Day: 08/14/2014

What does Ebola actually do?

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Behind the unprecedented Ebola outbreak in West Africa lies a species with an incredible power to overtake its host. Zaire ebolavirus and the family of filoviruses to which it belongs owe their virulence to mechanisms that first disarm the immune response and then dismantle the vascular system. The virus progresses so quickly that researchers have struggled to tease out the precise sequence of events, particularly in the midst of an outbreak. Much is still unknown, including the role of some of the seven proteins that the virus’s RNA makes by hijacking the machinery of host cells and the type of immune response necessary to defeat the virus before it spreads throughout the body. But researchers can test how the live virus attacks different cells in culture and can observe the disease’s progression in nonhuman primates—a nearly identical model to humans.

The Ebola virus

Here are some of the basic things we understand about how Ebola and humans interact.

What does Ebola do to the immune system?

Once the virus enters the body, it targets several types of immune cells that represent the first line of defense against invasion. It infects dendritic cells, which normally display signals of an infection on their surfaces to activate T lymphocytes—the white blood cells that could destroy other infected cells before the virus replicates further. With defective dendritic cells failing to give the right signal, the T cells don’t respond to infection, and neither do the antibodies that depend on them for activation. The virus can start replicating immediately and very quickly.

Ebola, like many viruses, works in part by inhibiting interferon—a type of molecule that cells use to hinder further viral reproduction. In a new study published today in Cell Host & Microbe, researchers found that one of Ebola’s proteins, called VP24, binds to and blocks a transport protein on the surface of immune cells that plays an important role in the interferon pathway.

Curiously, lymphocytes themselves don’t become infected with the virus, but a series of other factors—a lack of stimulation from some cells and toxic signals from others—prevent these primary immune cells from putting up a fight.

How does Ebola cause hemorrhaging?

As the virus travels in the blood to new sites, other immune cells called macrophages eat it up. Once infected, they release proteins that trigger coagulation, forming small clots throughout the blood vessels and reducing blood supply to organs. They also produce other inflammatory signaling proteins and nitrous oxide, which damage the lining of blood vessels, causing them to leak. Although this damage is one of the main symptoms of infection, not all patients exhibit external hemorrhaging—bleeding from the eyes, nose, or other orifices.

Does the virus target certain organs?

Ebola triggers a system-wide inflammation and fever and can also damage many types of tissues in the body, either by prompting immune cells such as macrophages to release inflammatory molecules or by direct damage: invading the cells and consuming them from within. But the consequences are especially profound in the liver, where Ebola wipes out cells required to produce coagulation proteins and other important components of plasma. Damaged cells in the gastrointestinal tract lead to diarrhea that often puts patients at risk of dehydration. And in the adrenal gland, the virus cripples the cells that make steroids to regulate blood pressure and causes circulatory failure that can starve organs of oxygen.

What ultimately kills Ebola patients?

Damage to blood vessels leads to a drop in blood pressure, and patients die from shock and multiple organ failure.

Why do some people survive infection?

Patients fare better with supportive care, including oral or intravenous rehydration that can buy time for the body to fight off infection. But studies on blood samples from patients during the 2000 outbreak of a different Ebola strain in Uganda have also identified genes and other markers that seem to be predictive of survival. Patients who recovered had higher levels of activated T cells in their blood and had certain variants of a gene that codes for surface proteins that white blood cells use to communicate. Earlier this year, researchers found a new association between survival and levels of sCD40L, a protein produced by platelets that could be part of the body’s attempt to repair damaged blood vessels. The authors note that markers like sCD40L could suggest new therapies that augment the repair mechanisms most important for survival.

 

Is Pain Real Or Is It All In Your Head? Neuroscience Explains

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is-pain-real-or-is-it-all-in-your-head-neuroscience-explains

“Pain feels like a fast stab wound to the heart. But then healing feels like the wind against your face when you are spreading your wings and flying through the air. We may not have wings growing out of our backs, but healing is the closest thing that will give us that wind against our faces.” ~ C. Joybell

Do you remember growing up, going to the doctor’s office to get a vaccine shot —only to be crippled by the thought of having a sharp needle stuck in you? But for some strange reason, when your doctor took your attention off of the shot and onto whatever they were saying; the pain of the needle became unnoticeable. Now did the pain magically go away with your doctor’s kind words or is it that pain goes beyond just the physical sensation attached to it? Neuroscience is illustrating for the world, that perhaps pain is more bio-psychological than we had previously thought. In fact, pain is more in your head than you ever realized.

THE DIFFERENT TYPES OF PAIN EXPLAINED

We first need to understand that there are different types of pain and how we perceive them is varied as well. For example, there is a difference between tissue-damage pain and the pain associated with a broken heart. Both feel just as intense as the other, the major difference is the origin of the pain and how your neurons interpret the pain associated with the stimulus.

Edwin S. Shneidman PhD, founder of the American Association of Suicidology, explains that the majority of pain, even physical pain has its roots in the body’s need for help. Dr. Shneidman goes on to say that the sensation of pain is a combination of physiological processes and psychological needs. Needs such as the need for love, freedom, achievement or even the need to avoid embarrassment, shame, and harm.

Another element that contributes to how you feel pain and the reason we all experience it slightly differently, is which needs take priority within our personal lives. Harvard University Psychologist Henry Murray enlightened the psychological community by explaining that there are no concrete forms expressing the caliber of someone’s pain. The only legitimate method is by gauging someone’s reactions to pain and what they have to say about what they are feeling. Henry Murray goes on to say that this phenomenon occurs because each one of us rates our psychological needs differently. Meaning, what is the most important need for me (emotional need) may not be the most important need for you (financial need), thus the reason in differing levels of pain.

Another factor that plays into how you perceive pain is your childhood and the experiences of pain as a child. Think about it, if you had never experienced pain before, you would be devastated the first time you broke a bone because you wouldn’t have the gained wisdom on how to deal with said pain. The same happens if a child is exposed to pain consistently and then reinforced by a negative emotion. This leads to two different types of pain sensitizations.

Peripheral Sensitization

This type of pain sensitivity has to deal with the inflammation or damage to your bodily tissue. For example, when you get a cut on your finger, you are experiencing peripheral sensitization. During this process, there is a change in the transduction proteins, which are the carriers of messages that affect the nociceptors, or the receptors of your body’s sensory neurons. When you burn your finger, the stimulus is transformed into electrical signals which are then carried throughout your nervous system and up to your brain via these proteins.

Central Sensitization

During this type of pain something different happens in people: instead of originating from bodily harm, this pain can manifest itself without tissue damage. What happens is that the neurons in your central nervous system become excited more easily —resulting in feeling pain for much longer periods of time and much more easily. The pain that would normally subside after the initial stimulus still lingers around, eventually leading to chronic pain.

THE MIND-BODY CONNECTION TO PAIN

Many doctors believe that disorders such as Fibromyalgia; where the patient has nothing physiologically wrong with them, can be tied back to central sensitization. I spoke with the former President of the Austin Pain Society, Dr. Brannon Frank, in order to better understand the mind and pain connection. After several discussions about single-case patients, Dr. Frank explained to me that the majority of his patients that come complaining of chronic stress usually begins with a life story.

Whereas athletes and other patients who have recently suffered tissue damage can immediately pinpoint the exact origin of pain and typically explain the situation behind the accident. Fibromyalgia patients and others suffering from chronic pain paint a picture of great emotional distress. Dr. Frank goes on to tell me that more often than not, the patients suffering from severe chronic pain, tell the story of their lives where they recently divorced, lost a loved one, or are undergoing severe depression.

This is a real life example of how pain is not just in the body, but in the mind of the beholder. So the next time you find yourself battling chronic pain or a bad back, before you run to your physical therapist — take a long and hard look at your life. Are you suffering from the loss of something valuable in your life or are you genuinely physically hurt? The answer won’t be easy or completely obvious, but I can tell you this much, how you react to the pain makes all the difference. It truly, may be all in your head.

To Learn More About Pain (References)

Journal of The American Physical Therapy Association: http://ptjournal.apta.org/content/91/5/700.long

US National Library of Medicine: http://www.ncbi.nlm.nih.gov/pubmed/7702468

US National Library of Medicine: http://www.ncbi.nlm.nih.gov/pubmed/9188037

Karen Byfield | Mental Health Advocate (original publication)

Written by Luis R. Valadez of www.learning-mind.com

Scientists Show How Ebola Disables Initial Immune Defenses

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Researchers report that they have discovered a mechanism unique to the Ebola virus that defeats attempts by interferon to block viral reproduction in infected cells. They say their study (“Ebola Virus VP24 Targets a Unique NLS Binding Site on Karyopherin Alpha 5 to Selectively Compete with Nuclear Import of Phosphorylated STAT1”), published in Cell Host & Microbe, explains for the first time how the production by the virus of a protein called Ebola Viral Protein 24 (eVP24) stops the interferon-based signals from ramping up immune defenses. With the body’s first response disabled, the virus is free to mass produce itself and trigger the too-large immune response that damages organs and often becomes deadly as part of Ebola virus disease (EVD).

Scientists Show How Ebola Disables Initial Immune Defenses

The study was led by scientists from Washington University School of Medicine in St. Louis in collaboration with researchers from the Icahn School of Medicine at Mount Sinai and the University of Texas Southwestern Medical Center.

“Our study is the first to show how Ebola viral protein 24 defeats the signal sent by interferons, the key signaling molecules in the body’s early response to Ebola virus infection,” notes Christopher F. Basler, Ph.D., professor of microbiology at the Icahn School of Medicine at Mount Sinai, and an author of the newly published paper. “These newfound details of Ebola biology are already serving as the foundation of a new drug development effort, albeit in its earliest stages.”

“We’ve known for a long time that infection with Ebola virus obstructs an important arm in our immune system that is activated by interferons,” adds senior author Gaya Amarasinghe, Ph.D., assistant professor of pathology and immunology at the Washington University School of Medicine. “By determining the structure of an eVP24 in complex with a cellular transporter, we learned how Ebola does this.”

To trigger an effective, early response to viral infection, interferons must pass on their signal to other cells. This occurs through other messengers inside cells as part of interferon signaling pathways, with the last of these messengers turning on genes inside the nuclei of cells to drive the immune response.

The current study determined the structure of eVP24 when bound to its cellular targets, karyopherin transport proteins. The study used these structures to show how, in place of interferon’s natural downstream signal carrier (phosphorylated STAT1), eVP24 docks into the karyopherins meant to escort STAT1 into cell nuclei where it turns on interferon-targeted genes. By elegantly interfering at this stage, eVP24 cripples innate immunity to cause EVD.

“eVP24 binds KPNA5 [karyopherin alpha5] with very high affinity to effectively compete with and inhibit PY-STAT1 nuclear transport,” wrote the investigators. “In contrast, eVP24 binding does not affect the transport of classical NLS cargo. Thus, eVP24 counters cell-intrinsic innate immunity by selectively targeting PY-STAT1 nuclear import while leaving the transport of other cargo that may be required for viral replication unaffected.”

In 2006, Dr. Basler and colleagues found that the Ebola virus suppresses the human immune response through eVP24, but not how. Through of combination of molecular biology techniques, cell studies, and tests that reveal protein structures, the current team led by Dr. Amarasinghe defined the molecular basis for how eVP24 achieves this suppression.

Understanding exactly how the Ebola virus targets the interferon pathway could help guide drug development moving forward. Dr. Basler believes it may be possible to find an antibody or molecule that interferes with eVP24, or that works around its competition with STAT1, such that treatment of patients with extra interferon, long used against the hepatitis C virus for instance, might become useful against the Ebola virus.

“We feel the urgency of the present situation, but still must do the careful research to ensure that any early drug candidates against the Ebola virus are proven to be safe, effective, and ready for use in future outbreaks,” says Dr. Basler, who is also principal Investigator of an NIH-funded Center of Excellence for Translational Research (CETR) focused on developing drugs to treat Ebola virus infections.

Cannabinoids increasingly recognized as powerful medicine for pain control, Alzheimer’s prevention, stress relief and more

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You may have noticed the flurry of new dietary supplements containingcannabinoids (CBDs) — active chemical constituents of the cannabis plant. People everywhere are discovering the power of CBDs to reduce pain, enhance mood, relax the nerves and even help prevent chronic disease.

But what most people don’t know — thanks to the systematic suppression of indigenous knowledge about plant-based medicine — is that CBDs have a long and rich history of medicinal use around the world. The history is fascinating, and it shows why the present-day system of monopoly medicine has worked so diligently to criminalize the cannabis plant and imprison its supporters. The following text is contributed by Natural News researchers:

5,000 years of medicinal use

Cannabis was used as a medicine well before the Christian era, especially in Asia and India (1). The introduction of cannabis to Western medicine took place during the 19th century and reached its peak during the last decade of that century, manifesting itself in the widespread use of cannabis extracts and tinctures. In the first decades of the 20th century, however, the medical use of cannabis declined, mostly due to difficulties to obtain consistent results from batches of plant material.

As early as 5,000 years ago, cannabis was found to have positive effects on the central nervous system. It showed consistent results in pain relief, stimulation of appetite and calming of nerves. Evidence for the medical use of cannabis goes back to Emperor Chen Nung, the father of Chinese agriculture and a discoverer of medicinal plants. Chen is believed to be the author of the oldest known Chinese pharmacy guide, in which he writes about cannabis’ medicinal uses to treat rheumatism, menstrual fatigue, constipation, malaria, and even absentmindedness.

Powerful medicinal alkaloids

During the 19th century, medicinal cannabis was widely used. At the time it was recognized that preparations of cannabis that were being distributed through pharmacies was varied; as the active ingredient was not yet known, quality control was almost impossible, which is part of the reason why use of cannabis plants fell out of practice.

One practical explanation for this was that the cannabis cultivated in places like China, India and Morocco might take as long as one year to reach Western markets. And since storage conditions were less than optimal in sailing vessels of the day, quality of the plant constituents degraded during storage.

During the Victorian Era, many alkaloids were extracted from plants for their unique properties. Plant chemists were successful because alkaloids they sought were water soluble organic bases that formed crystalline solids when combined with certain acids. Among the compounds isolated in the 19th century were quinine, cocaine and morphine; these represented significant advances in plant chemistry.

The molecules on the cannabis plant, though, were almost completely insoluble in water. The chemical nature of cannabinoids prevented early plant chemists during the Victorian period from creating efficient extracts of these polar compounds. The active ingredient, delta 9-Tetrahydrocannabinilol (or Delta-9-THC), was not isolated and summarily identified until 1964 (5).

Cannabinoid receptors discovered in the human body

In the 1990s, researchers made discoveries essential for the establishment of the cannabinoid research field. By the end of the decade scientists had discovered two distinct cannabinoid receptors (CB1 and CB2), isolated endogenous cannabinoids (Anandamide and 2-Arachidonylglycerol), synthesized a cadre of ligands, and generated cannabinoid receptor knockout mice (i.e., CB1 KO) (Gerard et al., 1990; Matsuda et al., 1990; Zimmer et al., 1999).

Efforts to identify and clone the CB1 receptor demonstrate that it is one of the most abundant proteins in the brain. Thus, cannabinoid receptors became an attractive target for drug development. The availability of synthetic THC and novel analogs has allowed researchers to begin characterizing the role of this neuronal G-protein coupled receptor (GPCR). The complex physiological mechanisms involving cannabinoid receptors and their ligands in mammals is referred to as the endocannabinoid system (ECS) (4).

According to History of Cannabis as a Medicine: A Review:

The identification of the chemical structure of cannabis components and the possibility of obtaining its pure constituents were related to a significant increase in scientific interest in such plant, since 1965. This interest was renewed in the 1990’s with the description of cannabinoid receptors and the identification of an endogenous cannabinoid system in the brain. A new and more consistent cycle of the use of cannabis derivatives as medication begins, since treatment effectiveness and safety started to be scientifically proven.

Cannabinoids effective against brain aging and Alzheimer’s

That said, cannabinoids are a class of diverse chemical compounds that act on cannabinoid receptors on cells that repress neurotransmitter release in the brain. In fact, the human brain contains an extensive network of special receptor sites that modulate nervous system function only when activated by the appropriate cannabinoid compounds, many of which are found in abundance in the marijuana plant. And emerging research continues to uncover the unique role these cannabinoids play in protecting brain function, which in turn helps deter the aging process and even reverse the damaging effects of Alzheimer’s disease and other forms of dementia and cognitive abnormality (2).

Notes the Cannabis International Foundation:

Cannabis provides highly digestible globular protein, which is balanced for all of the Essential Amino Acids. Cannabis provides the ideal ratio of omega 6 to omega 3 Essential Fatty Acids. Critically, cannabis is the only known source of the Essential Cannabinoid Acids. It is clear that all 7 billion individuals would benefit from access to cannabis as a unique functional food.

Web browsing and exchanging emails can boost memory

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Digital literacy, or the ability to engage, plan and execute actions such as web browsing and exchanging emails, can improve memory, scientists say.

Researchers led by Andre Junqueira Xavier at the Universidade do Sul de Santa Catarina in Brazil found a link between digital literacy and a reduction in cognitive decline.

Drawn from the English Longitudinal Study of Ageing, the study followed 6,442 participants in the UK between the ages of 50 and 89 for 8 years.

The data measured delayed recall from a 10-word-list learning task across 5 separate measurement points.

Higher wealth, education and digital literacy improved delayed recall, while people with functional impairment, diabetes, cardiovascular diseases, depressive symptoms or no digital literacy showed decline.

The researchers found that “digital literacy increases brain and cognitive reserve or leads to the employment of more efficient cognitive networks to delay cognitive decline.”

The authors concluded that “countries where policy interventions regarding improvement in digital literacy are implemented may expect lower incidence rates for dementia over the coming decades.”

Sweat-powered stick on batteries could power workouts of the future

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New biobatteries are applied like temporary tattoos to the skin and use electrons stripped from lactate in sweat to create power

Gym-goers and joggers are already used to bringing along a phone or MP3 player if they want some entertainment while they sweat, but what if these devices were actually being powered by the same bodily fluids?

Researchers at the University of California have created the first biobattery that sticks to the skin like a temporary tattoo and uses the lactate found in sweat to produce power. Even better, the same device also monitors how someone’s workout is going.

The device was invented almost accidently when the team from California set out to build a flexible, comfortable way to measure lactate levels in athletes. Lactate is produced by the body during high-intensity exercise as a side product of muscles creating energy anaerobically – the more there is in someone’s sweat, the harder they’ve had to push themselves.

The original sensor measured lactate by stripping electrons from the chemical to generate a tiny electrical current and measuring its resistance, but the team went a step further and converted this into a battery, passing the stream of electrons from a an anode to a cathode to harness the energy.
The result is a tiny portion of electricity produced from sweat. From a 2 by 3 millimetre patch the team were only able to generate around 4 microwatts (not enough to even power a digital watch – that would take at least 10 microwatts) but they have plans on developing it to power small electronic devices.

The research behind the device was first published last year, but the UC team now have new working prototypes that were presented at the American Chemical Society this week.

Interestingly, if the device was ever used to help encourage people to work out, it would ramp up difficulty as the wearer got fitter. The less fit someone is the more quickly they produce lactate and therefore the more power they generate – users would have a good incentive to start exercising, but as they got fitter, they’d have to work harder to keep the device running.

Fast food and you: The effects of too much fat, sugar, and salt in your diet

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With obesity rates rising and fast food chains profiting, Dr Nick Knight looks at what all of this fast food is really doing to our bodies

I try to hasten my pace past the neon-glow of the user-friendly menu, but the aroma has already conga-lined up my nose and trapped me. The environment screams innocence and ease, with its doors wide open and welcoming, like a hippopotamus lying in wait. I go in, order, and consume my burger and fries within 60 seconds of pure sensory joy – followed, by half an hour of indigestion.

Fast food is anchored firmly in our fast-paced world, providing us with the food aligned to the modus operandi for modern living – quick, easy and cheap. The effects on your body, however, are not as innocent.

Now we all know that fast food is tasty because it is packed with sugars and fats. It is also apparent that sugar is currently monopolising the limelight, with media and health groups holding their pitch forks aloft, and burning effigies of sugar cubes at dawn, calling for ‘sugar taxes’ and reform. With this in mind, I am going to focus my article on the saturated and trans-fats lurking in our fast food, and provide a snapshot of their unscrupulous activity in your body.

But before I sharpen my pitch-fork and strike-up my matches, I want to explain why fat, especially the healthier unsaturated fats that you get from foods like oily fish, are actually a welcomed, necessary component of your balanced diet. Let us begin with the big picture reasons first: protection, insulation and fuel.

Fat is your body’s natural cushion, providing protection and comfort for your internal organs and pressure areas like your bum (sitting on the ‘ischium’, a part of your pelvis, without any fat is not nice). Fat also provides you with some natural minor insulation, so that once our British summer has completed its annual 14 day stint, it supports your body’s thermoregulation.

Last but by no means least, your body fat acts as an impressive energy depot, with around 100,000 calories available for your body, if called upon. This, by comparison, dwarfs your quicker release carbohydrate stores that limp in at a weak second place, providing around 1900 calories – about 24 hours worth. So, if you are wondering how Tom Hanks survived in Castaway, no, it wasn’t just the company of Wilson that kept him going but that unsung hero, fat.

The positive roles of fat in your body – such as supporting the digestion, absorption, and transport of your fat-soluble essential vitamins A, D, E and K; and its secretion of the hormone, leptin, which acts as a ‘fat thermostat’ (or a ‘lipostat’) to regulate your body habitus by effecting your hunger – indeed, do go on. However, it is time to tool-up and light the match…

Fast food fats have the potential, when consumed in excess(Government daily recommendations are less than 20g for women and 30g for men of saturated fats, and less than 5g trans-fats for both) to deliver both troublesome short-term problems and more alarming long-term repercussions to your health. After-all, every bite adds up, with a fast food burger packing about 10g of saturated fat, and a quarter of your recommended calorie intake for the day (and that’s before you factor in the fries and fizzy drink!).

So, let us consider your brain for a moment. Now although with a mass, attributing only 2% of your body’s total, your brain has a staggeringly disproportionate metabolic demand, accounting for 25% of your total energy consumed. It needs this in order to allow you to make those smart business decisions, witty Facebook status updates, and think with clarity. “But you said fats have loads of energy!” I hear you shout. Sadly, like a disappointed under-18 at a night-club, the fats just can’t get in; the interface between the brain and the blood stream being largely (but not entirely) impermeable to fat. Quite simply, your brain needs carbohydrates for fuel.

To be honest though, a few dumb days are not your main concern. Instead it is the long-term risks of a fast food, high-fat diet lifestyle that are more worrisome. You only need to look around, or down at yourself, to see that we are an expanding society with over 64% of adults in the UK overweight or obese. It goes without saying that this carries significant mortality and morbidity risks. Yes, I agree, this is a product not just of a poor diet but of chronic physical inactivity (and numerous other factors) – but that is a story for another day.

Now before we move on, I want to clarify the two main types of fats in your body; you have ‘subcutaneous fat’ (some, admittedly more than others), which consists of fat cells called adipocytes, deposited under your skin in an area called the hypodermis and gives us all our, well, unique shapes, paving the way for the colourful phrases like ‘love handles’. Then, there is your ‘visceral fat’ which surrounds your organs. Depression, osteoarthritis, gout and increased infection risks are all associated with excess fat consumption and weight gain. Although both carry their own set of risks, when in chronic excess, visceral fat is by far more concerning both by its insidious existence and its consequences, so we shall focus on these.

So let us start with the more serious of the two – visceral fat, the fat that is packed between our organs. Excessive consumption of fast foods will chronically elevate the levels of fats in your blood. Alongside this, the amount of ‘bad’ cholesterol-carrying molecules, known as low density lipoproteins (LDL), also increases. This is bad news for you, as instead of helping to remove cholesterol from your body, the LDL carts it off to sites such as your liver and the walls of your blood vessels. The end result is that your blood vessel walls develop fatty plaques, in process known as atherosclerosis, narrowing them over time. This elevates your risk of interrupting blood supply to major organs like your heart and brain, increasing the risk of conditions like angina, myocardial infarctions (‘heart attacks’) and cerebro-vascular events (‘strokes’).

Organs, particularly your liver can also become infiltrated with fat. This is a gradual process that may begin with a ‘fatty liver’ but progress, over a lifetime, to conditions more serious such as non-alcoholic steatohepatitis (NASH), causing inflammation and damage to your liver. Excess fat can further unremorsefully impair your body’s sensitivity of peripheral tissues to insulin, causing type two diabetes. An excess of fat in your diet may also endorse the ‘metabolic syndrome’, a collection of conditions that includes hypertension (high blood pressure), diabetes, obesity, and hypercholesterolemia (high cholesterol), all present in one person. This can ultimately, as a result of dysregulation in energy usage and storage, greatly increase the risk of cardiovascular disease.

Now, I am going to break my promise to the salts and sugars, and very briefly give you a snap-shot of role in this fast food debate. The best way to explain the role of sugars is to talk about the ‘crash’. Not the Academy Award winning movie, no, but the feeling you get after you have demolished your fast food meal in record time, and then 60 minutes later slip into an exhausted, sluggish, and lethargic ‘food-coma’ to rival Sleeping Beauty. The simple, refined sugars in these foods give your blood sugar levels a huge, immediate spike – giving you that burst of energy – before being used up almost immediately. This is why you are left craving more – you are, in part, addicted to the sugar; just like kids and sweets.

High salt levels in fast food (roughly 2g in a fast food burger alone, equalling one third of your maximum daily allowance) can leave you feeling thirsty in the short term – but in the long-term can affect your blood pressure and subsequent risk of future cardiovascular disease.

The way in which high salt levels do this is, once in your blood stream, it separates into sodium and chloride, increasing the pressure in the blood by ‘holding water’ in you blood stream, and thereby exerting more mechanical stress on your blood vessel walls. A diet with chronically excessive salt will worsen blood vessel wall damage and promote hypertension.

Of course, the jackpot question is “why do you like fast foods so much?” As with most answers I give, there are, frustratingly, multiple factors – two of which I will highlight. Firstly there is that perfect combination of fats, sugars and salts in foods (that fast food companies look to perfect) that galvanises your brain’s reward centre; and secondly the orosensation (i.e. how the food feels in your mouth) and mouth-watering taste; both of which leave you craving more of the same guilty fast food pleasure.

As we draw to a close on this debate, cast your mind back to what I said in the beginning – some fat, the right fat, is good for you. It is a natural, supportive and healthy part of your diet. Just, perhaps, be mindful to select out the less desirable saturated- and trans-fats, high salts, and sugars that are within fast food. The NHS ‘Live Well’ website, for example, has mountains of information to help.

Remember too that the occasional fast food meal isn’t going to hurt you (I certainly have the occasional one), it is more that the cumulative effects of three or four each week will increase your health risks. I too appreciate that fast food chains do seem to be trying to become healthier – which is commendable. As always, if you are concerned about anything raised here, for example, your eating habits, want support for weight management, or further information on the health effects of high-fat diets, then please contact your GP – they are there to help.

Zebrafish discovery boosts stem cell research

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Australian researchers studying zebrafish have made one of the most significant ever discoveries in stem cell research.

They have uncovered the mystery of how a critical type of stem cell found in blood and bone marrow, and essential to replenishing the body’s supply of blood and immune cells, is formed.

The cells, called hematopoietic stem cells (HSC), are already used in transplants for patients with blood cancers such as leukaemia and myeloma.

But HSCs have significant potential to treat a broader range of conditions because they appear to be able to form all kinds of vital cells including muscle, blood vessel and bone.

The problem was scientists had no idea how HSCs formed, making growing them in a lab and using them to treat spinal cord injuries, diabetes and degenerative disorders impossible.

However, a research team led by Professor Peter Currie, from the Australian Regenerative Medicine Institute at Victoria’s Monash University, uncovered a major part of HSC’s development. Understanding how HSCs self-renew to replenish blood cells is considered the holy grail of advancing stem cell research.

Using high-resolution microscopy, Currie’s team filmed HSCs as they formed inside zebrafish embryos. “It’s a sad fact of life that humans are basically just modified fish, and our genomes are virtually identical to theirs,” Currie said. “Zebrafish make HSCs in exactly the same way as humans do, but what’s special about these guys is that their embryos and larvae develop free living and not in utero as they do in humans.

“So not only are these larvae free-swimming, but they are also transparent, so we could see every cell in the body forming, including HSCs.” The researchers were initially studying muscle mutations in the zebrafish. But when playing the film back they noticed that the muscle-deficient zebrafish had several times the normal population of HSCs.

They saw the pre-HSCs required a “buddy” cell, known as endotome cells, to turn into HSCs.

“Endotome cells act like a comfy sofa for pre-HSCs to snuggle into, helping them progress to become fully fledged stem cells,” Currie said.

“Not only did we identify some of the cells and signals required for HSC formation, we also pinpointed the genes required for endotome formation in the first place.

“I’m not an HSC biologist, I’m an muscle cell biologist, so this was a highly serendipitous finding we made because these helper cells are made next to the muscle stem cells we were initially examining.” He said researchers could now focus on finding the signals present in the endotome cells responsible for HSC formation in the embryo.

“Then we can use them in the lab to make different blood cells on demand for all sorts of blood-related disorders,” he said.

If they could do this, there would also be the potential for genetic defects in cells to be corrected and transplanted back into the body, he said.

Their findings were published in the international journal Nature.

Dr. Georgina Hollway, from the Garvan Institute of Medical Research in Sydney, said the work highlighted how molecular processes in the body play a key role in HSC formation.

“We now know that these migratory cells are essential in the formation of HSCs, and we have described some of the molecular processes involved,” Hollway said.

“This information is not the whole solution to creating them in the lab, but it will certainly help.

“It’s difficult to say exactly how close we are, but we have uncovered a vital step in the process.”

 

Caffeine May Reduce Tinnitus Risk

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A new study reports that caffeine intake is associated with a reduced risk for tinnitus — ringing or buzzing in the ears.

Researchers tracked caffeine use and incidents of tinnitus in 65,085 women in the Nurses’ Health Study II. They were 30 to 34 and without tinnitus at the start of the study. Over the next 18 years, 5,289 developed the disorder.

The women recorded their use of soda, coffee and tea (caffeinated and not), as well as intake of candy and chocolate, which can contain caffeine. The results appear in the August issue of The American Journal of Medicine.

Compared with women who consumed less than 150 milligrams of caffeine a day (roughly the amount in an eight-ounce cup of coffee), those who had 450 to 599 milligrams a day were 15 percent less likely to have tinnitus, and those who consumed 600 milligrams or more were 21 percent less likely. The association persisted after controlling for other hearing problems, hypertension, diabetes, use of anti-inflammatory Nsaid drugs, a history of depression and other factors. Decaffeinated coffee consumption had no effect on tinnitus risk.

“We can’t conclude that caffeine is a cure for tinnitus,” said the lead author, Dr. Jordan T. Glicksman, a resident physician at the University of Western Ontario. “But our results should provide some assurance to people who do drink caffeine that it’s reasonable to continue doing so.”

Giving antibiotics to babies may lead to obesity, researchers claim

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Mice given antibiotics for the first month of life were 25% heavier and more susceptible to the effects of a high-fat diet
The study found that wiping out some types of gut bacteria with antibiotics had a long-term impact on metabolism. Photograph: Michel Tcherevkoff/Getty

Long courses of antibiotics may put babies and toddlers at higher risk of obesity when they grow up, according to US researchers.

Low doses of penicillin early in life can alter natural populations of gut microbes, which in turn may affect metabolism and lead to higher rates of obesity later in life, the scientists said.

The findings emerged from a series of experiments in mice, but build onearlier work that found children who had antibiotics before six months of age were more likely to be overweight as seven-year-olds.

“This is part of a growing body of evidence that antibiotics have a biological cost,” said Martin Blaser, a microbiologist who led the study at New York University. “Our study shows that there can be permanent consequences.”

“If a kid is very ill, there is no question that they should get antibiotics, but if it’s marginal perhaps the doctor should be saying ‘let’s wait a day or two’ before taking another look. Doctors give out antibiotics thinking they won’t do any harm, but this provides evidence that they might,” Blaser added.

Humans and other animals are home to vast populations of microbes that live on the skin and in the gut. Humans carry around 100 trillion bacteria – meaning our microbes outnumber our human cells by 10 to one. But rather than causing us harm, studies suggest that a healthy “microbiome” is crucial for our wellbeing.

Blaser said that although his studies were in mice, they pointed to a window in early life when changes to the microbiome appeared to have a serious impact on metabolism and weight gain. In mice, the window was the first month of life. If a similar vulnerable period exists in humans, as Blaser suspects, it may be the first six months, the first year, or even three years, he said.

The mouse studies suggest that antibiotics are not directly to blame for weight gain later in life. Instead, the problem arose when antibiotics wiped out some types of gut bacteria but allowed hardier ones to thrive. This change in composition of the “microbiome” had a long-term impact on metabolism that persisted even when the population of gut microbes had returned to normal several weeks later.

“We found that four weeks of antibiotics was enough to perturb the microbiome, and even though it returned to normal after a few weeks, the mice still became fat,” Blaser said. Mice that had antibiotics for the first month of life were 25% heavier and had 60% more fat than controls, according to the study published in the journal, Cell.

Disrupting the microbiome seemed to exacerbate the effects of a high-fat diet, too, with animals on antibiotics gaining more weight than others who were not given the drugs. For unknown reasons, males put on more weight than females.

Knocking out four particular species of bacteria with antibiotics seemed to trigger metabolic changes, namely Lactobacillus, Allobaculum, Rikenelleceae, and Candidatus arthromitus. The last of these is found in mice, but does not seem to live in humans.

The New York group has now begun a series of experiments to test whether administering “good microbes” to mice can restore the microbiome quickly enough to prevent metabolic changes and weight gain. Other studies will look at whether more realistic courses of antibiotics that last only three to five days have a similar effect on weight gain.

Paul Cotter at the Teagasc Food Research Centre in Ireland said the findings highlighted the risks of overusing antibiotics. “While these studies were carried out with mice, the insights gained may well be applicable to humans, especially given that previous human studies have established that early life exposure to antibiotics can impact on weight gain later in life,” he said.

Naveed Sattar, professor of metabolic medicine at Glasgow University, said that while the results were interesting, they should not alter current clinical practice. “Antibiotics in children or newborns should be given on the basis of clinical needs, whereas the usual advice about lifestyle remains the most important means to tackle obesity,” he said.