Arizona State University

DO GUT BACTERIA RULE OUR MINDS?

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It sounds like science fiction, but it seems that bacteria within us — which outnumber our own cells about 100-fold — may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.

In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.

Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem — our digestive tracts — they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.

While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.

“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.

Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.

Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”

There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.

Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.

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In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.

Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?

The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.

“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.

The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago. Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.

In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.

“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.

HOW STRESS HORMONES PROMOTE BRAIN’S BUILDING OF NEGATIVE MEMORIES.

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When a person experiences a devastating loss or tragic event, why does every detail seem burned into memory; whereas, a host of positive experiences simply fade away?

It’s a bit more complicated than scientists originally thought, according to a study recently published in the journal Neuroscience by Arizona State University researcher Sabrina Segal.

When people experience a traumatic event, the body releases two major stress hormones: norepinephrine and cortisol. Norepinephrine boosts heart rate and controls the fight-or-flight response, commonly rising when individuals feel threatened or experience highly emotional reactions. It is chemically similar to the hormone epinephrine – better known as adrenaline.

In the brain, norepinephrine in turn functions as a powerful neurotransmitter or chemical messenger that can enhance memory.

Research on cortisol has demonstrated that this hormone can also have a powerful effect on strengthening memories. However, studies in humans up until now have been inconclusive – with cortisol sometimes enhancing memory while at other times having no effect.

A key factor in whether cortisol has an effect on strengthening certain memories may rely on activation of norepinephrine during learning, a finding previously reported in studies with rats.

In her study, Segal, an assistant research professor at the Institute for Interdisciplinary Salivary Bioscience Research (IISBR) at ASU, and her colleagues at the University of California– Irvine showed that human memory enhancement functions in a similar.

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Conducted in the laboratory of Larry Cahill at U.C. Irvine, Segal’s study included 39 women who viewed 144 images from the International Affective Picture Set. This set is a standardized picture set used by researchers to elicit a range of responses, from neutral to strong emotional reactions, upon view.

Segal and her colleagues gave each of the study’s subjects either a dose of hydrocortisone – to simulate stress – or a placebo just prior to viewing the picture set. Each woman then rated her feelings at thetime she was viewing the image, in addition to giving saliva samples before and after. One week later, a surprise recall test was administered.

What Segal’s team found was that “negative experiences are more readily remembered when an event is traumatic enough to release cortisol after the event, and only if norepinephrine is released during or shortly after the event.”

“This study provides a key component to better understanding how traumatic memories may be strengthened in women,” Segal added. “because it suggests that if we can lower norepinephrine levels immediately following a traumatic event, we may be able to prevent this memory enhancing mechanism from occurring, regardless of how much cortisol is released following a traumatic event.”

Further studies are needed to explore to what extent the relationship between these two stress hormones differ depending on whether you are male or female, particularly because women are twice as likely to develop disorders from stress and trauma that affect memory, such as in Posttraumatic Stress Disorder (PTSD). In the meantime, the team’s findings are a first step toward a better understanding of neurobiological mechanisms that underlie traumatic disorders, such as PTSD.

New theory uncovers cancer’s deep evolutionary roots.

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A new way to look at cancer – by tracing its deep evolutionary roots to the dawn of multicellularity more than a billion years ago – has been proposed by Paul Davies of Arizona State University’s Beyond Center for Fundamental Concepts in Science in collaboration with Charles Lineweaver of the Australian National University. If their theory is correct, it promises to transform the approach to cancer therapy, and to link the origin of cancer to the origin of life and the developmental processes of embryos.

Paul Davies

Davies and Lineweaver are both theoretical physicists and cosmologists with experience in the field of astrobiology – the search for life beyond Earth. They turned to cancer research only recently, in part because of the creation at Arizona State University of the Center for the Convergence of Physical Science and Cancer Biology. The center is one of twelve established by the National Cancer Institute to encourage physical scientists to lend their insights into tackling cancer.

The new theory challenges the orthodox view that cancer develops anew in each host by a series of chance mutational accidents. Davies and Lineweaver claim that cancer is actually an organized and systematic response to some sort of stress or physical challenge. It might be triggered by a random accident, they say, but thereafter it more or less predictably unfolds.

Their view of cancer is outlined in the article “Exposing cancer’s deep evolutionary roots,” written by Davies. It appears in a special July issue of Physics World devoted to the physics of cancer.

“We envisage cancer as the execution of an ancient program pre-loaded into the genomes of all cells,” says Davies, an Arizona State University Regents’ Professor in ASU’s College of Liberal Arts and Sciences. “It is rather like Windows defaulting to ‘safe mode’ after suffering an insult of some sort.” As such, he describes cancer as a throwback to an ancestral phenotype.

The new theory predicts that as cancer progresses through more and more malignant stages, it will express genes that are more deeply conserved among multicellular organisms, and so are in some sense more ancient. Davies and Lineweaver are currently testing this prediction by comparing gene expression data from cancer biopsies with phylogenetic trees going back 1.6 billion years, with the help of Luis Cisneros, a postdoctoral researcher with ASU’s Beyond Center.

But if this is the case, then why hasn’t evolution eliminated the ancient cancer subroutine?

“Because it fulfills absolutely crucial functions during the early stages of embryo development,” Davies explains. “Genes that are active in the embryo and normally dormant thereafter are found to be switched back on in cancer. These same genes are the ‘ancient’ ones, deep in the tree of multicellular life.”

The link with embryo development has been known to cancer biologists for a long time, says Davies, but the significance of this fact is rarely appreciated. If the new theory is correct, researchers should find that the more malignant stages of cancer will re-express genes from the earliest stages of embryogenesis. Davies adds that there is already some evidence for this in several experimental studies, including recent research at Harvard University and the Albert Einstein College of Medicine in New York.

“As cancer progresses through its various stages within a single organism, it should be like running the evolutionary and developmental arrows of time backward at high speed,” says Davies.

This could provide clues to future treatments. For example, when life took the momentous step from single cells to multicellular assemblages, Earth had low levels of oxygen. Sure enough, cancer reverts to an ancient form of metabolism called fermentation, which can supply energy with little need for oxygen, although it requires lots of sugar.

Davies and Lineweaver predict that if cancer cells are saturated with oxygen but deprived of sugar, they will become more stressed than healthy cells, slowing them down or even killing them. ASU’s Center for the Convergence of Physical Science and Cancer Biology, of which Davies is principal investigator, is planning a workshop in November to examine the clinical evidence for this.

“It is clear that some radically new thinking is needed,” Davies states. “Like aging, cancer seems to be a deeply embedded part of the life process. Also like aging, cancer generally cannot be cured but its effects can certainly be mitigated, for example, by delaying onset and extending periods of dormancy. But we will learn to do this effectively only when we better understand cancer, including its place in the great sweep of evolutionary history.”

Source: asunews.asu.edu

Why is cancer so common?.

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Hundreds of thousands of people are diagnosed with cancer every year in the UK. It is not one disease; there are over 200 different types, each with its own symptoms, methods of diagnosis and treatment.

What is cancer?

Cancer starts when cells in our bodies start to reproduce out of control, forming new, abnormal cells. These abnormal cells form lumps, known as tumours.

If the cells from tumours cannot spread, then the tumours are benign. They are not cancerous and can usually be removed.

If the cells are able to invade nearby healthy tissue and organs, or spread around the body through the blood or lymphatic system causing further tumours to grow, then the tumours are malignant or cancerous. These cancer cells are likely to spread if the tumour is not treated.

What causes cancer?

Every cell in our body contains DNA. It carries our genetic code and contains the instructions for all the cell’s actions.

If the DNA inside cells is damaged, these instructions go wrong. In fact damage to the DNA or “mutations” as they are known, constantly occur in our cells as they divide and reproduce. Most of the time, the cells recognise that a mutation has occurred and repair the DNA, or self-destruct and die.

When a number of mutations have occurred in the DNA of a cell, control of cell growth may be lost and the cells do not die. Instead they start to follow abnormal instructions that make them reproduce and grow, producing more and more of these mutated cells – this is the start of a cancer.

Many factors such as smoking or too much exposure to the sun can also trigger DNA damage – leading to a faster accumulation of the mutations which lead to cancer.

A family history of cancer can also increase chances of getting the disease, because it usually means that person starts their life already having inherited some of the DNA mutations that take them down the path to cancer.

Even when in remission, those who have had the disease have a higher risk of it developing again. In most cases however, the exact cause or sequence of events by which cancer develops, is not yet known

A recent study has found that there are more than 80 genetic markers (i.e. mutated genes) that can increase the risk of developing breast, prostate or ovarian cancer, for example. Scientists believe the results could soon lead to widespread use of DNA profiling for these cancers, though individual genetic testing for those likely to be at increased risk – such as when there is a strong family history of a type of cancer – is already in use.

Why is it so deadly?

Cancer cells are able to invade other parts of the body, where they settle and grow to form new tumours known as secondary deposits – the original site is known as the primary tumour. The cells spread by getting into the blood or lymph vessels and travelling around the body.

For example, if bowel cancer has spread through the wall of the bowel itself, it can start growing on the bladder. If cells enter the bloodstream they can travel to distant organs, such as the lungs or brain. Over time, the tumours will then replace normal tissue.

The process of cancer cells spreading is called metastasis. Once a cancer has started to spread, the chances of a cure often begin to fall, as it becomes more difficult to treat for a variety of reasons.

Cancer harms the body in a number of ways. The size of the tumour can interfere with nearby organs or ducts that carry important chemicals. For example, a tumour on the pancreas can grow to block the bile duct, leading to the patient developing obstructive jaundice. A brain tumour can push on important parts of the brain, causing blackouts, fits and other serious health problems. There may also be more widespread problems such as loss of appetite and increased energy use with loss of weight, or changes in the body’s clotting system leading to deep vein thrombosis.

Why is it so hard to stop?

Cancer is an extremely complex condition. Each type of cancer is biologically different from any other type. For example, skin cancer is biologically different from the blood cancer called lymphoma, of which there are then many different types.

That is then coupled with genetic differences between individuals and the often random nature of the DNA mutations that cause cancer.

All this makes it difficult to identify the way the particular cancer cells are behaving and how they are likely to spread or damage the body. Without a full understanding of the physiology of the cancer, effective treatments are hard to develop.

How common is cancer?

  • More than one in three people will develop some form of cancer during their lifetime
  • In 2010 324,579 people in the UK were diagnosed with cancer (excluding non-melanoma skin cancer).

Source: Cancer Research UK

Early surgery to remove tumours can work. But the cancer can return if any cells are left behind. It can also return if cells have broken away from the primary tumour and formed microscopic secondary tumours elsewhere in the body before an operation to remove the primary.

And because cancer cells are our own body’s cells, many treatments to destroy them also risk destroying our healthy cells.

One controversial theory of why cancer is so hard to stop is that it is rooted in the ancient traits of our genes.

Prof Paul Davies from Arizona State University believes cancer may use tried-and-tested genetic pathways going back a billion years to the dawn of multicellular life, when unregulated cell growth would have been an advantage.

He argues that this tendency was suppressed by later, more sophisticated genes, but lies dormant in all living organisms. Cancer occurs when something unlocks these ancient pathways.

Other scientists disagree, saying that these pathways would not have survived millions of years of evolution.

One thing is for sure – our genes hold the key to understanding cancer and how to treat it.

The future of cancer research

The field of cancer research is moving away from defining a cancer by where it is in the body, as one type of breast cancer can have more in common with an ovarian cancer than another cancer in the breast.

Instead scientists are looking deeper at what is going wrong inside cancerous cells – a tumour can have 100,000 genetic mutations and these alter over time.

By pinpointing the mutations that can cause certain cancers, doctors hope to personalise treatment – choosing the drug most likely to work on a particular type of tumour.

Scientists are creating targeted cancer therapies using their latest insights into cancer at a molecular level. These treatments block the growth of cancer by interfering with genetic switches and molecules specifically involved in tumour growth and progression.

Clinical trials using gene therapy are also underway. This experimental treatment involves adding genetic material into a person’s cells to fight or prevent disease.

Source: BBC

 

 

Aspartame: Safety Approved in 90 Nations, but Damages the Brain.

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More than 90 countries have given the artificial sweetener aspartame the green light to be used in thousands of food and beverage products.1

Two hundred times sweeter than sugar, aspartame allows food manufacturers to produce sweet foods they can market as “low calorie,” “diet,” or sugar-free,” appealing to hundreds of millions of consumers looking to cut sugar from their diets.

No doubt about it, the less sugar you include in your diet, the better. But replacing sugar with aspartame is not the solution, and in fact is likely to be even worse for your health.

Despite assurances from the U.S. Food and Drug Administration (FDA) and other public health agencies that aspartame is safe, the research says otherwise…

So What the Heck is Aspartame Made Of?

Virtually all of the marketing material emphasizes the fact that aspartame is natural and made of two amino acids, the building blocks of protein. But, like many deceptions, this is only partially true. While there are two amino acids that comprise 90% of aspartame, aspartic acid and phenylalanine, they are held together in a methyl ester bond that comprises 10% of the molecule.

The methanol is released from the aspartame within hours of consumption after hydrolysis of the methyl group of the dipeptide by chymotrypsin in the small intestine. Once this methyl ester bond is broken it liberates free methyl alcohol or methanol, which is commonly called wood alcohol. The problem with methanol is that it passes into your blood-brain barrier and is converted into formaldehyde, which causes the damage. You may recognize formaldehyde as embalming fluid.

Interestingly, methanol is only toxic in humans. All other animals are able to detoxify it before it causes damage.

Methanol is a toxin that destroys the myelin tissue in your body, which is the insulating material around your nerves that allows nerve signals to travel properly. Once injured, one can have what are called demyelinating symptoms that are commonly seen in diseases like MS and also migraines that can include bizarre and inconsistent visual field disruptions.

My sister that helped me start my practice in 1985 is actually one of the people that develops these symptoms when exposed to aspartame. In the late ‘80s I helped to diagnose her with this sensitivity and she has avoided it for over 25 years.

Why is Methanol So Toxic?

Methanol breaks down into formic acid and formaldehyde in your body. Many experts believe formic acid is the problem but the real problem is the formaldehyde, which is a deadly neurotoxin and carcinogen. An EPA assessment of methanol states that methanol “is considered a cumulative poison due to the low rate of excretion once it is absorbed. In the body, methanol is oxidized to formaldehyde and formic acid; both of these metabolites are toxic.”2

They recommend a limit of consumption of 7.8 mg/day. But according to Woodrow Monte, Ph.D, R.D., director of the Food Science and Nutrition Laboratory at Arizona State University:3

“When diet sodas and soft drinks, sweetened with aspartame, are used to replace fluid loss during exercise and physical exertion in hot climates, the intake of methanol can exceed 250 mg/day or 32 times the Environmental Protection Agency’s recommended limit of consumption for this cumulative toxin.”

Further, he states that due to the lack of a couple of key enzymes, humans are many times more sensitive to the toxic effects of methanol than animals. Therefore, tests of aspartame or methanol on animals do not accurately reflect the danger for humans.

“There are no human or mammalian studies to evaluate the possible mutagenic, teratogenic, or carcinogenic effects of chronic administration of methyl alcohol,” he said.

Symptoms from methanol poisoning are many, and include headaches, ear buzzing, dizziness, nausea, gastrointestinal disturbances, weakness, vertigo, chills, memory lapses, numbness and shooting pains in the extremities, behavioral disturbances, and neuritis. The most well known problems from methanol poisoning are vision problems including misty vision, progressive contraction of visual fields, blurring of vision, obscuration of vision, retinal damage, and blindness. Formaldehyde is a known carcinogen that causes retinal damage, interferes with DNA replication and may cause birth defects. The researchers in the featured study then reasoned that the aspartame-induced methanol exposure was likely possible for oxidative stress in the brain.

New Study Shows Aspartame Damages Your Brain

A newly published study with rats investigated the chronic effect of aspartame on oxidative stress in the brain. Researchers found that there was a significant increase in lipid peroxidation levels, superoxide dismutase activity, GPx levels and CAT activity, showing that chronic exposure of aspartame resulted in detectable methanol in the blood, which may be responsible for the generation of oxidative stress and damage in the brain.4

So the study found that aspartame exposure did result in “detectable levels” of methanol in the blood. Methanol is gradually released in the small intestine when the methyl group of aspartame encounters the enzyme chymotrypsin.

Are Artificial Sweeteners Stressing Out Your Brain?

Oxidative stress can be defined as the state in which damaging free radicals outnumber your antioxidant defenses. Oxidative stress tends to lead to accelerated tissue and organ damage.

Case in point, earlier this year another study investigated the effect of long-term intake of aspartame on the antioxidant defense status in the rat brain and also found it leads to oxidative stress.5 Male rats that were given a high dose of the artificial sweetener exhibited a lowered concentration of reduced glutathione (the active, antioxidant form of glutathione), and reduced glutathione reductase activity, a sign of increased oxidative stress-induced damage in the body.

Glutathione deficiency has also been linked to age-related diseases such as Alzheimer’s. Examination also revealed mild vascular congestion – an obstruction of the normal flow of blood within the brain – in these rats. Researchers concluded:

“The results of this experiment indicate that long-term consumption of aspartame leads to an imbalance in the antioxidant/pro-oxidant status in the brain, mainly through the mechanism involving the glutathione-dependent system.”

Adding to the problem, one of the amino acids in aspartame, aspartic acid is capable of crossing your blood-brain barrier. There it attacks your brain cells, creating a form of cellular overstimulation called excitotoxicity, which can lead to cell death.

Your blood-brain barrier, which normally protects your brain from excess aspartate, as well as toxins, is not able to adequately protect you against the effects of aspartame consumption because it:

  • Is not fully developed during childhood
  • Does not fully protect all areas of the brain
  • Is damaged by numerous chronic and acute conditions
  • Allows seepage of excess aspartate into the brain even when intact

That excess aspartate slowly begins to destroy neurons, and the large majority (75 percent or more) of neural cells in a particular area of the brain are killed before any clinical symptoms of a chronic illness are noticed. Then, when they do occur, they may or may not be associated with aspartame consumption, even though examples of chronic illnesses that are made worse by long-term exposure to excitatory amino acid damage include:

Multiple sclerosis (MS) ALS Memory loss
Hormonal problems Hearing loss Epilepsy
Alzheimer’s disease and dementia Parkinson’s disease Hypoglycemia
AIDS Brain lesions Neuroendocrine disorders

Why Was Aspartame Ever Approved?

If it causes brain damage, why is aspartame allowed in our food and drinks? The truth of the matter is the FDA rejected aspartame not once but multiple times. The scientific data just did not support it as a safe product. But the FDA is a federal agency subject to the political winds, and the people in charge of the agency have repeatedly and notoriously been accused of many conflicts of interest, both economically and ethically.

In 1975, the FDA came to the conclusion that aspartame should not be allowed on the market. They requested that further studies be conducted. The FDA’s next move was to set up a public board of inquiry composed of outside experts to investigate the safety of aspartame, and in 1980 that board unanimously rejected aspartame’s request for approval. Another internal FDA panel convened in 1980 also rejected aspartame for approval.

So it was three strikes against aspartame at this point, four strikes if you count the Bressler Report. This report was compiled in 1977 after FDA scientists looked into the field studies conducted on aspartame. The Bressler Report uncovered fraud and manipulation of data so serious that the FDA forwarded their files to the Chicago U.S. Attorney’s office for prosecution.

Basically the results of the scientific data were fairly clear up until 1980: Aspartame was a dangerous, brain-tumor-causing man-made poison and the company trying to get it into the food supply was recommended for prosecution by the FDA. You would think that would be the end of aspartame, right?

Not by a long shot.

For more details on the story of how aspartame made it through the FDA approval process despite warning signs of potential health hazards and alleged scientific fraud, please watch the 60-Minutes report below, as Mike Wallace does a nice job of summarizing an otherwise very long story.

Did You Know Aspartame May Make You Fat?

If you’re one of the people who suffers from headaches/migraines, vision problems, fatigue, anxiety attacks, abdominal pains or other symptoms when you consume aspartame, deciding to eliminate it from your diet was probably an easy choice.

For the rest of you, doing so based on the possibility that it could “one day” cause symptoms of brain damage is much more abstract, and probably much less likely to make you take action today.

That’s why I want to share with you one of the major deceptions surrounding artificial sweeteners like aspartame, which is that they will help you lose weight by avoiding sugar.

This is a MYTH. Research has shown that artificial sweeteners can:

  • Stimulate your appetite
  • Increase carbohydrate cravings
  • Stimulate fat storage and weight gain. In fact, diet sodas, which are well-known sources of artificial sweeteners, may actually double your risk of obesity!6

So much for being a dieter’s best friend… The point is, if you’re having a hard time giving up aspartame based on its potential to damage your brain, maybe the fact that it could make you pack on the pounds in the very near future will motivate you toward positive change.

My Favorite Tool for Addressing Artificial Sweetener Addictions

Artificial sweeteners tend to trigger enhanced activity within your brain’s pleasure centers, yet at the same time provide less actual satisfaction. This separation of the taste of sweetness from caloric content means that when you consume artificial sweeteners, your brain actually craves more of it because your body receives no satisfaction on a cellular level by the sugar imposter. This can actually contribute to not only overeating and weight gain, but also an addiction to artificial sweeteners.

In order to break free, be sure you address the emotional component to your food cravings using a tool such as the Emotional Freedom Technique (EFT). More than any traditional or alternative method I have used or researched, EFT works to overcome food cravings and helps you reach dietary success. If diet soda is the culprit for you, be sure to check out Turbo Tapping, which is an extremely effective and simple tool to get rid of your soda addiction in a short amount of time.

If you’re determined to sweeten your foods and beverages, I urge you to consider using stevia extract – a safe and natural sweet herb, which is my personal sweetener of choice. Lo Han is another herbal sweetener that doesn’t have the aftertaste of stevia that many object to.

Source: Dr. Mercola