Autoimmune kidney disease

Monash researchers have solved a mystery, revealing how certain immune cells work together to instigate autoimmune kidney disease.The study, led by Professor Michael Hickey and Professor Richard Kitching from Monash University's Centre for Inflammatory Diseases. In glomerulonephritis, an immune disease of the kidney, rogue immune cells damage the kidney via a misdirected inflammatory attack.

Special cells called monocytes continuously patrol the glomeruli by crawling within its blood vessels. Monocytes are very good at 'picking up and removing rubbish' and being on the lookout for signs of infection and tissue injury. However in autoimmunity, some immune cells in the circulation are highly reactive to molecules picked up in the kidney.

Patrolling monocytes can display these molecules to the reactive immune cells in the bloodstream, resulting in the rogue cells remaining in the kidney and turning on an unnecessary and damaging inflammatory attack. This autoimmune damage to the kidney can severely impact on the normal function of the kidney, if left untreated.

 This damage occurs while the cells are moving around in the kidney blood vessels. This process, known as intravascular antigen recognition, has never been described before for the key helper T cells that direct and control the immune response.
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How liver responds to food

Minutes after eating, as nutrients rush into the bloodstream the body makes massive shifts in how it breaks down and stores fats and sugars. Within half an hour, the liver has made a complete switch  from burning fat for energy to storing as much glucose, or sugar, as possible. It's too short a time span for the liver's cells to activate genes and produce the RNA blueprints needed to assemble new proteins to guide metabolism.

Liver cells store up pre-RNA molecules involved in glucose and fat metabolism. ''The switch from fasting to feeding is a very quick switch and human physiology has to adapt to it in the right time frame," says Satchidananda Panda, a professor in the Salk Institute's Regulatory Biology Laboratory. It was known that a RNA-binding protein called NONO was implicated in regulating daily ("circadian") rhythms in the body.

Researchers analyzed levels of NONO in response to feeding and fasting in mice. After the animals ate, speckled clumps of NONO suddenly appeared in their liver cells, newly attached to RNA molecules. Within half an hour, the levels of corresponding proteins-those encoded by the NONO-bound RNA increased.

After mice eat, it looks as if NONO brings all these RNAs together and processes them so they can be used to make proteins. When mice lacked NONO, it took more than three hours for levels of the same proteins involved in processing glucose to increase. During that time lag, blood glucose levels shot up to unhealthy levels.

Since blood glucose levels are also heightened in diabetes, the researchers think that the mice without NONO may act as a model to study some forms of the disease. NONO has been found at high levels in the brain and muscle cells.
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Mechanism behind autoimmune disorder

Northwestern Medicine scientists discovered a previously-unknown mechanism of disease behind a specific autoimmune disorder. The scientists observed antibodies that targeted phosphatidylethanolamine, an important phosopholipid, from within the endosomes of cells. This discovery was the first observation of a pathogenic mechanism behind anti-phosphatidylethanolamine (aPE) autoimmunity, an immune system disorder that's been correlated with thrombosis, transplant failure and pregnancy loss.

It was first reported decades ago, but exactly how aPE autoimmunity worked had remained a mystery despite a large body of literature documenting its prevalence, according to Ming Zhao, PhD, associate professor of Medicine in the Division of Cardiology and senior author on the paper. Autoimmune diseases usually develop when antibodies-proteins which neutralize pathogens erroneously attack cells while circulating through the bloodstream. To target those cells, the antibodies bind to accessible antigen targets on the exterior surface of cells.

The internalization happens through the endosome, a part of the cell that samples the external environment and gathers in signaling molecules. In this case, the endosome also draws in the antibodies, making the cells vulnerable.This creates an opportunity for anti-PE antibodies that are brought into the cells to bind to the PE in these tiny vesicles and attack the cells from within a miniature 'Trojan Horse' process, this causes chaos within the cell, sending it into an inflammatory state, leading to a greater risk of blood clot formation and pregnancy complications.

It's important to note the inflammatory response may be the principal effect of aPE because it means anti-inflammatory treatment is likely to be more effective than anti-coagulants. These novel discoveries shed light on how cellular vulnerability to aPE is mediated and explain some of its clinical symptoms, according to the study. Because endosomes are an integral part of nearly every type of cell, linking the activity of aPE antibodies to clinical symptoms will be a priority for scientists in future investigations.
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Gene therapy may kill HIV

Gene therapy may have the potential to eradicate HIV in people infected with the virus, new animal research suggests. The science centers around the use of "chimeric antigen receptor" (CAR) genes. In laboratory work with monkeys, these engineered cells have destroyed HIV-infected cells for more than two years, scientists reported.

T-cells are the cells that are largely responsible for human ability to fight off pathogens and get rid of infections in the body. Every T-cell has a unique receptor, or molecule, on it. That receptor allows the cell to recognize a specific target-a bacteria, or fungus or virus. And when it recognizes that target, it's called into duty to clear it from the body. Taking artificial receptors- CAR that can go on to these cells and allow them to recognize what we want them to recognize," he noted. "In this case that's HIV."

First, the team genetically engineered CAR to find and bind to simian/human immunodeficiency virus (SHIV), a lab-engineered HIV hybrid composed of human virus and monkey virus. Then the researchers modified the DNA of certain blood-forming stem cells so they would carry SHIV-killing CAR. The resulting cells were introduced into the bloodstream of four male juvenile SHIV-infected macaque monkeys.

The engineered cells successfully took up residence in each monkey's bone marrow. The cells moved widely throughout the body, targeting and killing SHIV-infected cells, without producing any notable adverse side effects. The advantage of the stem cell-based approach is that once these cells are grafted into the body, they continuously produce new T-cells that have this gene in them that can target HIV cells.

Plans are underway for a human trial, this study shows both that these cells will respond to HIV and that it's safe. This strategy is unlikely to fully work on its own, CAR will most likely need to be used with antiretroviral therapy. CAR therapy is already leading to impressive results in cancer and holds promise for HIV eradication.
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Reovirus could treat brain tumours

A virus injected directly into the bloodstream could be used to treat people with aggressive brain tumours, Scientists have found that the naturally occurring virus could act as an effective immunotherapy in patients with brain cancer or other cancers that have spread to the brain. They showed that a type of virus called reovirus could cross the blood-brain barrier to reach tumours, where it replicates and kills the cancer cells.

They also found that the virus was able to 'switch-on' the body's own defense systems to attack the cancer. The study authors, from the University of Leeds and The Institute of Cancer Research in London, believe reovirus therapy could be used in conjunction with other cancer therapies to make them more potent - and a clinical trial is currently underway. Because the virus infects cancer cells and leaves healthy cells alone, patients receiving the treatment reported only mild flu-like side effects.

Scientists thought it was unlikely that the virus would be able to pass from the blood into the brain because of the blood-brain barrier, a protective membrane around the brain. That would have meant that the only way they could get the virus into the brain was to inject it directly into the brain - which is challenging, would not be suitable for all patients, and cannot be regularly repeated. But the research demonstrated that the virus could be administered through a single-dose intravenous drip.

Nine patients took part in the study, they had cancers that had either spread to the brain from other parts of the body or were fast-growing gliomas, a type of brain cancer that is difficult to treat, and has a poor prognosis. All the patients were due to have the tumours removed surgically. But in the days before the surgeons operated, the patients were given the virus drip.

Once the tumours were removed, samples were taken and analysed for signs that the virus had been able to reach the cancer, sometimes deep within the brain. In all nine patients, there was evidence that the virus had reached its target. The researchers also found that the presence of reovirus stimulated the body's own immune system, with white blood cells or 'killer' T-cells being attracted to the tumour site to attack the cancer.

Tissue samples from patients who had surgery but not the virus therapy served as a control. When compared with the control samples, the tissue taken from the people who had received the reovirus had higher levels of interferons, proteins that 'switch-on' the body's immune system. According to Dr Adel Samson, co-lead author and medical oncologist at the Leeds Institute of Cancer and Pathology, at the University of Leeds, "This is the first time it has been shown that a therapeutic virus is able to pass through the brain-blood barrier, and that opens up the possibility this type of immunotherapy could be used to treat more people with aggressive brain cancers.

Human immune systems aren't very good at detecting cancers, because cancer cells look like human body's own cells, and partly because cancers are good at telling immune cells to turn a blind eye. But the immune system is very good at seeing viruses. In the study, they were able to show that reovirus could infect cancer cells in the brain. And, importantly, brain tumours infected with reovirus became much more visible to the immune system.

Although the earlier trial demonstrated that the reovirus was reaching the cancer cells after just a single dose, doctors have decided to give it repeatedly to patients because of the way it 'kick starts' the body's own defences. The presence of cancer in the brain dampens the body's own immune  system. The presence of the reovirus counteracts this and stimulates the defence system into action. Additional effect of the virus on enhancing the body's immune response to the tumour will increase the amount of tumour cells that are killed by the standard treatment, radiotherapy and chemotherapy.
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Skin patch for management of type 2 diabetes

Researchers with NIH's National Institute of Biomedical Imaging and Bioengineering (NIBIB) have devised an innovative biochemical formula of mineralized compounds that interacts in the bloodstream to regulate blood sugar for days at a time. In a proof-of-concept study performed with mice, the researchers showed that the biochemically formulated patch of dissolvable microneedles can respond to blood chemistry to manage glucose automatically.

Insulin is a hormone made in the pancreas and secreted into the bloodstream to regulate glucose in response to food intake. It is needed to move glucose from the bloodstream into cells where the sugar can be converted to energy or stored. In type 1 diabetes, usually diagnosed in children and young adults, the body does not make insulin at all. Type 2 diabetes, which can be diagnosed at any age but more commonly as an adult, progressively lessens the body's ability to make or use insulin.

Untreated, diabetes can result in both vascular and nerve damage throughout the body, with debilitating impacts on the eyes, feet, kidneys, and heart. The base of the experimental patch is material called alginate, a gum-like natural substance extracted from brown algae. It is mixed with therapeutic agents and poured into a microneedle form to make the patch. Alginate is a pliable material -- it is soft, it has to be able to poke the dermis, and while not a commonly used material for needles, it seems to work pretty well in this case.

Researchers infused the alginate with a formula of biochemical particles that stimulates the body's own insulin production when needed and curtails that stimulation when normal blood sugar concentration is reached. The responsive delivery system of the patch can meet the body's need for days instead of being used up all at once. Diabetes is a very serious disease and affects a lot of people. Researchers puts two drug compounds -- exendin-4 and glucose oxidase -- into one patch. The two compounds react with the blood chemistry to trigger insulin secretion. Each is matched with a phosphate mineral particle, which stabilizes the compound until it is needed. Acidity that occurs when sugar concentrations rise weakens the bond with the drug being held by one, but not the other mineral.

Exendin-4 is similar in genetic makeup to a molecule the body produces and secretes in the intestine in response to food intake. Though it is somewhat weaker than the naturally occurring molecule, the team chose exendin-4 for its application because exendin-4 does not degrade in the bloodstream for an hour or more, so can have long-lasting effect after being released. However, it can induce nausea when too much is absorbed. To control how quickly it is absorbed, the researchers combined exendin-4 with mineral particles of calcium phosphate, which stabilize it until another chemical reaction occurs. That chemical reaction is caused by the second drug compound in the patch -- glucose oxidase -- that is held in its mineral buffer of copper phosphate.

When blood sugar is elevated beyond a precise point, it triggers a reaction with copper phosphate and glucose oxidase to produce slight acidity, which causes calcium phosphate to release some exendin-4. Rising glucose levels trigger the release of exendin-4; but exendin-4 then gets insulin flowing to reduce the glucose level, which slows down and stops release of exendin-4. The researchers demonstrated that a patch about half an inch square contained sufficient drug to control blood sugar levels in mice for a week.

 For the approach to advance as an application that people with type-2 diabetes can use, the team will need to perform tests to treat larger animals with a patch that contains proportionately more therapeutic compound. In addition to its size, the patch would need to be altered for application on human skin, likely requiring longer needles.
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Link between obesity and diabetes

Researchers have identified a major mechanism by which obesity causes type 2 diabetes, which is a common complication of being overweight. In obesity, insulin released into the blood by the pancreas is unable to pass through the cells that form the inner lining of blood vessels.

As a result, insulin is not delivered to the muscles, where it usually stimulates most of the body's glucose to be metabolized. Blood glucose levels rise, leading to diabetes and its related cardiovascular, kidney and vision problems.

 A major problem in obesity is the delivery of circulating insulin to the muscle, this problem involves immunoglobulins, which are the proteins that make up circulating antibodies. The researchers found that obese mice have an unexpected chemical change in their immunoglobulins.

The abnormal immunoglobulins then act on cells lining blood vessels to inhibit an enzyme needed to transfer insulin from the bloodstream into the muscle. Type 2 diabetes patients have the same chemical change, and if immunoglobulins from a type 2 diabetic individual is given to a mouse, the mouse will becomes diabetic.
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How obesity causes breast cancer

Obesity leads to the release of cytokines into the bloodstream which impact the metabolism of breast cancer cells, making them aggressive to treatment.
Severe overweight can lead to various health impairments. Besides inducing cardiovascular diseases, obesity for example also promotes the development of cancer and metastases.

ACC1 acetyl-CoA-carboxylase 1, a central component of fatty acid synthesis. ACC1 mediates the chemical addition of carbon dioxide to acetyl-CoA, which results in malonyl-CoA. This reaction is the first and speed determining step in the fatty acid synthesis of all living organisms.

ACC1 enzymes is a key component of fatty acid synthesis, its function is impaired by the cytokines leptin and TGF-β. The levels of these cytokines are increased particularly in the blood of severely overweight people.

Fatty acid precursors promote metastasis. The inhibition of ACC1 leads to the accumulation of the fatty acid precursor acetyl-CoA. This precursor is transferred to certain gene switches that in turn increase the metastatic capacity of cancer cells by activating a specific gene program.

Scientists used human tissue from breast cancer metastases to show that ACC1 was less active. When the scientists blocked the unknown signaling pathway with an antibody directed against the leptin receptor, this led to a significantly reduced metastatic spread of breast cancer tumors in an experimental model.
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Gene mutation linked with liver cancer

Presently, there is no effective treatment for the cancer found in the liver called fibrolamellar hepatocellular carcinoma, which is mainly found among children and young people. Operation of the tumour is the only treatment, some of the patients do not survive after five years.

Coupling of the two genes through a mutation causes a cancer tumour to develop in the liver. The researchers have made sure the genetic composition of the mutation in the mice is identical with the mutation found in human patients. This makes the researchers conclude that the gene mutation also leads to cancer in humans.

Sequencing the DNA of the patients tumour showed that all the patients suffering from the disease had the same mutation in their DNA. The researchers used the revolutionary technology CRISPR/Cas9 that makes it possible to 'edit' genetic material on mice.
They have produced CRISPR/Cas9 reagents, which would provoke precisely the desired fusion of the two genes.

The reagents were injected into the mice's tails and then transported through the bloodstream to the liver.
 In the liver they created a mutation identical with the human mutation, then the researchers were able to conclude that the mice developed the expected type of tumour in the liver.

In other studies, researchers deliberately damage the mice's liver to imitate a liver disease found among human patients or expose them to several different forms of mutations which may cause cancer. This was not necessary here. Because of our genetic design based on CRISPR/Cas9-technology we are certain that the main factor that can explain the cancer is the fusion of the two genes.

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Bacteria imbalances and breast cancer

Breast cancer develops from breast tissue, common symptoms of breast cancer are lump in the breast, change in breast shape, fluid coming out from the nipple and red scaly patch of skin.

Bacteria imbalances allow disease-causing bacteria and toxins to move into the bloodstream and upset the normal body function, it exposes the body to different diseases.

Healthy breast tissue contains more of the bacterial species Methylobacterium, bacteria that live in the body, known as the microbiome, influence many diseases. Bacterial composition of breast tissue of healthy women and women with breast cancer are different.

Researchers examined the tissues of some patients who underwent mastectomy for invasive carcinoma or elective cosmetic breast surgery, they examined oral rinse and urine to determine the bacterial composition of these distant sites in the body. They discovered that cancer patients' urine samples had increased levels of gram-positive bacteria, including Staphylococcus and Actinomyces.
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Alcohol affects levels of cholesterol through epigenetics

In an analysis of the epigenomes of people and mice, researchers discovered that drinking alcohol may induce changes to a cholesterol regulating gene. The findings suggest that these changes to the gene, PCSK9, may be responsible for some of the differences in how cholesterol is processed in people who drink alcohol, or may affect those taking a relatively new class of PCSK9 cholesterol-lowering drugs designed to reduce LDL cholesterol.

Chronic alcohol use can have detrimental effects on the liver and the cardiovascular system. Regulation of PCSK9 seems to correlate with this pattern and may be a significant underlying factor behind the variations in the relationship between cholesterol and cardiovascular disease when it comes to alcohol use. Researchers measure how drinking of alcohol can leads to changes in which genes are expressed.

They examined information from DNA chips- microarrays that can show which genes have chemical methyl groups added across the whole genome. These chips looked at about 500,000 methyl groups at a time. methylation affects the level of gene expression. The researchers used different sets of data: DNA from the brains of deceased people with documented alcohol dependence compared to healthy controls and DNA from blood samples of people who had documented alcohol dependence with healthy controls.

When the investigators cross-compared epigenetic data from the sets of data to find out what changes occurred in common in the two data sets and what changes did not, the common factor highlighted the gene PCSK9. The human liver samples from people with alcohol dependence who underwent a liver transplant and noticed a similar pattern: more methylation on PCSK9 and unexpectedly lower PCSK9 protein levels. In samples from people who abused alcohol, the researchers detected that PCSK9 gene expression was only a third of the level in people who didn't abuse alcohol.

Alcohol is metabolized by the liver and can cause liver damage if used in large amounts over long periods of time. In people, PCSK9 is found at its highest levels in liver, but is also found in other tissues, such as brain and blood. PCSK9 binds to the bad cholesterol receptors and blocks uptake and breakdown of bad cholesterol by cells, leading to accumulation in the bloodstream, where it presumably clogs arteries.
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Human semen keeps viruses

The current analysis revealed genetic evidence of many infectious viruses found in semen. Semen provides a hiding place and breeding ground for many dangerous viruses

Zika, Ebola, Marburg, Lassa fever, Chikungunya, Mumps, Epstein-Barr and Chhicken pox are present in human semen. Non-sexually transmitted viruses can persist in semen, and this increases the risk of sexual transmission.

 The presence of viruses in semen does not mean that every virus can be sexually transmitted, common viruses in semen are: hepatitis viruses, herpes viruses, and range of other viruses that can be pass from person-to-person via blood, saliva or other means.

It is easy for viruses to get in to the semen, but relatively hard for the immune system to kill the viruses, the immune system recognized sperm as foreign objects in the body and this subject sperm to attack from the immune system.

For sperm to survive, the testes are immunologic locations in the body, where the immune system does not have much access to, this immunological location can also protect dangerous viruses.

Zika is cleared from the bloodstream within one week of treatment, but can persist in semen for months, Ebola survivors can reigniting an outbreak because the virus remained latent and active in their testicles.
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Causes of abdominal fat

Excess abdominal fat may be the result of excess consumption of sugar and simple white carbohydrates. However,
sleep deprivation, stress or wrong exercise can leads to abnormal fat.

Having abdominal fat increases the risk of type 2 diabetes and heart problems.
Cortisol, the stress hormone, plays a part in laying down central adipose tissue. You can avoid stress by engaging in yoga practice and mindfulness to your daily routine.

High-sugar diet can increase abdominal fat, cut down on sugar, saturated fats and white refined foods such as white bread, pasta, rice and potatoes, as they metabolise quickly, resulting in elevated blood sugar levels that promotes fat storage.

Eat more of lean meats, vegetables, fruits, monounsaturated and polyunsaturated fats, such as those found in nuts and avocados. Avoid eating fruit after a meal, as fruit can cause food to ferment in your stomach, leading to bloating and lots of gas.

Fat can play a vital role in weight loss, by slowing the release of nutrients into the bloodstream, add little fat to your meal. Hormonal disruption can affect fat distribution, seek medical help.
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Mylotarg for treating acute myeloid leukemia

Mylotarg (gemtuzumab ozogamicin) has been approved for the treatment of adults with newly diagnosed acute myeloid leukemia whose tumors express the CD33 antigen (CD33-positive AML).

AML is a rapidly progressing cancer that forms in the bone marrow and results in an increased number of white blood cells in the bloodstream.

Mylotarg is a targeted therapy that consists of an antibody connected to an anti-tumor agent that is toxic to cells. It is thought to work by taking the anti-tumor agent to the AML cells that express the CD33 antigen, blocking the growth of cancerous cells and causing cell death.

Common side effects of Mylotarg are fever, nausea, infection, vomiting, bleeding, low levels of platelets in the blood, swelling and sores in the mouth, constipation, rash, headache, liver damage, and low levels of certain white blood cells.
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Fatty liver can damage other organs

Nonalcoholic fatty liver disease  NAFL increases the risk of chronic liver diseases such as liver cirrhosis, liver cancer, type 2 diabetes and cardiovascular diseases. Altered secretion of the fatty liver increases production of glucose, fats, and proteins like hepatokine fetuin-A, which are releases into the bloodstream.

The secreted substances of the fatty liver enter other organs and trigger further reactions. People who had experienced an increased pancreatic fatty degeneration have reduced insulin secretion.

Fatty liver and fatty degeneration of the pancreas triggers increased local immune cell infiltration and inflammation that increase the disease.
However, adipose tissue is not harmful, it can even have protective effects: adipose tissue located around the blood vessels of the kidney has regenerative properties.

The factor that leads to pathological changes is fetuin-A, which is produced by the fatty liver, instead of protecting tissue as before, the adipose tissue brings out inflammatory processes that leads to a restriction of renal function.
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Vyxeos for Acute Myeloid Leukemia

Food and Drug Administration has approves Vyxeos (daunorubicin and cytarabine) Liposome for Injection for Certain Types of Poor-Prognosis Acute Myeloid Leukemia

The drug is for the treatment of adults with two types of acute myeloid leukemia (AML): newly diagnosed therapy-related AML (t-AML) or AML with myelodysplasia-related changes (AML-MRC).

Vyxeos is a fixed-combination of chemotherapy drugs daunorubicin and cytarabine. Vyxeos combines two commonly used chemotherapies into a single formulation that may help some patients live longer than if they were to receive the two therapies separately.

Acute myeloid leukemia AML is a rapidly progressing cancer that forms in the bone marrow and results in an increased number of white blood cells in the bloodstream. It occurs as a complication of chemotherapy or radiation in patients treated for cancer five years after treatment.

Patients who have a history of serious hypersensitivity to daunorubicin, cytarabine or any component of the formulation should not use Vyxeos.
Patients taking Vyxeos should be monitored for hypersensitivity reactions and decreased cardiac function.

Common side effects of Vyxeos are: hemorrhage, fever with low white blood cell count, rash, swelling of the tissues, nausea, inflammation of the mucous membranes, diarrhea, constipation, musculoskeletal pain, fatigue, abdominal pain, shortness of breath, headache, cough, decreased appetite, abnormal heart rhythm, lung infection, blood infection, sleep disorders and vomiting.
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Meningococcal B vaccine may prevents gonorrhoea

Vaccine used against a bacteria that causes brain inflammation can prevents gonorrhoea. Presently, using a condom or abstaining from sex are ways of preventing gonorrhoea.

Gonorrhoea can cause painful pelvic inflammation in women, and infertility in men and women. It can also spread into the bloodstream to cause life-threatening infections in other parts of the body. Infected pregnant woman can pass it to her fetus and cause blindness.

The disease spreads easily because many carriers are unaware of the disease, until they experience the symptoms. Gonorrhoea is becoming untreatable because of antibiotic resistance, there is an increased imperative to examine different vaccine for the treatment.

Researchers examined gonorrhoea cases among people who have used meningococcal B vaccine for Meningococcal bacteria, they noticed a decline in gonorrhoea after the use of meningococcal B vaccine.
This shows that meningitis vaccine can prevents gonorrhoea.
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Treat sepsis with vitamins C

Sepsis is a progressive disease process caused by an aggressive and dysfunctional immune response to an infection in the bloodstream. Illnesses like bronchitis, pneumonia and kidney infection can turn septic.

 Sepsis starts with symptoms of an infection, the condition can progress to septic shock, which may be lethal.
Lack of vital vitamins in the body can increase the risk of Sepsis.

Chronic diseases like AIDS, cancer, diabetes, lung, kidney and liver raises the risk of Sepsis. Being exposed to
infection-causing bacteria in health centers can also increase the risk of Sepsis.

The condition can leads to extremely low blood pressure that is unresponsive to fluid replacement, weakening of the heart and multiple-organ failure if treatment is delayed.

Steroid hydrocortisone, intravenous   (IV) vitamin C, thiamine (vitamin B-1) can be used to treat Sepsis. Vitamin C
prevents and treat infectious diseases.
Thiamine is required for metabolism of some of the metabolites of vitamin C. It
reduces the risk of renal failure and mortality.
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High sugar intake and your facial beauty

High sugar intake can cause obesity, chronic disease, tooth decay, cause wrinkles on your face and change your complexion.

Glycation is when sugar in your bloodstream bonds onto proteins in the body. The more sugar we eat, the more glycation end products we produce.

Since collagen that keeps our skin plump and firm is the body’s most prevalent protein, it will be affected most and can result in saggy, loose and red facial skin.

Glycation can cause other skin problems, like redness, rosacea and acne. Foods with higher glycemic index
can trigger breakouts.

Sugar triggers the pancreas to produce more insulin, which increases the hormones that stimulate sebum production. Sugar changes complexion by depleting water in the cells causing dark under-eye circles.

Vigorous exercise increases health risks

Vigorous exercise for a long period of time can change the composition of gut bacteria.

The research looked at soldiers taking part in an intensive training programme and found that pro-longed exercise caused the protective barrier in their guts to become permeable and triggered leaky gut syndrome.

Gut health and overall health are linked, intense physiological stress could raise the risks of many types of illnesses.

 Poor gut health is linked to conditions ranging from irritable bowel syndrome, diabetes, high blood pressure, depression, obesity, childhood asthma, colitis and colon cancer.

The study is the first to investigate the response of gut microbiome - the term for the population of microbes in the intestine - during military training.

It looked at a group of 73 Norwegian Army soldiers taking part in a military-style cross country skiing training programme.

The group skied 31 miles (51 km) while carrying 99-pound (45 kg) packs, across four days. Before and after the training
exercise, researchers collected blood and stool samples from the soldiers.

It was found that the microbiome and metabolites - the substance formed in or necessary for metabolism - in the soldiers' blood and stool altered 'significantly' by the end of the aggressive training period.

Furthermore, sucralose excretion in their urine samples rose considerably, indicating an increase in intestinal permeability (IP).

Scientists know that healthy intestines have a semi-permeable barrier, which acts as a defense to keep bacteria and other harmful substances out, while allowing healthy nutrients into the bloodstream.