Wednesday, January 30, 2013


(Byron J. Richards, CCN) - Thyroid Helper® has been used by thousands of happy customers. As an expert clinician in thyroid-related issues, I designed it to safely and naturally work your metabolism to help promote the normal function of thyroid hormone in your body.* By nourishing the formation and activation of thyroid hormone you will be amazed how much better you feel. There is no need to struggle with hibernating metabolism, a dull and heavy head, feeling too cold, and too much fatigue. Thyroid Helper® was designed and tested in clinical practice based on advanced nutritional science and helping many people struggling with thyroid-related health concerns. It is our top thyroid product and the best thyroid supplement on the market.*
Thyroid Helper® sets the gold standard for natural thyroid support. I am flattered that many other companies try to copy my time-tested formulation; it obviously works. Before describing the details of the nutrients in Thyroid Helper® and how they work, I would like to tell you what is not in Thyroid Helper®.
  • There are no animal glandulars in Thyroid Helper® or any Wellness Resources product. I do not consider animal glandulars safe to take especially for individuals with multiple health concerns. My concern is that if you are taking some form of thyroid animal gland extract then you are running the risk of your immune system adversely reacting to foreign animal tissue which may provoke an autoimmune reaction. Animal glands also contain residues of every pollutant the animal was exposed to, and thyroid tissue is susceptible to accumulation of numerous toxins.
  • There are no herbal stimulants in Thyroid Helper® or any Wellness Resources product. In fact, I refused to put ephedra in any of my products long before it was removed from the market. Other common herbal stimulants are bitter orange, yohimbine, or khat. Some products rely on caffeinated herbs such as guarana, kola nut, or green tea (I use decaffeinated green tea in my products). I'm not against caffeine, and you can easily control your intake in the coffee or tea you consume. However, taking an herbal stimulant dietary supplement for weight loss or thyroid support is a waste of money and may actually make thyroid problems worse by revving up nerves too much.
  • There is no potassium iodide in Thyroid Helper®. This cheap salt of iodine is very hard for your body to use and may clog thyroid function if consumed in high amounts. Iodine is important, but I only recommend the unique water soluble liquid form known as Iosol Iodine, which works great with Thyroid Helper®.
  • Most importantly, there is no excessive price mark-up in Thyroid Helper®. I'm sure we could sell Thyroid Helper® in an infomercial or through inflated health professional networks, you would just need to pay three times the current price to pay for the advertising and marketing expense. We keep our costs down by selling real quality directly to you.
Thyroid Helper® is a truly innovative product and blends nicely with other Wellness Resources products that naturally support healthy metabolism (such as Iosol Iodine and Daily Energy Multiple Vitamin - see the Thyroid Energy Package). Thyroid Helper® works by enhancing the formation of thyroid hormone, protecting the thyroid gland and liver so they can more efficiently produce and activate thyroid hormone, and making it easier for your body to increase its production of biologically active thyroid hormone (T3).* The nutrients in Thyroid Helper® also supports weight loss and cholesterol fitness topics that are typically important to most people struggling to maintain healthy thyroid function.*
Thyroid Helper® may be used along with your thyroid medication as it will simply help the medication work better within the tissues. Thyroid Helper® is not replacement thyroid hormone, rather it provides nutrients that improves the conversion of inactive thyroid hormone (T4) to active thyroid hormone (T3), along with improving the transport and absorption of activated thyroid hormone into cell tissues to turn on metabolism. Each of these mechanisms requires proper nourishment in order to adequately function. Thyroid Helper® provides that nourishment. View more information about Thyroid and Metabolism.

Learn more about Thyroid Helper®:

Millions Struggle with Low Thyroid Function
The Thyroid Helper® Strategy
Selenium is Vital to Thyroid Function
Warming Up and Energizing
Manganese: Thyroid and Liver Protector
Supports Fat Burning and Insulin Function
Guggul A True Friend of Healthy Thyroid Function
Ashwagandha: Stress-Busting Thyroid Nutrient

Millions Struggle with Low Thyroid Function

Thyroid function is weakened by stress, pollution, poor lifestyle, bad eating habits, and a history of yo-yo dieting. It is now proven that various nutrients directly support the healthy structure of the thyroid gland, the formation of thyroid hormone, and the activation of thyroid hormone throughout the body. These are all normal and natural functions that need to be properly maintained to support health.*
New science is showing that free radical problems stress thyroid hormone function, especially when there are deficiencies of selenium and manganese containing antioxidant enzymes. If these nutritional deficiencies are not corrected a person is much more likely to struggle with body weight, insulin function, and poor metabolism.*
Sluggish thyroid hormone function is common, a different issue than medical thyroid problems such as hypothyroidism. Many individuals have symptoms of slow metabolism, including low body temperature, fatigue, weight gain, trouble losing weight and keeping it off, constipation, poor mood, heavy head, dry skin, and energy problems in the afternoon. Thyroid Helper® offers significant nutritional support to help maintain the normal function of thyroid hormone. A considerable amount of exciting new science helps to explain why Thyroid Helper® is such a popular product.*

The Thyroid Helper® Strategy

A main reason why you may have the symptoms of poor thyroid function is a lack of nutrients that are vital for the normal function of thyroid hormone. Nutrient deficiencies place a major stress on the thyroid gland itself, helping to lock in sluggish and inefficient metabolism of calories. Various nutrients are needed to form thyroid hormone, activate thyroid hormone, and protect the thyroid and liver during this process.
I have tried to make this easy for people by designing nutritional products that provide the most needed nutrients. Thyroid Helper® is our top thyroid support product. It is a mix of tyrosine, selenium, manganese, guggul, and Ashwaganda.
Tyrosine is an amino acid that converts to dopamine and norepinephrine with the help of vitamin B6 and vitamin C. Norepinephrine is a sympathetic nerve neurotransmitter that is the stimulus for your subconscious brain (hypothalamus and pituitary) to activate the production of thyroid hormone in the first place (TRH and TSH).
Brain levels of leptin act as a traffic cop, regulating the amount of norepinephrine allowed to stimulate the production of thyroid (leptin bases this on the adequacy of stored fat a perception that is often faulty). Norepinephrine-transmitting nerves are also wired directly to the thyroid gland, which act as a catalyst to get the thyroid moving.
Supplemental tyrosine is well known to promote brain activation, mental clarity, and better mood.* Tyrosine is also the central molecule of thyroid hormone (four iodine molecules are attached to one tyrosine to make thyroxine, T4).
Most people do not realize that the natural process of making and activating thyroid hormone is highly oxidative, meaning a lot of free radicals are made even when the thyroid is running normally. Once the thyroid starts to struggle the increase in free radicals and related inflammatory signals (like TNFa and IL6) is significant and may induce stressful wear and tear on metabolic processes.
Free radicals are neutralized by antioxidants. Once your antioxidant reserves are depleted your thyroid function must slow down otherwise there will be too much metabolic friction and health-deteriorating inflammation. Unfortunately, the modern diet is lacking in antioxidants and other nutrients needed to support thyroid health.
Key nutrients that facilitate thyroid-related antioxidant function are selenium and manganese.*

Selenium is Vital to Thyroid Function

Selenium is highly concentrated in the thyroid gland, more so than in any other organ in the human body, indicating its vital need in normal thyroid function. It acts as an antioxidant that protects the thyroid gland, a cofactor nutrient that facilitates the production of thyroid hormone, and as a nutrient that is required to facilitate the conversion of T4 to T3 (triiodothyronine, active thyroid hormone that works inside cells to set the pace of metabolism).
Selenium combines with the sulfur-containing amino acid cysteine to make a special protein known as selenocysteine, a selenoprotein. There are 30 selenoproteins that are currently identified, mostly involving the antioxidant defense system and thyroid function.
The selenium-containing antioxidant enzymes are known as glutathione peroxidases (GSH). Six different GSH enzymes have now been identified; helping to protect the inside of cells, the GI tract, the reproductive system, and operating in fluids between cells. GSH enzymes are vital to maintaining normal health. They are now proven to protect the thyroid gland during thyroid hormone formation.
The formation of thyroid hormone occurs on cell membranes of thyroid cells known as thyrocytes. This process requires selenium as a cofactor nutrient. During this process the enzyme thyroid peroxidase (TPO) prepares iodine for attachment to tyrosine to form thyroid hormone. The normal activity of TPO generates tremendous numbers of free radicals within the thyroid gland in the form of H2O2 and lipid peroxides. These must be deactivated by GSH enzymes, otherwise the production of thyroid hormone stresses and inflames the thyroid gland. This can easily result in a reduced rate of thyroid hormone formation. Its like trying to run on a sprained ankle, except it is a sprained thyroid.
Selenoproteins also act in various ways to change T4 into T3 (active thyroid hormone) and reverseT3 (which inactivates T3). Three main selenoproteins activate and inactivate thyroid hormone, known as D1, D2, and D3.
D1 is the primary activator of thyroid hormone for your body, working mostly in the liver and to some degree in the kidneys. D2 is active in the thyroid gland, brain, nerves, and heart. It plays the primary role in thyroid activation in the brain under normal conditions, and produces thyroid hormone for the rest of the body under stressed conditions. D3 is mostly a brake on thyroid hormone activity, turning off active hormone.
When your body starts to run low on selenium the activation of thyroid hormone by D1 may drop by 90%. Your body compensates by turning on the back up system, using the D2 enzyme to maintain active thyroid hormone. The problem with this back up system running for any great length of time is that is causes significantly increased production of free radicals. Even worse, the lack of selenium already handicapped the primary antioxidant that protects the thyroid gland and liver, GSH. Thus, selenium deficiency forces the body into a very uncomfortable metabolic coping strategy that eventually leads to slower metabolism, increased oxidative stress, and wear and tear to the thyroid gland and liver.*

Warming Up and Energizing

Thyroid hormone acts in cells to set the basal metabolic rate. When this is working properly cells burn calories, producing 65% energy and 35% heat. This results in a good energy level as well as normal body temperature. The brain is especially sensitive to thyroid hormone function, thus a tired head feeling, especially in the afternoon, is a key sign energy is not being produced adequately.*
Many nutrition-related factors inside cells determine if energy and heat are made properly. Energy and heat production take place in the mitochondria of cells. Think of them as the car engine of the cell. Think of thyroid hormone as the idling speed of the engine. If the idling speed is too low the engine may backfire or conk out, resulting in fatigue and poor metabolism.*
Daily Energy Multiple Vitamin, Iosol Iodine, and Thyroid Helper® are frequently used together to provide basic nutritional support for thyroid hormone and for cell engines. The goal is to get energy going in the morning and keep it going through the day, especially in the late afternoon. Some people find that taking a Thyroid Helper® and Daily Energy Multiple Vitamin in the afternoon helps keep their head awake and energy level maintained through this often difficult period of the day.*

Manganese, a Thyroid and Liver Protector

Manganese has long been known as the anti-pear nutrient. New science is showing the vital role of manganese in liver function, fat metabolism, and liver anti-oxidant status. This relates to thyroid hormone activation, as most activation occurs on cell membranes in the liver. If the liver is suffering from excessive free radical stress, then cell membranes are not as functional and the activation of thyroid hormone may become distressed.*
Manganese is a mineral that is required to form a special antioxidant enzyme called manganese-dependent superoxide dismutase (MnSOD). It is a key part of the cell engine's antioxidant defense system that enables the cell engine to produce energy and heat efficiently. Poor function of this enzyme reduces the ability of cells to make energy and heat.*
MnSOD is now found to be a primary protector of the thyroid hormone. This enzyme naturally rises as thyroid hormone activity is increased, acting as a protective buffer to support increased metabolic rate. If this enzyme, or the selenium-dependent GSH are lacking, then activation of thyroid hormone generates friction and stress in the form of excessive free radicals. This results in wear and tear to the thyroid gland, liver, and nerves.* A lack of manganese is clearly associates with reduced function of thyroid hormone in the body.*

Supports Healthy Fat Metabolism and Insulin Function

New science has shown that as free radical stress increases, due to lacking GSH and MnSOD activity, fat begins to accumulate in the liver, generating further free radical stress in the form of damaged fats, known as lipid peroxides. This makes a stressed metabolic situation worse. Once this happens a person is more likely to struggle with weight loss.*
Recent discoveries show that this free radical issue stresses normal insulin function in the liver.. As the liver and thyroid become inefficient, the problems play off each other like a chicken and egg proposition.*
Since Thyroid Helper® enhances the function of antioxidant enzymes normal insulin function and liver-related fat metabolism are supported.*

Guggul A True Friend of Healthy Thyroid Function

Thyroid Helper® includes the Ayurvedic herb called Commiphora mukul, known as guggul. The thyroid stimulating properties of guggul have been reported for the past twenty years. Animal studies show it works partly by stimulating thyroid hormone production and partly by increasing liver antioxidant status.*
The active component in this herb is gugglesterone. Intense research is now being conducted with gugglesterones as they have been found to naturally regulate a gene receptor called farnesoid X receptor (FSX). As it turns out, FSX specifically turns on and off fat burning in the liver.*
The rate of bile flow is also regulated by the FSX. Gugglesterones have been shown to help the FSX receptor pump bile more efficiently, helping to clear LDL cholesterol, triglycerides, and toxins.*
Gugglesterones have been used in traditional Ayurvedic medicine in India for several thousand years to help weight loss. Any nutrient that enhances the burning of fat will at least have an indirect benefit to thyroid function, since obesity itself is a major stress to the thyroid gland.*

Ashwagandha, the Stress-Busting Thyroid Booster

Ashwagandha is another Ayurvedic herb that has been used for thousands of years to boost stress tolerance and generally rejuvenate the body. It has been shown to enhance thyroid hormone levels by directly working as an antioxidant that reduces the amount of lipid peroxides forming in the liver.*
A variety of animal experiments show that Ashwagandha helps maintain normal antioxidant function even during intentionally induced stress trauma, not only boosting antioxidant protection but also reducing the amount of cortisol that is released in response to stress. When excess cortisol is combined with poor thyroid function, it is a recipe for weight gain especially around the abdominal area.*
Studies show that Ashwagandha supports normal antioxidant enzymes, such as GSH, so they don't have to work so hard. This has a sparing effect on selenium, thus supporting healthy thyroid function. Living in a high-stress world, Ashwagandha is another helpful nutrient to offset the demands and wear of living.*


Thyroid Helper® is designed to support metabolism by helping issues that stress the natural conversion of T4 to T3. Part of optimal health is managing body weight and maintaining a good energy level. The proper functioning of thyroid hormone is essential for this to occur.
For more information on nutrition and healthy thyroid function see our Thyroid and Metabolism health topic page.
Ingredients & Dosage
Directions: Take 1 capsule, three times per day, before meals. May be taken in between meals for energy, as needed. Take up to 6 per day for more thyroid support.

Supplement Facts

Serving Size: 1 capsule
Amount Per Serving% Daily Value
Selenium (from L-Selenomethione)75 mcg105
Manganese (from picolinate)1 mg50
L-Tyrosine200 mg*
Ashwagandha (Withania somnifera)(standardized for 1.7% withanaloids)300 mg*
Gugulipid (Commiphora mukul)(2.5% guggulsterones)300 mg*
* Daily Value not established.
Other Ingredients: silica, magnesium stearate, and cellulose capsule (Vcap).
This product does NOT contain milk, egg, fish, gluten, corn, peanuts, crustacean shellfish, soybeans, tree nuts, wheat, yeast, or rice. This product does NOT contain hidden fillers, preservatives, artificial sweeteners, colors or flavors, or sugar

Tuesday, January 29, 2013

Late Lunching Can Slow Weight Loss

29 Jan 2013   

A new study suggests if you are trying to lose weight, then you shouldn't just keep an eye on the calories you consume, but also when you consume them: if lunch is your big meal of the day, then a tendency to eat it later means you will lose weight more slowly and lose less of it, than if you ate it earlier.

In other words, the later you eat your main meal of the day, the harder it is to lose weight, say researchers from Brigham and Women's Hospital (BWH) and Tufts University in Boston in the US, and the University of Murcia in Spain, who write about their findings in the 29 January online issue of the International Journal of Obesity.

Senior author Frank Scheer, director of the Medical Chronobiology Program and associate neuroscientist at BWH, says in a statement:

"This is the first large-scale prospective study to demonstrate that the timing of meals predicts weight-loss effectiveness."

"Our results indicate that late eaters displayed a slower weight-loss rate and lost significantly less weight than early eaters, suggesting that the timing of large meals could be an important factor in a weight loss program," adds Scheer, who is also assistant professor of medicine at Harvard Medical School.

The researchers were interested in doing the study because while there is lots of evidence from animal research of a link between timing of food intake and weight regulation, there is scarcely any to show whether this is true of humans.

For their investigation, Scheer and colleagues looked at data on 420 overweight people who took part in a 20-week weight loss program in Murcia, Spain, where the main meal of the day in this Mediterranean region is lunch. For this population, lunch also accounts for about 40% of daily calorie intake.

About half the participants were female, their average age was 42, and around half ate lunch early (up to 3 pm) and half ate it late (after 3 pm). 

The researchers found those who ate lunch early lost significantly more weight than those who ate it late. 

The late-eaters also showed a much slower rate of weight loss, and a lower estimated rate of insulin sensitivity, which is a known risk factor for diabetes. 

The study also looked at other factors that can influence weight loss, for example total calories consumed, energy burned, levels of appetite hormones (leptin and ghrelin), amount of sleep, and presence of clock gene (which has been linked to difficulty in losing weight).

The researchers found no significant differences between the two groups when they took these factors into account.

The timing of other meals, which were much smaller than lunch, also made little difference to the rate and quantity of weight loss, but the researchers noted that:

"Nevertheless, late eaters were more evening types, had less energetic breakfasts and skipped breakfast more frequently that early eaters." 

Lead author Marta Garaulet, professor of Physiology at the University of Murcia, says their findings show that timing of food intake may play a significant role in weight regulation in humans, and weight loss programs should therefore take into account not only "the caloric intake and macronutrient distribution, as it is classically done, but also the timing of food".

It is not clear, however, from these study results, how applicable the findings would be to populations where a significant proportion of calories is consumed outside mealtimes. For instance, in the US, snacking accounts for 25% of calorie intake.

Written by Catharine Paddock PhD 

Thursday, January 24, 2013

Good Bacteria in the Intestine Prevent Diabetes, Study Suggests

The picture shows the intestinal cells in blue with a very thick and dense layer of bacteria in red just above the top of the intestinal surface. The red bacteria produce chemicals that enter the body and help keep it healthy, for example by protecting it from diabetes. (Credit: Dr. Li Hai, UCVM, University of Bern)
Jan. 18, 2013 — All humans have enormous numbers of bacteria and other micro-organisms in the lower intestine. In fact our bodies contain about ten times more bacteria than the number of our own cells and these tiny passengers are extremely important for our health. They help us digest our food and provide us with energy and vitamins. These 'friendly’ commensal bacteria in the intestine help to stop the 'bad guys’ such as Salmonella that cause infections, taking hold. Even the biochemical reactions that build up and maintain our bodies come from our intestinal bacteria as well as our own cells.
Pretty important that we get along with these little bacterial friends... definitely. But as in all beautiful relationships, things can sometimes turn sour. If the bacteria in the intestine become unbalanced, inflammation and damage can occur at many different locations in the body. The best known of these is the intestine itself: the wrong intestinal bacteria can trigger Crohn’s disease and ulcerative colitis. The liver also becomes damaged when intestinal bacteria are unbalanced.
Research groups led by Professor Jayne Danska at the Sick Children’s Hospital of the University of Toronto and Professor Andrew Macpherson in the Clinic for Visceral Surgery and Medicine at the Inselspital and the University of Bern have now shown that the influence of the intestinal bacteria extends even deeper inside the body to influence the likelihood of getting diabetes. In children and young people, diabetes is caused by the immune cells of the body damaging the special cells in the pancreas that produce the hormone insulin. By chance, 30 years ago, before the development of genetic engineering techniques, Japanese investigators noticed that a strain of NOD laboratory mice tended to get diabetes. These mice (also by chance) have many of the same genes that make some humans susceptible to the disease. With the help of the special facilities of the University of Bern and in Canada, these teams have been able to show that the intestinal bacteria, especially in male mice, can produce biochemicals and hormones that stop diabetes developing.
Diabetes in young people is becoming more and more frequent, and doctors even talk about a diabetes epidemic. This increase in diabetic disease has happened over the last 40 years as our homes and environment have become cleaner and more hygienic. At the moment, once a child has diabetes, he or she requires life-long treatment.
"We hope that our new understanding of how intestinal bacteria may protect susceptible children from developing diabetes, will allow us to start to develop new treatments to stop children getting the disease," says Andrew Macpherson of the University Bern

Wednesday, January 23, 2013

New culprit for high blood pressure discovered

Published January 15, 2013
| LiveScience
High blood pressure has just gotten a new culprit: a newly discovered brain cell.
While the usual suspects of heart risk — weight problems, stress, smoking, those salty slices of bacon — do contribute to high blood pressure, researchers think they've discovered a new cluster of neurons that also play a role.
Researchers from Sweden spotted the previously unknown cluster of nerve cells in the brains of mice, finding the cells affected the animals' blood pressure and other cardiovascular functions. If these neurons also exist in human brains, scientists and doctors may have a new avenue for tackling hypertension (chronically high blood pressure) and other heart problems.
These cells, which are part of a family of nerves known as parvalbuminergic neurons, are located in the hypothalamus of the mouse brain, a region that helps control involuntary functions such as thirst, body temperature and blood pressure.
Jens Mittag, a molecular biologist at Sweden's Karolinska Institutet, and his team focused on mice that had mutations in a cell receptor for thyroid hormone. This defect prevented their hearts from responding normally to stressful stimuli, such as environmental temperature changes. [10 Odd Facts About the Brain]
Thyroid hormone problems have been known to affect the heart directly in humans. To determine whether the hypothalamus also played a role, Mittag and his team scanned the brains of the mutated mice, finding the hypothalamus was missing a significant number of parvalbuminergic neurons.
Here's what the researchers think is happening: The thyroid hormone, produced by the thyroid gland in the brain in the neck, is partly responsible for making these special neurons. Mice with a lack of thyroid hormone activity didn't successfully form these parvalbuminergic neurons during embryonic development.
The researchers confirmed the role of these neurons in another experiment in which they destroyed these cells in other mice with the help of a virus. This action led to hypertension and heart-rate problems in the presence of temperature changes.
"There's lots of anatomical areas in the brain that we know regulate the control of cardiovascular function. These are the first neurons in the hypothalamus on the cellular level that we know regulate these parameters," Mittag told LiveScience.
"I have no idea why no one has stumbled over these cells before," he added. "I guess we were lucky to be the first to describe them."
Before scientists can think about targeting these neurons for hypertension treatment in humans, further studies are needed to confirm that these cells are present in human brains and perform the same jobs.
In the meantime, Mittag said the study underscores the importance of making sure that pregnant women produce a sufficient amount of thyroid hormone. Without it, the brain of the fetus may not develop properly and, according to this study, cardiovascular issues from a lack of parvalbuminergic neurons may be just one more problem for the fetus that can be caused by insufficient thyroid hormone production in the mother.
The research was detailed online Dec. 21 in the Journal of Clinical Investigation.

Read more:

Saturday, January 19, 2013

Insulin breakthrough could mean no more needles for diabetics

Scientists uncovered what they called a 'molecular handshake' between insulin and its receptor cells, a discovery 20 years in the making that could lead to different kinds of treatments for diabetes.

Updated: Thursday, January 10, 2013, 6:50 PM

 Lead researcher and Associate Professor Mike Lawrence from the Colman Lab, Structural Biology, examines modes for docking insulin (modeled in white) into a three-dimensional structure of the human insulin receptor ectodomain (modeled in yellow and red) in Melbourne.

Walter and Eliza Hall Institute/AFP

Lead researcher and associate professor Mike Lawrence of the Walter and Eliza Hall Institute of Medical Research in Melbourne examines modes for docking insulin (modeled in white) into a three-dimensional structure of the human insulin receptor ectodomain (modeled in yellow and red).

Breakthrough research mapping how insulin works at a molecular level could lead to new diabetes treatments and end daily needle jabs, helping hundreds of millions of suffers, scientists said Thursday.
A joint US-Australian team said it has been able to lay out for the first time in atomic detail how the insulin hormone binds to the surface of cells, triggering the passage of glucose from the bloodstream to be stored as energy.
Lead researcher Mike Lawrence said the discovery, more than 20 years in the making and using powerful x-ray beams, would unlock new and more effective kinds of diabetes medication.
"Until now we have not been able to see how these molecules interact with cells," said Lawrence, from the Walter and Eliza Hall Institute of Medical Research in Melbourne.
"We can now exploit this knowledge to design new insulin medications with improved properties, which is very exciting."
Lawrence said the team's study, published in the latest edition of Nature, had revealed a "molecular handshake" between the insulin and its receptor on the surface of cells.
"Both insulin and its receptor undergo rearrangement as they interact -- a piece of insulin folds out and key pieces within the receptor move to engage the insulin hormone," he said of the "unusual" binding method.
Understanding how insulin attaches to cells was key to developing "novel" treatments of diabetes, a chronic condition in which the pancreas does not produce enough insulin or the body cannot use it properly.
"The generation of new types of insulin have been limited by our inability to see how insulin docks into its receptor in the body," Lawrence said.
"This discovery could conceivably lead to new types of insulin that could be given in ways other than injection, or an insulin that has improved properties or longer activity so that it doesn't need to be taken as often."
Importantly, Lawrence said the discovery could also have ramifications for the treatment of diabetes in developing nations, allowing for the creation of more stable insulins that do not need refrigeration.
It could also have applications in the treatment of cancer and Alzheimer's, with insulin playing a role in both diseases, he added.
"Our finding is a fundamental piece of science that ultimately might play across all three of those very serious diseases," Lawrence told AFP.
The Australian Diabetes Council, a lobby group representing people with the condition, said the development was welcome news.
"While we do not currently have a cure for diabetes, discoveries such as this insulin docking breakthrough give us hope that it is coming ever closer," said council chief Nicola Stokes.
Stokes said one Australian was diagnosed with diabetes every five minutes and its prevalence was growing by eight percent every year, making it the country's fastest-growing chronic disease and biggest health issue.
There are an estimated 347 million diabetes sufferers worldwide and diagnoses are increasing, particularly in developing countries, due to growing levels of obesity and physical inactivity.
It is expected to be the seventh leading cause of death in the world by 2030, with the World Health Organisation projecting total deaths from diabetes will rise by more than 50 percent in the next 10 years.
Complications of diabetes include heart disease, blindness, limb amputation and kidney failure

Read more:

Friday, January 18, 2013


Fecal transplants cure diarrhea, modulate testosterone levels

Nutella was not used as a placebo control.

From some perspectives, we humans aren't really so much individuals as we are walking ecosystems—our bodies carry more bacterial cells—with their own genomes and agendas—than the total count of human cells we're composed of. Bacteria cover our skin, get to our food before we have the chance to absorb it, and in many cases stay helpfully out of the way of the immune system.
Given all that, it shouldn't be a surprise that we're finding that bacteria can have significant effects on the human body in ways that go well beyond causing an infection. Two articles that appeared this week drive that home. In one, doctors cured a recurring, diarrhea-causing infection simply by transplanting gut bacteria from a healthy individual. And in the second, the bacterial transplants altered the progression of type 1 (autoimmune) diabetes in mice—by altering the animal's testosterone levels.

Fighting bacteria with bacteria

Clostridium difficile, or C. diff, is a bacteria that tends to cause extended bouts of diarrhea. In about 20 percent of the cases that end up under a doctor's care, it will get into the digestive system and refuse to come back out, creating recurring bouts of illness that don't respond to most antibiotics. At that point, the standard of care is an intensive course of vancomycin, which only works in about 60 percent of patients. With each further recurrence, the rate of success goes down even further.
Anecdotal evidence and case reports had suggested that the problem wasn't so much the presence of C. diff as the fact that it had grown out of balance with the rest of the gut's bacterial ecosystem. To get the gut back into balance, fecal transplants had been tried and, anecdotally at least, they worked. So some doctors in the Netherlands decided to do a clinical trial, comparing a fecal transplant to standard care with vancomycin. The trial was what the researchers called "open label," meaning that people were aware they were having a feeding tube stuffed down their nose to deliver someone else's poop into their body. (A Twitter pundit suggested a Nutella infusion might make for a good placebo control.)
A few dozen healthy volunteers were screened for a huge panel of infectious diseases, and those who came through clean were asked to rush their bodies' first deliveries of the day to the hospital, where it was mixed with saline and had the particulates removed. The results then went into the gastro-nasal tube, given to patients after their original gut flora had been cleared out by a "bowel lavage."
The authors had originally planned to get 40 patients for each group, but the fecal transplants were so successful, they stopped the trial after only 16 patients had received a transplant. Of these, 13 (80 percent) were cured after a single transplant. Two of the remaining three were cured after their second, bringing the success rate up to over 90 percent. In contrast, the success rate of vancomycin treatments was down around 30 percent.
The biggest problem? Enrolling patients. Most people who agreed to participate in the trial only did so after conventional treatments failed several times, "reflecting the reluctance of patients and physicians to choose donor-feces infusion at an early stage."

Bacteria, sex, and immunity

It's easy to view this as a demonstration of the hygiene hypothesis, which posits that all sorts of health issues are linked to exposure to a variety of infectious agents, which the immune system then learns to live in harmony with. But a second paper appeared this week that cautioned against viewing things as being quite that simple.
The paper focused on the progression of type 1 diabetes, which is the product of an autoimmune attack on the insulin-producing cells. There's a special strain of mice, called NOD (for non-obese diabetic) that are prone to developing this disorder. The mice show properties that are very much like the human version of the disease: it's genetically complex, the progression is influenced by environmental factors, and it strikes females more severely than males.
And, unexpectedly, it's influenced by gut bacteria. There was some hint of this, given that other researchers had shown that a systematic exposure to bacterial proteins was able to suppress the development of the disease. But the authors found an unexpected effect when they tested how the disorder progressed in mice raised in germ-free conditions. Rather than accelerating the development of symptoms in all mice, the germ-free conditions accelerated the progression in males, making them (at least in this assay) indistinguishable from females.
So the researchers tried an experiment: they took germ-free NOD mice and did a fecal transplant from adult male animals (mice are naturally coprophagic, so the mice took a lot less convincing than did the humans). When female NOD mice received gut bacteria from males, it actually slowed the disease progression down. The apparent sex difference in autoimmune function was mediated in part by gut bacteria.
Your first thought might be that testosterone in males could create a different environment in the gut, causing it to host a different diversity of species. It's a reasonable guess, but it's wrong. Instead, the researchers found that the transplant of gut bacteria caused a surge in testosterone production by females that lasted for up to 14 weeks. This had no effect on the female's fertility, but it did clearly alter immune function. If the authors injected these mice with a testosterone inhibitor, the diabetes protection went away.
All of which indicates that the other intuitive idea—that gut bacteria influence immune function by interacting directly with immune cells—also can't be right, or at least can't be everything. Clearly, the production of testosterone, by whatever cells may be producing it, plays a key role.
Although the papers argue against some of the simpler views of human health—bacteria are all bad, or not having exposure to pathogens means an overactive immune system—they both argue that viewing our bodies as a complex ecosystem can help provide insight into human health.