Ergosterol Peroxide

Ergosterol Peroxide: A Mushroom-Derived Compound with Promising Biological Activities-A Review.


Ergosterol peroxide (EP; 5α,8α-epidioxy-22E-ergosta-6,22-dien-3β-ol) is a C28-sterol and a component of many medicinal mushrooms. Since its discovery nearly a century ago, many sources and biological effects of this compound have been described. Effects range from antimicrobial to cytotoxic to immunosuppressive and other activities. This review covers biological investigations of EP, its activities, and possible mechanisms of action. EP is a promising candidate for drug development and contributes to the health-promoting effects of medicinal mushrooms.

More on Vitamin D, Ergosterol and Cholesterol

Do Vitamin D Levels Affect Cholesterol?

~Content Source

Higher vitamin D levels appear to be associated with higher total cholesterol levels and higher HDL cholesterol levels, according to a new study presented at the American College of Cardiology’s (ACC) 65th Annual Scientific Sessions.1 

Investigators looked 13 039 adults and found that higher 25-hydroxyvitamin D (25[OH]D) was cross-sectionally and prospectively associated with higher total cholesterol and HDL cholesterol levels and lower total cholesterol-to-HDL cholesterol ratio after considering factors such as diabetes and adiposity.

“We wanted to see the association of low vitamin D with low HDL cholesterol and high total cholesterol-to-HDL cholesterol ratio, but I think we were most surprised to not find an association of vitamin D deficiency with elevated triglycerides, as has been noted in other studies. This may be in part that we carefully adjusted for other confounding lifestyle variables such as physical activity and 2 measures of adiposity (BMI and waist circumference),” said senior study author Erin Michos, MD, MHS, associate professor of medicine and epidemiology and associate director of preventive cardiology at Johns Hopkins School of Medicine in Baltimore.

“We also were surprised that we did not see any association of low vitamin D with elevated LDL cholesterol in our overall sample. However, when we performed a sensitivity analysis looking at individuals who were not taking lipid-lowering therapy at the baseline exam or at any of the follow-up visits, we did see the association of low vitamin D with elevated LDL cholesterol.”

Dr Michos and her colleagues measured lipids at baseline (1990-1992), in 1993-1994, and in 1996-1998. The mean follow-up was 5.2 years.

The investigators used linear and mixed model regression methods to assess associations of 25(OH) D with cross-sectional and lipid trends. They also adjusted for clinical characteristics. The mean age at baseline was 57.6 years, 57% were women, and 24% were black.

Among those individuals without baseline dyslipidemia, participants with low 25(OH) D (<20 ng/mL) compared with optimal levels (≥30 ng/mL) had increased risk for incident dyslipidemia in demographic-adjusted models (hazard ratio [HR]=1.19; 95% CI, 1.02-1.39). Nevertheless, this finding was attenuated in fully-adjusted models (HR=1.12; 95% CI, 0.95-1.32).1

Dr Michos said low concentrations of vitamin D, defined as serum 25(OH)D below 30 ng/mL, are present in more than two-thirds of the US adult population and in an estimated 1 billion individuals worldwide. 

“So, this is a major relevant public health issue. Vitamin D deficiency has been associated with a number of non-bone-related adverse health outcomes, including increased risk for cardiovascular diseases (CVDs). One of the mechanisms by which vitamin D may influence CVD risk is through an effect on lipids,” Dr Michos told Endocrinology Advisor. “The potential link between vitamin D deficiency and adverse lipid profile should be of great interest to a large number of practitioners who treat both vitamin D and lipid disorders, including endocrinologists, internists, lipidologists, and cardiologists.”

Previous studies, including one study conducted by her team and recently published in the Journal of Clinical Lipidology, suggested that low levels of vitamin D were associated with an atherogenic lipid profile consisting of elevated LDL cholesterol, elevated triglycerides, and lower HDL cholesterol, noted Dr Michos.2 However, most of the evidence supporting this association was obtained in cross-sectional analyses. 

For this current investigation, the researchers analyzed the association between vitamin D status and the lipid profile prospectively using data from the Atherosclerosis Risk in Communities (ARIC) study. This large study of a US community-based sample of blacks and whites collected data on numerous demographic, lifestyle, and clinical variables spanning multiple clinic visits. Unlike prior investigations, ARIC allowed for extensive adjustment of possible confounders over time, according to Dr Michos. It also contained information regarding initiation of lipid-lowering medication use during follow-up. 

Dr Michos said further research is warranted, including randomized, controlled trials, to assess whether treating vitamin D deficiency can impact lipids and thereby influence CVD risk.

References

  1. Faridi K, Zhao D, Martin SS, et al. Vitamin D and Change in Lipids Over 5 Years: The Atherosclerosis Risk in Communities (ARIC) Study. Presented at: ACC 65th Annual Scientific Session & Expo; April 2-4, 2016; Chicago, IL.
  2. Lupton JR, Faridi KF, Martin SS, et al. Deficient serum 25-hydroxyvitamin D is associated with an atherogenic lipid profile: The Very Large Database of Lipids (VLDL-3) study. J Clin Lipidol. 2016;10(1):72-81. doi:10.1016/j.jacl.2015.09.006.

Cytomegalovirus, Epstein-barr, Diet and Leukemia.

‘For 30 years I’ve been obsessed by why children get leukaemia. Now we have an answer’

Newly knighted cancer scientist Mel Greaves explains why a cocktail of microbes could give protection against disease.

Mel Greaves has a simple goal in life. He is trying to create a yoghurt-like drink that would stop children from developing leukaemia.

The idea might seem eccentric; cancers are not usually defeated so simply. However, Professor Greaves is confident and, given his experience in the field, his ideas are being taken seriously by other cancer researchers.

Based at the Institute of Cancer Research in London, Greaves has been studying childhood leukaemia for three decades. On Friday, it was announced that he had received a knighthood in the New Year honours list for the research he has carried out in the field.

“For 30 years I have been obsessed about the reasons why children get leukaemia,” he says. “Now, for the first time, we have an answer to that question – and that means that we can now start thinking about ways to halt it in its tracks. Hence my idea of the drink.”

In the 1950s, common acute lymphoblastic leukaemia – which affects one in 2,000 children in the UK – was lethal. Today 90% of cases are cured, although treatment is toxic, and there can be long-term side effects. In addition, for the past few decades, scientists have noticed that numbers of cases have actually been increasing in the UK and Europe at a steady rate of around 1% a year.

“It is a feature of developed societies but not of developing ones,” Greaves adds. “The disease tracks with affluence.”

Acute lymphoblastic leukaemia is caused by a sequence of biological events. The initial trigger is a genetic mutation that occurs in about one in 20 children.

“That mutation is caused by some kind of accident in the womb. It is not inherited, but leaves a child at risk of getting leukaemia in later life,” adds Greaves.

For full leukaemia to occur, another biological event must take place and this involves the immune system. “For an immune system to work properly, it needs to be confronted by an infection in the first year of life,” says Greaves. Without that confrontation with an infection, the system is left unprimed and will not work properly.”

And this issue is becoming an increasingly worrying problem. Parents, for laudable reasons, are raising children in homes where antiseptic wipes, antibacterial soaps and disinfected floorwashes are the norm. Dirt is banished for the good of the household.

In addition, there is less breast feeding of infants and a tendency for them to have fewer social contacts with other children. Both trends reduce babies’ contact with germs. This has benefits – but also comes with side effects. Because young children are not being exposed to bugs and infections as they once were, their immune systems are not being properly primed.

“When such a baby is eventually exposed to common infections, his or her unprimed immune system reacts in a grossly abnormal way,” says Greaves. “It over-reacts and triggers chronic inflammation.”

As this inflammation progresses, chemicals called cytokines are released into the blood and these can trigger a second mutation that results in leukaemia in children carrying the first mutation.

“The disease needs two hits to get going,” Greaves explains. “The second comes from the chronic inflammation set off by an unprimed immune system.”

In other words, a susceptible child suffers chronic inflammation that is linked to modern super-clean homes and this inflammation changes his or her susceptibility to leukaemia so that it is transformed into the full-blown condition.

From this perspective, the disease has nothing to with power lines or nuclear fuel reprocessing stations, as has been suggested in the past, but is caused by a double whammy of interacting prenatal and environmental events, as Greaves outlined in the journal Nature Reviews Cancer earlier this year.

Crucially, this new insight offers scientists a chance to intervene and to stop leukaemia from developing in the first place, he adds. “We do not yet know how to prevent the occurrence of the initial prenatal mutation in the womb, but we can now think of ways to block the chronic inflammation that happens later on.”

To do this, Greaves and his team have started working on the bacteria, viruses and other microbes that live in the human gut. These help us digest our food but they also give an indication of the bugs we have been exposed to in life. For example, people in developed countries tend to have far fewer bacterial species in their guts, it has been found – and that is because they have been exposed to fewer species of microbes in the early stages of their lives, a reflection of those “cleaner” lives they are now living.

“We need to find ways of reconstituting their microbiomes – as we term this community of microbes. We also need to find which are the most important species of bacteria for priming a child’s immune system.”

To do this, Greaves is now experimenting on mice to find out which bugs are best at stimulating rodent immune systems. The aim would then be to follow up with trials on humans in two or three years.

“The aim is to find six or maybe 10 species of microbes that are best able to restore a child’s microbiome to a healthy level. This cocktail of microbes would be given, not as a pill, but perhaps as yoghurt-like drink to very young children.

“And it would not just help prevent them getting childhood leukaemia. Cases of conditions such as type 1 diabetes and allergies are also rising in the west and have also been linked to our failure to expose babies to bacteria to prime children’s immune systems. So such a drink would help cut numbers of cases of these conditions as well.

“I think the prospect is incredibly exciting. I think we could use this to reduce the risk not just of leukaemia but a number of other very debilitating conditions.”

Leukaemia: the facts

Blood cells are manufactured in bone marrow. Red blood cells, which carry oxygen round our bodies, white blood cells, which fight infection, and platelets, which stop bleeding, are created when your body needs them. But when a person develops leukaemia, too many white blood cells are released, which stop the normal cells in your bone marrow from growing. As a result, the amount of normal red cells, white cells and platelets in your blood is reduced – and your health suffers.

Of the many types of leukaemia, the most common in young people are acute lymphoblastic leukaemia and acute myeloid leukaemia.

Source: Teenage Cancer Trust

Hugh O’Connor and Hodgkin’s Lymphoma

Hugh O’Connor was born in Rome, Italy. When he was six days old, he was adopted by Carroll O’Connor and his wife Nancy. Carroll was in Rome filming Cleopatra. He was named after Carroll O’Connor’s brother, who died in a motorcycle accident in 1961.

When he was 16, Hugh was diagnosed with Hodgkin’s lymphoma. He survived the cancer with chemotherapy and two surgeries but became addicted to drugs. He had been taking prescription drugs for the pain and marijuana for nausea but later became dependent on harder drugs. Despite numerous stays at rehabilitation clinics, he never conquered his addiction and remained in recovery.


Hodgkin’s lymphoma (HL) is a type of lymphoma in which cancer originates from a specific type of white blood cells called lymphocytes. Symptoms may include fever, night sweats, and weight loss. Often there will be non-painful enlarged lymph nodes in the neck, under the arm, or in the groin.[ Those affected may feel tired or be itchy.

About half of cases of Hodgkin’s lymphoma are due to Epstein–Barr virus (EBV). Other risk factors include a family history of the condition and having HIV/AIDS.[ There are two major types of Hodgkin lymphoma: classical Hodgkin lymphoma and nodular lymphocyte-predominant Hodgkin lymphoma.[ Diagnosis is by finding Hodgkin’s cells such as multinucleated Reed–Sternberg cells (RS cells) in lymph nodes.[ The virus-positive cases are classified as a form of the Epstein-Barr virus-associated lymphoproliferative diseases.

More on Vitamin D…Friend or Foe?

Mushrooms are the >>>ONLY<<< vegetarian/produce based food that can make vitamin D. Actually, they contain a “pro-vitamin,” or precursor, called ergosterol that is converted into vitamin D when exposed to the sun’s ultraviolet (UV) radiation—similar to how your skin synthesizes the vitamin in response to sun exposure. -Berkeley Wellness

Ergosterol is a sterol found in cell membranes of fungi and protozoa, serving many of the same functions that cholesterol serves in animal cells. Because many fungi and protozoa cannot survive without ergosterol, the enzymes that synthesize it have become important targets for drug discovery. Ergosterol is a provitamin form of vitamin D2; exposure to ultraviolet (UV) light causes a chemical reaction that produces vitamin D2.

Ergosterol powder is an irritant to skin, eyes, and the respiratory tract. Ingestion of large amounts can cause hypercalcemia, which (if prolonged) can lead to calcium salt deposits in the soft tissues and, in particular, the kidneys. -Wikipedia

The Skin

Our body tries in many different ways to get rid of toxins. If liver, kidneys and lungs do not fulfill their tasks sufficiently, the body needs help from the skin.

The skin is the largest organ of protection and defense. It is a sensory organ. It serves for thermo regulation, secretion and excretion. The skin plays an important role in the elimination of toxins and can assist the kidneys in their work.

It evacuates the waste products that are classified as crystals. They are soluble in liquids and are evacuated in the form of sweat through the sweat glands. Crystals are the residues of the metabolism of food rich in protein, such as meat, fish, eggs, dairy products, legumes and cereals. Uric acid and urea are part of the group of crystals.

These may also result from an excess of refined sugar or very acidic food. Other types of waste products and toxins are excreted in the form of rashes. -Issels Immuno Oncology

Lipofuscin – Wikipedia

Liver Spots – Wikipedia

Tinnitus is the result of the brain trying, but failing, to repair itself

Date:January 15, 2011

Source: Georgetown University Medical Center – Link

Summary: Tinnitus appears to be produced by an unfortunate confluence of structural and functional changes in the brain, say neuroscientists.


Tinnitus appears to be produced by an unfortunate confluence of structural and functional changes in the brain, say neuroscientists at Georgetown University Medical Center (GUMC).

The phantom ringing sounds heard by about 40 million people in the U.S. today are caused by brains that try, but fail to protect their human hosts against overwhelming auditory stimuli, the researchers say in the January 13th issue of Neuron. They add that the same process may be responsible for chronic pain and other perceptual disorders.

The researchers say that the absence of sound caused by hearing loss in certain frequencies, due to normal aging, loud-noise exposure, or to an accident, forces the brain to produce sounds to replace what is now missing. But when the brain’s limbic system, which is involved in processing emotions and other functions, fails to stop these sounds from reaching conscious auditory processing, tinnitus results.

“We believe that a dysregulation of the limbic and auditory networks may be at the heart of chronic tinnitus,” says the study’s lead investigator, Josef P. Rauschecker, PhD, a neuroscientist. “A complete understanding and ultimate cure of tinnitus may depend on a detailed understanding of the nature and basis of this dysregulation.”

Tinnitus isn’t curable, although antidepressants appear to help some patients, as does the use of masking noise to diminish focus on the ringing sensations.

Using functional Magnetic Resonance Imaging (fMRI), the Georgetown researchers tested 22 volunteers, half of whom had been diagnosed with chronic tinnitus. They found that moderate hyperactivity was present in the primary and posterior auditory cortices of tinnitus patients, but that the nucleus accumbens exhibited the greatest degree of hyperactivity, specifically to sounds that were matched to frequencies lost in patients.

The nucleus accumbens is part of the corticostriatal circuit, which is involved in evaluation of reward, emotion, and aversiveness, says Rauschecker. “This suggests that the corticostriatal circuit is part of a general ‘appraisal network’ determining which sensations are important, and ultimately affecting how or whether those sensations are experienced,” he says. “In this study, we provide evidence that these limbic structures, specifically the nucleus accumbens and the ventromedial prefrontal cortex, do indeed differ in the brains of individuals with tinnitus.”

Functional lapses in these same areas have also been implicated to altered mood states and to chronic pain. “Both of these conditions may also involve the inability to suppress unwanted sensory signals,” Rauschecker says.

Based on their findings, the researchers argue that the key to understanding tinnitus lies in understanding how the auditory and limbic systems interact to influence perception — be it sound, emotions, pain, etc.

Grant support was provided by the National Institute on Deafness and Other Communication Disorders, the Tinnitus Research Consortium, the Tinnitus Research Initiative, and the Skirball Foundation.

Story Source:

Materials provided by Georgetown University Medical CenterNote: Content may be edited for style and length.


Journal Reference:

  1. Amber M. Leaver, Laurent Renier, Mark A. Chevillet, Susan Morgan, Hung J. Kim and Josef P. Rauschecker. Dysregulation of Limbic and Auditory Networks in TinnitusNeuron, Volume 69, Issue 1, 13 January 2011, Pages 33-43 DOI: 10.1016/j.neuron.2010.12.002