vanished from the earth without a trace in our genetic record! In addition, there is no evidence from the mitochondrial DNA data that Eve's descendants interbreeded with the older man types at all. The overtaking of the world's population by Eve's descendants in the last wave, a mere 100,000 years ago, is a point of contention because many of the paleoanthropologists saw a continuity of genetic traits between Homo erectus (the older type of man that Eve's descendants are thought to have killed off) and modern man. A continuity of genetic traits of the fossil remains suggests that Homo erectus actually had a direct genetic link to the more modern form of man. So, the modern chinese would be the decendants of Chinese erectus. Paleoanthropologists see this continuity as happening in separate parts of the world at the same time, in a parallel evolutionary process. What they see in the field is: African erectus evolving into modern africans, Chinese erectus evolving into modern chinese, European erectus evolving into Neandertals then modern Europeans, etc. So, the mitochondrial data seems to be at odds with fossils found in the field. The idea that Eve's children had conquered the whole world without any interbreeding at all, goes against the evidence showing that Homo erectus in various places of the world like China and Africa, look like the modern people of those same regions. Why do the chinese have traits associated with Asian erectus if all the Asian erectus had been wiped out when Eve's descendants arrived in Asia with no interbreeding at all? One paleoanthropologist, Milford Wolpoff, made the point that the out-of-Africa hypothesis was "Wacko"! When Eve's descendants left Africa, they left as Africans, but when they arrived in Asia, they were Asians! The Chinese and other Asians of today resemble the old erectus populations with the flat faces of the oriental people. The mitochondrial DNA data says the Asian erectus are extinct but the characteristics of modern man says they are not. The same phenomenon occurs in other regions of the world such as Europe where modern Europeans are actually closer to classic Neandertal than they are to any living human population with such features as a prominent nose and the shape of the rear end of the cranium. These kinds of arguments were countered by Chris Stringer who said: "Your fossils are not ancestors of modern men. What you have done for the last ten, twenty years was a complete waste of time". Rebeca Cann, one of the original authors of the study (mentioned above) had also said that paleoanthropologists could never tell for certain if a specific fossil actually left any descendants. On the other hand, there was "100 percent certainty that genes in modern populations have a history that can be examined and will trace back in absolute time to real ancestors". It is easy to tell that feelings were running high over this fight between the "out-of-Africa" theory and the "multi-regional continuity" theory that modern man arose from various place on the earth at the same time. The critics of the Eve story, who saw that the mitochondrial data did not fit with the fossils in the field that show a multi-regional continuity, so they started voicing several complaints against the mitochondrial data: The mitochondrial data was determined using restriction analysis rather than DNA sequencing. Restriction analysis is an enzymeatic method which can give false results at times. They used African Americans rather than Africans from Africa to represent native Africans in their study. So they did not get a proper sampling of the African population. They used an inferior method to build a phylogenetic tree. They used a program called PAUP which had been written to determine evolutionary relationships. However, the program gave different results when you entered the data in a different order. The answer was dependant upon the order that the data was entered into the computer. A big problem! Blair Hedges and his group in Penn State, found that when the data was entered in different orders, that sometimes some other part of the world was indicated as the place where Eve lived, rather than Africa. Newslines Headings in 1992 and 1993 such as: "Mitochondrial Eve: Wounded, But Not Dead Yet" and "Mitochondrial Eve Refuses to Die" are indications that the Mitochondrial Eve Hypothesis was in real trouble. At the 1993 AAAS (American Association for the Advancement of Science) meeting, Milford Wolpoff anounced: "It's over for Eve". Ever since it was admitted that there were serious problems with the statistics that supports the Eve idea, Wolpoff had wanted to give her last rites. However, in the very same meeting, Maryellen Ruvolo, from Harvard U. presented new data that used DNA sequencing rather than restriction analysis to study a part of the cytochrome oxidase gene found in the mitochondrial genome. The original work was criticized because it was based on a rapidly evolving part of the mitochondria. Ruvolo's work was based on a slowly evolving portion of the mitochondrial genome and he got the same answer as is found in the original work. What his work shows is that the short time for Eve is essentially correct. The "multi-regional continuity" people were hoping for an older date, like maybe 1 million years. That would have allowed the mitochondrial Eve data to fit with the "multi-regional continuity" theory. However that did not happen. Currently the battle is still raging over the history of Modern Human Origins and we still have the same two irreconcilable scientific camps: The mitochondrial Eve data, that supports the "out-of-Africa" theory where Eve's decendents, on coming out of Africa, are seen as taking over the whole world and overcoming all the other man types with no sign of interbreeding, only 100,000 years ago. The continuous genetic change of fossil data in many places on the globe seems to suggest to many that mankind has been advancing across the globe in a parallel multiregional evolutionary process. if Eve's descendants overtook the whole world suplanting all other peoples, there would be a break in the type of fossils seen in the field. The older fossils would not relate to the newer fossils that descend from Eve. There would be no way to explain the continuous change of fossil remains that is seen around the world, using the mitochondrial Eve data. So, there seems to be no way for all the data to presently fit together. It is true, as "Kip" Thorne from Australian National University, mentioned: "The fossil evidence is really scrappy. There just isn't enough of it." However, it does not look like the situation will change anytime soon. Wolpoff thinks that the controversy will continue until they are all dead. Then the next generation, he says, will have to decide.     Interesting Journal Articles with abstracts if available Mitochondrial DNA and human evolution. Cann RL, Stoneking M, Wilson AC. Nature. 1987 Jan 1-7;325(6099):31-6. Department of Biochemistry, University of California, Berkeley, California 94720, USA Mitochondrial DNAs from 147 people, drawn from five geographic populations have been analysed by restriction mapping. All these mitochondrial DNAs stem from one woman who is postulated to have lived about 200,000 years ago, probably in Africa. All the populations examined except the African population have multiple origins, implying that each area was colonised repeatedly. Mitochondrial COII sequences and modern human origins. Ruvolo M, Zehr S, von Dornum M, Pan D, Chang B, Lin J. Mol Biol Evol. 1993 Nov;10(6):1115-35. The aim of this study is to measure human mitochondrial sequence variability in the relatively slowly evolving mitochondrial gene cytochrome oxidase subunit II (COII) and to estimate when the human common ancestral mitochondrial type existed. New COII gene sequences were determined for five humans (Homo sapiens), including some of the most mitochondrially divergent humans known; for two pygmy chimpanzees (Pan paniscus); and for a common chimpanzee (P. troglodytes). COII sequences were analyzed with those from another relatively slowly evolving mitochondrial region (ND4-5). From class 1 (third codon position) sequence data, a relative divergence date for the human mitochondrial ancestor is estimated as 1/27 th of the human-chimpanzee divergence time. If it is assumed that humans and chimpanzees diverged 6 Mya, this places a human mitochondrial ancestor at 222,000 years, significantly different from 1 Myr (the presumed time of an H. erectus emergence from Africa). The mean coalescent time estimated from all 1,580 sites of combined mitochondrial data, when a 6-Mya human-chimpanzee divergence is assumed, is 298,000 years, with 95% confidence interval of 129,000-536,000 years. Neither estimate is compatible with a 1-Myr-old human mitochondrial ancestor. The mitochondrial DNA sequence data from COII and ND4-5 regions therefore do not support this multiregional hypothesis for the emergence of modern humans. Erratum in: Mol Biol Evol 1994 May;11(3):552. Identification of the remains of the Romanov family by DNA analysis. Gill P, Ivanov PL, Kimpton C, Piercy R, Benson N, Tully G, Evett I, Hagelberg E, Sullivan K Nat Genet 1994 Feb;6(2):130-5 Central Research and Support Establishment, Forensic Science Service, Aldermaston, Reading, Berkshire, UK. Comment in: Nat Genet 1994 Feb;6(2):113-4 Nine skeletons found in a shallow grave in Ekaterinburg, Russia, in July 1991, were tentatively identified by Russian forensic authorities as the remains of the last Tsar, Tsarina, three of their five children, the Royal Physician and three servants. We have performed DNA based sex testing and short tandem repeat (STR) analysis and confirm that a family group was present in the grave. Analysis of mitochondrial (mt) DNA reveals an exact sequence match between the putative Tsarina and the three children with a living maternal relative. Amplified mtDNA extracted from the remains of the putative Tsar has been cloned to demonstrate heteroplasmy at a single base within the mtDNA control region. One of these sequences matches two living maternal relatives of the Tsar. We conclude that the DNA evidence supports the hypothesis that the remains are those of the Romanov family. Mitochondrial DNA sequence heteroplasmy in the Grand Duke of Russia Georgij Romanov establishes the authenticity of the remains of Tsar Nicholas II. Ivanov PL, Wadhams MJ, Roby RK, Holland MM, Weedn VW, Parsons TJ Nat Genet 1996 Apr;12(4):417-20 Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow. In 1991, nine sets of skeletal remains were excavated from a mass grave near Yekaterinburg, Russia which were believed to include the Russian Tsar Nicholas II, the Tsarina Alexandra, and three of their daughters. Nuclear DNA testing of the remains verified such a family group, and mitochondrial DNA (mtDNA) sequences of the presumed Tsarina matched a known maternal relative, Prince Philip. mtDNA sequences from bone of the presumed Tsar matched two living maternal relatives except at a single position, where the bone sample had a mixture of matching (T) and mismatching (C) bases. Cloning experiments indicated that this mixture was due to heteroplasmy within the Tsar; nevertheless, the 'mismatch' fueled a lingering controversy concerning the authenticity of these remains. As a result, the official final report on the fate of the last Russian Royals has been postponed by Russian authorities pending additional, convincing DNA evidence. At the request of the Russian Federation government, we analysed the skeletal remains of the Tsar's brother Georgij Romanov in order to gain further insight into the occurrence and segregation of heteroplasmic mtDNA variants in the Tsar's maternal lineage. The mtDNA sequence of Georgij Romanov, matched that of the putative Tsar, and was heteroplasmic at the same position. This confirms heteroplasmy in the Tsar's lineage, and is powerful evidence supporting the identification of Tsar Nicholas II. The rapid intergenerational shift from heteroplasmy to homoplasmy, and the different heteroplasmic ratios in the brothers, is consistent with a 'bottleneck' mechanism of mtDNA segregation. How rapidly does the human mitochondrial genome evolve? Howell N, Kubacka I, Mackey DA Am J Hum Genet 1996 Sep;59(3):501-9 Department of Radiation Therapy, University of Texas Medical Branch, Galveston 77555-0656, USA. nhowell@mspo3.med.utmb.edu The results of an empirical nucleotide-sequencing approach indicate that the evolution of the human mitochondrial noncoding D-loop is both more rapid and more complex than is revealed by standard phylogenetic approaches. The nucleotide sequence of the D-loop region of the mitochondrial genome was determined for 45 members of a large matrilineal Leber hereditary optic neuropathy pedigree. Two germ-line mutations have arisen in members of one branch of the family, thereby leading to triplasmic descendants with three mitochondrial genotypes. Segregation toward the homoplasmic state can occur within a single generation in some of these descendants, a result that suggests rapid fixation of mitochondrial mutations as a result of developmental bottlenecking. However, slow segregation was observed in other offspring, and therefore no single or simple pattern of segregation can be generalized from the available data. Evidence for rare mtDNA recombination within the D-loop was obtained for one family member. In addition to these germ-line mutations, a somatic mutation was found in the D-loop of one family member. When this genealogical approach was applied to the nucleotide sequences of mitochondrial coding regions, the results again indicated a very rapid rate of evolution. The mutation rate of the human mtDNA deletion mtDNA4977. Shenkar R, Navi di W, Tavare S, Dang MH, Chomyn A, Attardi G, Cortopassi G, Arnheim N Am J Hum Genet 1996 Oct;59(4):772-80 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Science Center, Denver, USA. Comment in: Am J Hum Genet 1996 Oct;59(4):749-55 The human mitochondrial mutation mtDNA4977 is a 4,977-bp deletion that originates between two 13-bp direct repeats. We grew 220 colonies of cells, each from a single human cell. For each colony, we counted the number of cells and amplified the DNA by PCR to test for the presence of a deletion. To estimate the mutation fate, we used a model that describes the relationship between the mutation rate and the probability that a colony of a given size will contain no mutants, taking into account such factors as possible mitochondrial turnover and mistyping due to PCR error. We estimate that the mutation rate for mtDNA4977 in cultured human cells is 5.95 x 10(-8) per mitochondrial genome replication. This method can be applied to specific chromosomal, as well as mitochondrial, mutations. Mutational analysis of the human mitochondrial genome branches into the realm of bacterial genetics. Howell N Am J Hum Genet 1996 Oct;59(4):749-55 Comment on: Am J Hum Genet 1996 Oct;59(4):772-80 Comment in: Am J Hum Genet 1997 Oct;61(4):983-90 mtDNA mutation rates--no need to panic. Macaulay VA, Richards MB, Forster P, Bendall KE, Watson E, Sykes B, Bandelt HJ Am J Hum Genet 1997 Oct;61(4):983-90 As part of this letter to the editor, a reply to Macaulay et al. by Neil Howel and David Mackey is included. Comment on: Am J Hum Genet 1996 Oct;59(4):749-55 A high observed substitution rate in the human mitochondrial DNA control region. Parsons TJ, Muniec DS, Sullivan K, Woodyatt N, Alliston-Greiner R, Wilson MR, Berry DL, Holland KA, Weedn VW, Gill P, Holland MM Nat Genet 1997 Apr;15(4):363-8 Armed Forces DNA Identification Laboratory, Armed Forces Institute of Pathology, Rockville, Maryland 20850, USA. The rate and pattern of sequence substitutions in the mitochondrial DNA (mtDNA) control region (CR) is of central importance to studies of human evolution and to forensic identity testing. Here, we report a direct measurement of the intergenerational substitution rate in the human CR. We compared DNA sequences of two CR hypervariable segments from close maternal relatives, from 134 independent mtDNA lineages spanning 327 generational events. Ten substitutions were observed, resulting in an empirical rate of 1/33 generations, or 2.5/site/Myr. This is roughly twenty-fold higher than estimates derived from phylogenetic analyses. This disparity cannot be accounted for simply by substitutions at mutational hot spots, suggesting additional factors that produce the discrepancy between very near-term and long-term apparent rates of sequence divergence. The data also indicate that extremely rapid segregation of CR sequence variants between generations is common in humans, with a very small mtDNA bottleneck. These results have implications for forensic applications and studies of human evolution. Intraspecific nucleotide sequence variability surrounding the origin of replication in human mitochondrial DNA. Greenberg BD, Newbold JE, Sugino A. Gene. 1983 Jan-Feb;21(1-2):33-49. We have cloned the major noncoding region of human mitochondrial DNA (mtDNA) from 11 human placentas. Partial nucleotide sequences of five of these clones have been determined and they share a maximum of 900 bp around the origin of H-strand replication. Alignment of these sequences with others previously determined has revealed a striking pattern of nucleotide substitutions and insertion/deletion events. The level of sequence divergence significantly exceeds the reported estimates of divergence in coding regions. Two particularly hypervariable regions have also been defined. More than 96% of the base changes are transitions, and length alterations have occurred exclusively by addition or deletion of mono-or dinucleotide segments within serially repeating stretches. This region of the mitochondrial genome, which contains the initiation sites for replication and transcription, is the least conserved among species with respect to both sequence and length (Anderson et al., 1981; Walberg and Clayton, 1981). Despite this overall lack of primary sequence conservation, several consistencies appear among the available mammalian mtDNA sequences within this region. Between species, a conserved linear array of characteristic stretches exists which nonetheless differ in primary sequence. Among humans, several conserved blocks of nucleotides appear within domains deleted from the mtDNA of other species. These observations are consistent with both a species-specificity of nucleotide sequence, and a preservation of the necessary genetic functions among species. This provides a model for the evolution of protein-nucleic acid interactions in mammalian mitochondria. The mutation rate in the human mtDNA control region. Sigurgardottir S, Helgason A, Gulcher JR, Stefansson K, Donnelly P. Am J Hum Genet. 2000 May;66(5):1599-609. Epub 2000 Apr 7. deCODE Genetics, Inc., Reykjavik, Iceland 110. The mutation rate of the mitochondrial control region has been widely used to calibrate human population history. However, estimates of the mutation rate in this region have spanned two orders of magnitude. To readdress this rate, we sequenced the mtDNA control region in 272 individuals, who were related by a total of 705 mtDNA transmission events, from 26 large Icelandic pedigrees. Three base substitutions were observed, and the mutation rate across the two hypervariable regions was estimated to be 3/705 =.0043 per generation (95% confidence interval [CI].00088-.013), or.32/site/1 million years (95% CI.065-.97). This study is substantially larger than others published, which have directly assessed mtDNA mutation rates on the basis of pedigrees, and the estimated mutation rate is intermediate among those derived from pedigree-based studies. Our estimated rate remains higher than those based on phylogenetic comparisons. We discuss possible reasons for-and consequences of-this discrepancy. The present study also provides information on rates of insertion/deletion mutations, rates of heteroplasmy, and the reliability of maternal links in the Icelandic genealogy database. Mitochondrial mutation rate revisited: hot spots and polymorphism. Jazin E, Soodyall H, Jalonen P, Lindholm E, Stoneking M, Gyllensten U Nat Genet 1998 Feb;18(2):109-10 As part of this correspondence, Parsons and Holland respond Comment on: Nat Genet 1997 Apr;15(4):363-8 Mitochondrial genome variation and the origin of modern humans. Ingman M, Kaessmann H, Paabo S, Gyllensten U. Nature. 2000 Dec 7;408(6813):708-13. Department of Genetics and Pathology, Section of Medical Genetics, University of Uppsala, Sweden. The analysis of mitochondrial DNA (mtDNA) has been a potent tool in our understanding of human evolution, owing to characteristics such as high copy number, apparent lack of recombination, high substitution rate and maternal mode of inheritance. However, almost all studies of human evolution based on mtDNA sequencing have been confined to the control region, which constitutes less than 7% of the mitochondrial genome. These studies are complicated by the extreme variation in substitution rate between sites, and the consequence of parallel mutations causing difficulties in the estimation of genetic distance and making phylogenetic inferences questionable. Most comprehensive studies of the human mitochondrial molecule have been carried out through restriction-fragment length polymorphism analysis, providing data that are ill suited to estimations of mutation rate and therefore the timing of evolutionary events. Here, to improve the information obtained from the mitochondrial molecule for studies of human evolution, we describe the global mtDNA diversity in humans based on analyses of the complete mtDNA sequence of 53 humans of diverse origins. Our mtDNA data, in comparison with those of a parallel study of the Xq13.3 region in the same individuals, provide a concurrent view on human evolution with respect to the age of modern humans. Erratum in: Nature 2001 Mar 29;410(6828):611. Comment in: Nature. 2000 Dec 7;408(6813):652-3. References     Please criticise or comment WebMaster: Michael Brown center@mhrc.net Copyright © 1998 - 2017 by Michael Brown all rights reserved Officially posted January 1, 1998 last revised January 1, 2017