Carbohydrate Abuse Disorder

This will be fun. The Sinclair Method. Time to achieve recovery addiction to carbohydrates. TSM works wonders for Carbohydrate Addicted People.


Research shows that traditional treatment for alcohol abuse fails 85-90 percent of the time. Government data indicates a 90% relapse rate over four years. About half of those relapses happen within six months.

The treatment method I’m here to talk about flips those statistics. It SUCCEEDS for about 80 percent of those who use it, and most people see dramatic improvement in about four months.


The American Medical Association first labeled alcoholism as a disease of the brain in 1956, but those with AUD are not treated as though they have a disease. What if other diseases were treated like addiction? Would your doctor refuse to address your high cholesterol or blood pressure until after you had a heart attack? Would your doctor tell you to see a nutritionist, but withhold insulin until after you’ve proven you are ready to stop eating sugar entirely? Would he or she tell you it’s your fault that your cancer has returned? This is the reality for someone with an addiction to alcohol. Society, and many treatment professionals, believe a person has to hit rock bottom and lose it all before they can commit to recovery.

Rock bottom is unethical. It is the polar opposite of harm reduction. It’s immoral…and making patients reach rock bottom before medical treatment is given should be considered malpractice.

Crucifers, Cancer and Indole-3-Carbinol(I3C)

The glucosinolate breakdown product indole‐3‐carbinol acts as an auxin antagonist in roots of Arabidopsis thaliana.

Indolebutyric Acid–Derived Auxin and Plant Development

The phytochemical indole‐3‐carbinol (I3C) functions in cruciferous vegetables as a protective agent against foraging insects (Kim and Jander, 2007), and is used in humans as a dietary supplement with anti‐carcinogenic properties (Aggarwal and Ichikawa, 2005). I3C is a breakdown product of glucosinolates, which are a diverse group of small molecules produced in the Cruciferae family, including Brassica vegetables, such as broccoli and cauliflower, and also Arabidopsis thaliana.


Glucosinolate – Wikipedia

The glucosinolates are natural components of many pungent plants such as mustardcabbage, and horseradish. The pungency of those plants is due to mustard oils produced from glucosinolates when the plant material is chewed, cut, or otherwise damaged. These natural chemicals most likely contribute to plant defence against pests and diseases, but are also enjoyed in small amounts by humans and are believed to contribute to the health promoting properties of cruciferous vegetables.

Fungal Cell Body and Development

Article Source ~ Science Direct

Fungal Cell Biology and Development

Nicholas P. Money, in The Fungi (Third Edition), 2016

Cords and Rhizomorphs

Attack Hyphae

The use of the term ‘organ’ to describe the multicellular structures of fungi is subjective. Animal organs are differentiated structures that perform specific functions. A mycelium may be viewed as an organ by this definition, but the degree of differentiation among its hyphae is very limited. A higher degree of differentiation is achieved through the formation of cords by mycelia of wood-decay and ectomycorrhizal fungi and it seems justifiable to describe the more complex of these structures as organs. We will return to this issue of terminology when we consider the structure and function of fruit bodies later in the chapter.

Babylon Battery or Hyphal Tip

Strandscords, and rhizomorphs vary in complexity from bundles of hyphae, whose cell walls adhere to one another to produce slender cylinders of unpigmented cells on the surface of a culture dish, to fat pipes with a diameter of a few centimetres that can extend for hundreds of metres. The larger pipes are formed from hundreds of thousands of hyphae, develop a complex internal anatomy, and are sometimes tipped with a rounded, mucilaginous cap. Variations in the internal structure of these organs make it difficult to discriminate between strands, cords, and rhizomorphs. The term rhizomorph may be useful to designate the larger of these invasive organs that have an identifiable tip that pushes through the soil.

Hyphae Tip

Cord is the preferred term for other linear organs without an organised tip.

What is my Vagus Nerve Trying to Tell Me?

Article Source ~ Wikipedia

Physical and emotional effects

Excessive activation of the vagal nerve during emotional stress, which is a parasympathetic overcompensation of a strong sympathetic nervous system response associated with stress, can also cause vasovagal syncope due to a sudden drop in cardiac output, causing cerebral hypoperfusion. Vasovagal syncope affects young children and women more than other groups. It can also lead to temporary loss of bladder control under moments of extreme fear.

Research has shown that women having had complete spinal cord injury can experience orgasms through the vagus nerve, which can go from the uteruscervix, and, it is presumed, the vagina to the brain.[8][9]

Insulin signaling activates the adenosine triphosphate (ATP)-sensitive potassium (KATP) channels in the arcuate nucleus, decreases AgRP release, and through the vagus nerve, leads to decreased glucose production by the liver by decreasing gluconeogenic enzymes: Phosphoenolpyruvate carboxykinaseGlucose 6-phosphatase.[10][11]


Vagotomy

Vagotomy (cutting of the vagus nerve) is a now-obsolete therapy that was performed for peptic ulcer disease. Vagotomy is currently being researched as a less invasive alternative weight-loss procedure to gastric bypass surgery.[18] The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients’ stomachs, resulting in average weight loss of 43% at six months with diet and exercise.[19]

One serious side effect of a vagotomy is a vitamin B12 deficiency later in life — perhaps after about 10 years — that is similar to pernicious anemia. The vagus normally stimulates the stomach’s parietal cells to secrete acid and intrinsic factor. Intrinsic factor is needed to absorb vitamin B12 from food. The vagotomy reduces this secretion and ultimately leads to the deficiency, which, if left untreated, causes nerve damage, tiredness, dementia, paranoia, and ultimately death.[20]

Researchers from Aarhus University and Aarhus University Hospital have demonstrated that vagotomy prevents (halves the risk of) the development of Parkinson’s disease, suggesting that Parkinson’s disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain.[21]


Vagus nerve stimulation (VNS) therapy using a neurostimulator implanted in the chest is a treatment used since 1997 to control seizures in epilepsy patients and has been approved for treating drug-resistant cases of clinical depression.[12] A non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon[when?]undergo trials.[13]

Clinical trials are underway in AntwerpBelgium, using VNS for the treatment of tonal tinnitus[14] after a breakthrough study published in early 2011 by researchers at the University of Texas – Dallas showed successful tinnitus suppression in rats when tones were paired with brief pulses of stimulation of the vagus nerve.[15]


Vagotomy (cutting of the vagus nerve) is a now-obsolete therapy that was performed for peptic ulcer disease. Vagotomy is currently being researched as a less invasive alternative weight-loss procedure to gastric bypass surgery.[18] The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients’ stomachs, resulting in average weight loss of 43% at six months with diet and exercise.[19]

One serious side effect of a vagotomy is a vitamin B12 deficiency later in life — perhaps after about 10 years — that is similar to pernicious anemia. The vagus normally stimulates the stomach’s parietal cells to secrete acid and intrinsic factor. Intrinsic factor is needed to absorb vitamin B12 from food. The vagotomy reduces this secretion and ultimately leads to the deficiency, which, if left untreated, causes nerve damage, tiredness, dementia, paranoia, and ultimately death.[20]

Researchers from Aarhus University and Aarhus University Hospital have demonstrated that vagotomy prevents (halves the risk of) the development of Parkinson’s disease, suggesting that Parkinson’s disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain.[21]

Not Just in the Kidneys – Stones – Oxalate

Hyphae Tip

Even though oxalate crystals are most common in the kidney, they also can form in virtually any other tissue in the body, including the brain and the blood-brain barrier. Oxalate crystals resembling pieces of glass can form in the heart muscle. As the heart muscle contracts, these pieces of oxalate crystals actually tear into the tissue. If these crystals are deposited in skeletal muscle, normal movement and exercise can be very painful. Other diseases in which oxalates may play a role include arthritis, joint pain and interstitial cystitis.

Data Source – Quora – Good conductors, such as most metals, e.g. copper and gold, have a ‘sea’ of free electrons, which are charged particles, that are free to move around, and therefore carry charge, which is what makes up electricity. this causes them to be good conductors of electricity

silicon is a poor conductor of electricity due to the free electrons being locked in giant lattice structures, and being unable to move around and carry the charge that makes up electricity.

however, when silicon is heated up, the giant lattice structures start to break down, and the electrons are released. this is important, because the electrons so not just conduct electricity, but also heat. when heated, the electrons are free to move around and therefore conduct heat. it is for the same reason that silicon becomes a better conductor of electricity the more you heat it up, since more of the giant lattice structures break, releasing more electrons to conduct electricity.


As pointed out, pure silicon is a semiconductor and has a resistance about halfway between good conductors and good insulators.

Pathogenesis of Aspergillus fumigatus in Invasive Aspergillosis

Article Source ~ Clinical Microbiology Review

No Fun Guys

A. fumigatus interactions with phagocytes. Alveolar macrophages phagocytose inhaled conidia via PRRs. Conidial swelling (within or outside of the macrophage) releases the protective rodlet layer, exposing β(1,3)-glucan for recognition by dectin-1. Dectin-1-β(1,3)-glucan interactions are primarily responsible for the activation of macrophage proinflammatory responses, including conidial killing. Neutrophils attach to hyphae and degranulate, damaging hyphae by oxidative and nonoxidative mechanisms. Neutrophils may also aggregate conidia and prevent germination. Compromised phagocyte function is the primary risk factor for IA. Fungal products (shown in red) may contribute to fungal pathogenicity in these immunocompromised hosts by evading or modulating host defenses.

Cytomegalovirus – Walking Dead

How did I get to 45 years of age and not ever hear of this? ~ slideshare.net

Infects 60-90% of the population worldwide. Typically asymptomatic. W.T.Fungal?

infection in immunocompromised individuals life threatening.

Infection in utero: Leading cause of infectious disease related birth defects. 1 in 100 infected. Again…W.T.Fungus?

  1. Mild to severe hearing loss.
  2. Cognitive deficits(ADHD, Autism?)
  3. Physical abnormalities.

Human cytomegalovirus (HCMV  or Human herpesvirus 5) is a large DNA virus (>235 kb) that belongs to theBetaherpesvirinae genus of the Herpesviridaefamily. Primary HCMV infection in immunocompetent individuals is usually benign but establishes a lifelong latent state. Immune suppressed transplant recipients or AIDS patients are particularly susceptible to life-threatening end-organ disease. The other vulnerable population is the developing fetus in utero. During pregnancy, the vertical transmission of the virus across the placenta to the fetus (congenital infection) can lead to serious symptomatic disease in newborns that include mental retardation and deafness. Congenital CMV is the leading cause of mental retardation/deafness in newborns with over 5,000 children each year in the US. HCMV is also considered to be a contributing factor to vascular disease and specific cancers (eg. glioblastoma).

Cytomegalovirus-Mother to Child Invasion

Anatomy of the maternal-fetal interface, where the fetus-derived placenta attaches to the mother’s uterus. The basic structural unit of the placenta is the chorionic villus, composed of a stromal core with blood vessels, surrounded by a basement membrane, and overlaid by cytotrophoblast stem cells. As part of their differentiation pathway, stem cells detach from the basement membrane and adopt one of two lineage fates. They fuse to form the syncytiotrophoblast, which covers floating villi, or they join a column of extravillus cytotrophoblasts that invade the uterine stroma. The syncytiotrophoblast mediates nutrient and gas exchange across the maternal-fetal interface. The anchoring villi (AV) establish physical connections between the mother and fetus through the attachment of cytotrophoblast columns. The floating villi (FV), bathed by maternal blood, contain the fetal capillaries (zone I). Cytotrophoblasts in the AV attach the placenta to the uterine wall (zone II). Cytotrophoblasts then invade the decidua up to the first third of the myometrium (zone III), anchoring the placenta to the uterus and gaining access to the maternal circulation. Sites proposed as routes of CMV infection in utero are numbered 1 to 4.

An Institute of Medicine report placed a vaccine to cytomegalovirus as a high priority for vaccines for the 21st century and various vaccine strategies are being investigated. An alternative intervention therapy, in lieu of a vaccine against HCMV, is the use of antivirals. Licensed antivirals are available for the treatment of transplant and AIDS patients. These drugs act at late stages of the virus life cycle and can lead to the development of resistant strains.  There is an additional risk to the fetus of toxic side effects from extended drug therapy. Importantly, we have recently demonstrated in a novel humanized chimeric animal model that antiviral ganciclovir (the most commonly used HCMV antiviral for transplant patients) will reduce but not prevent congenital infection. Consequently, a vaccine against HCMV would be the best intervention strategy.

Ambergris, Aspergillus and Manganese Nodules.

Article Source ~ Atlas Obscura

According to Christopher Kemp, author of Floating Gold: A Natural (and Unnatural) History of Ambergris, ambergris is formed when the indigestible remnants of the sperm whale’s favorite meal—squid-meets up with a malfunctioning, leaky sphincter between the last of the whale’s four stomachs and its intestine:

Curved like a parrot’s beak, the squids’ [indigestible] beaks pass from the stomach, chafing and irritating the delicate intestinal lining on the way. As a growing mass, they are pushed farther along the intestines and become a tangled indigestible solid, saturated with feces, which begins to obstruct the rectum. It also acts as a dam. Feces builds up behind it. The whale’s gastrointestinal system responds by increasing water absorption from the lower intestines, and gradually the feces saturating the compacted mass of squid beaks becomes like cement, binding the slurry together permanently. It becomes a concentration- a smooth and striated boulder.

This process is thought to occur in about one percent of the world’s 350,000 sperm whales, who roam in every part of the ocean except the very coldest. It has led to the very common mis-assumption that ambergris is “whale vomit.”


Ambergris is, in fact, most likely passed by the living whale, or the last byproduct of the dead whale, floating up from its eaten carcass. Ambergris cut from whales is black and tar-like, with a strong fecal smell. The longer it is in the ocean, the paler, smoother and more fragrant it becomes, shaped by the smells of the sea. The most valuable ambergris is light grey and lightweight, and may be peppered with the black beaks of squids, like so many little sesame seeds.


Ambergris derives from a sperm whale’s intestines.

Cytomegalovirus (CMV) and Congenital CMV Infection

Article Source ~Centers for Disease Control and Prevention

Babies Born with CMV (Congenital CMV Infection)

When a baby is born with cytomegalovirus (CMV) infection, it is called congenital CMV infection. About one out of every 200 babies are born with congenital CMV infection. However, only about one in five babies with congenital CMV infection will be sick from the virus or will have long-term health problems.

Transmission

Women can pass CMV to their baby during pregnancy. The virus in the woman’s blood can cross through the placenta and infect the baby. This can happen when a pregnant woman experiences a first-time infection, a reinfection with a different CMV strain (variety), or a reactivation of a previous infection during pregnancy.

Signs & Symptoms

Most babies with congenital CMV infection never show signs or have health problems. However, some babies may have health problems that are apparent at birth or may develop later during infancy or childhood. Although not fully understood, it is possible for CMV to cause the death of a baby during pregnancy (pregnancy loss).

Some babies may have signs of congenital CMV infection at birth. These signs include

  • Premature birth,
  • Liver, lung and spleen problems,
  • Small size at birth,
  • Small head size, and
  • Seizures.

Some babies with signs of congenital CMV infection at birth may have long-term health problems, such as

Some babies without signs of congenital CMV infection at birth may have hearing loss. Hearing loss may be present at birth or may develop later in babies who passed their newborn hearing test.

Diagnosis

Congenital CMV infection can be diagnosed by testing a newborn baby’s saliva, urine, or blood. Such specimens must be collected for testing within two to three weeks after the baby is born in order to confirm a diagnosis of congenital CMV infection.

Treatment and Management

Medicines, called antivirals, may decrease the risk of health problems and hearing loss in some infected babies who show signs of congenital CMV infection at birth.

Use of antivirals for treating babies with congenital CMV infection who have no signs at birth is not currently recommended.

Babies with congenital CMV infection, with or without signs at birth, should have regular hearing checks.

Regularly follow-up with your baby’s doctor to discuss the care and additional services your child may need.