Alcohol Plus Liver Equals Vinegar

Content Source ~ Wikipedia ~ Disulfiram(Antabuse)

Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to a harmless acetic acid derivative (acetyl coenzyme A).

Cancer Treatment

When disulfiram creates complexes with metals (dithiocarbamate complexes), it is a proteasome inhibitor and can represent a new approach to proteasome inhibition. Clinical trials are recommended. A clinical trial of disulfiram with copper gluconate against liver cancer is being conducted in Utah (ClinicalTrials.gov Identifier: NCT00742911) and a clinical trial of disulfiram as adjuvant against lung cancer is happening in Israel (ClinicalTrials.gov Identifier: NCT00312819).

How Are Hangovers Related To Candida?

Content Source ~

Have you ever noticed that the symptoms of a hangover are similar to those of a Candida overgrowth? Symptoms like brain fog, headaches, nausea, and fatigue are present in both alcohol-induced hangovers and Candida Related Complex.


The common factor that we see in both hangovers and Candida overgrowth is an organic chemical named acetaldehyde. It is actually all around us – there is acetaldehyde in polluted air, tobacco smoke, synthetic fragrances, and many of the foods we eat. However, the amounts that we get from environment exposure alone are pretty low. Acetaldehyde usually only becomes a problem during a Candida overgrowth or when we drink alcohol.

Why does it matter if our levels of acetaldehyde become elevated? For starters, it is a known neurotoxin and possibly carcinogenic. But you’re probably more familiar with the more immediate effects of acetaldehyde – headaches, fatigue, brain fog, and nausea.

In today’s article I’m going to examine how alcohol and Candida can both lead to higher levels of acetaldehyde, and look at what you can do to prevent this from happening.

Alcohol And Acetaldehyde

Higher levels of acetaldehyde are often caused by one of two things – alcohol metabolism and Candida overgrowth. Let’s take a look at the alcohol first.

The metabolism of alcohol is a multi-stage process that happens in your liver. First, the alcohol is oxidized into acetaldehyde by an enzyme named alcohol/dehydrogenase. Second, the acetaldehyde is broken down again into acetic acid, a harmless substance that is ultimately broken down further into carbon dioxide and water.

When this process is running efficiently, the acetaldehyde exists only for a short period of time before being broken down. It doesn’t have any time to circulate through your body and cause unpleasant symptoms like headaches and nausea.

However, when the liver runs out of the substances (like molybdenum) and enzymes that it needs to complete this metabolic process, large amounts of acetaldehyde can remain. This is what happens when you drink too much, and it’s one of the major causes of your hangover.

Candida And Acetaldehyde

Candida overgrowth is another significant contributor to elevated acetaldehyde levels, but through a very different process. If you are suffering from a Candida overgrowth, the Candida colonies in your gut continually produce a number of toxins as metabolic byproducts. Among these toxins are uric acid, ammonia, and (you guessed it) acetaldehyde.

According to a team of researchers looking at the link between Candida overgrowth and Parkinson’s disease, “Patients with chronic polysystemic candidiasis exhibit significantly elevated levels of acetaldehyde in the gastrointestinal (GI) tract. This phenomenon is a direct result of the metabolic processes of the invading organism – Candida albicans.”

Now you can see why many of the same symptoms regularly associated with hangovers (fatigue, nausea etc.) frequently appear in Candida sufferers too. The toxic chemical that contributes to bad hangovers is the very same toxin that is released by the Candida albicans living in your gut.

On a related noted, have you noticed that your hangovers are particularly bad recently? That could be a sign that your liver is overloaded and already coping with the acetaldehyde produced by a Candida overgrowth. After you drink alcohol, your over-stressed liver is simply unable to cope with the extra workload.

Reducing Your Acetaldehyde Levels

Cutting back on your alcohol intake is one sure way to reduce your acetaldehyde levels. You should consider doing this anyway, as part of a healthy, low-inflammatory, low sugar diet. But if you’re suffering from chronic Candida, your body is going to need a little more assistance.

Supplements like molybdenum and milk thistle can help your liver to process the acetaldehyde into acetic acid and remove it more efficiently. This is certainly a useful way to get relief from your symptoms, but it’s only a short-term fix.

To achieve a long-term reduction in your acetaldehyde levels (and relief from those annoying Candida symptoms), you need to attack your Candida overgrowth. As we describe in our Ultimate Candida Diet program, the best way to do this is through a staggered approach that incorporates a low-sugar diet, some natural anti-fungal’s, and a good probiotic. If you regularly suffer from symptoms like fatigue, headaches, and brain fog, an effective Candida treatment plan will offer relief.

Candida Albicans, Cryptococcus Neoformans, and Aspergillus Fumigatus

Content Source ~ Journal of Clinical Microbiology ~ Rare and Emerging Opportunistic Fungal Pathogens

Current clinical management of infections by dimorphic fungal pathogens is limited to azole-class antifungal drugs and amphotericin B. While orally available, the azoles are not without host toxicity issues and the treatment course is lengthy for infections by dimorphic fungi. Development of resistance to azoles is not widespread, although treatment failures due to azole resistance have occurred.106-108 Unfortunately, the better tolerated echinocandin antifungals lack efficacy against the pathogenic-phase of the dimorphic fungal pathogens raising the need for alternative or second-line treatment options. While a number of strides have been made in repurposing existing drugs and development of new inhibitors of fungal growth, careful attention must be paid to challenges posed by dimorphic fungi. As the yeasts/spherules of the dimorphic fungi are the state present within the mammalian host, antimicrobial susceptibilities need to be performed with these pathogenic-phase cells, not the mycelia which has led to erroneous conclusions. Testing of the pathogenic-phase in vitro should follow recently optimized procedures as the CLSI methodology for yeasts is inadequate for the dimorphic fungi. Since yeast cells of the dimorphic fungi reside within host phagocytes, it is also advisable for in vitro tests to be followed with tests on drug effectiveness on intracellular yeasts, at least during initial drug development stages. The overall selectivity of antifungal drug candidates is
critical for progression of drugs through the development pipeline. Structure-guided rational design is one approach that has improved the selectivity of an azole structure (VT-1161). Many of the repurposed drugs have relatively high MICs (greater than 100 ug/mL) questioning their therapeutic utility, however if their selectivity is sufficiently high, formulations may be developed to facilitate
sufficiently high serum and tissue levels. Lower MICs have been found for drugs targeting the folate pathway, an isoniazid-hydrazone derivative, antiretroviral protease inhibitors, and the anti-cancer drug AR-12, all of which are expected to be reasonably well-tolerated by the mammalian host. Novel drugs with good in vitro MICs and good selectivity include thioredoxin-reductase inhibitors, an aminothiazole compound, and nikkomycin Z. Since nikkomycinZ targets an enzyme absent from the host, nikkomycin
has an excellent basis for high selectivity for fungi. In addition, nikkomycin Z has maintained antifungal
effectiveness against multiple dimorphic fungal pathogens in animal models of disease. While the current antifungal armament is limited, there are exciting prospects on the horizon for treating dimorphic fungal infections.

Chronic Granulomatous Disease

Chronic Granulomatous Disease (CGD) is an inherited primary immunodeficiency disease (PIDD) which increases the body’s susceptibility to infections caused by certain bacteria and fungi. Granulomas are masses of immune cells that form at sites of infection or inflammation.

People with CGD are unable to fight off common germs and get very sick from infections that would be mild in healthy people. This is because the presence of CGD makes it difficult for cells called neutrophilsto produce hydrogen peroxide. The immune system requires hydrogen peroxide to fight specific kinds of bacteria and fungi.

These severe infections can include skin or bone infections and abscesses in internal organs (such as the lungs, liver or brain).

Data Source & Further Reading ~ CGD


NIH ~ Chronic Granulomatous Disease ~ Genetics Home Reference

Chronic granulomatous disease is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. Immunodeficiencies are conditions in which the immune system is not able to protect the body from foreign invaders such as bacteria and fungi. Individuals with chronic granulomatous disease may have recurrent bacterial and fungal infections. People with this condition may also have areas of inflammation (granulomas) in various tissues that can result in damage to those tissues. The features of chronic granulomatous disease usually first appear in childhood, although some individuals do not show symptoms until later in life.

Lactic Acid and Cancer. Friends, Foes, or Both Depending?

Content Source ~ Lactic Acid Found to Fuel Tumors


A team of researchers at Duke University Medical Center and the Université catholique de Louvain (UCL) has found that lactic acid is an important energy source for tumor cells. In further experiments, they discovered a new way to destroy the most hard-to-kill, dangerous tumor cells by preventing them from delivering lactic acid.

“We have known for more than 50 years that low-oxygen, or hypoxic, cells cause resistance to radiation therapy,” said senior co-author Mark Dewhirst, DVM, Ph.D., professor of radiation oncology and pathology at Duke. “Over the past 10 years, scientists have found that hypoxic cells are also more aggressive and hard to treat with chemotherapy. The work we have done presents an entirely new way for us to go after them.”

Many tumors have cells that burn fuel for activities in different ways. Tumor cells near blood vessels have adequate oxygen sources and can either burn glucose like normal cells, or lactic acid (lactate). Tumor cells further from vessels are hypoxic and inefficiently burn a lot of glucose to keep going. In turn, they produce lactate as a waste product.

Tumor cells with good oxygen supply actually prefer to burn lactate, which frees up glucose to be used by the less-oxygenated cells. But when the researchers cut off the cells’ ability to use lactate, the hypoxic cells didn’t get as much glucose.

For the dangerous hypoxic cells, “it is glucose or death,” said Pierre Sonveaux, professor in the UCL Unit of Pharmacology & Therapeutics and lead author of the study, published in the Nov. 20 online edition of the Journal of Clinical Investigation. He formerly worked with Dr. Dewhirst at Duke.

The next challenge was to discover how lactate moved into tumor cells. Because lactate recycling exists in exercising muscle to prevent cramps, the researchers imagined that the same molecular machinery could be used by tumor cells.

“We discovered that a transporter protein of muscle origin, MCT1, was also present in respiring tumor cells,” said Dewhirst. The team used chemical inhibitors of MCT1 and cell models in which MCT1 had been deleted to learn its role in delivering lactate.

“We not only proved that MCT1 was important, we formally demonstrated that MCT1 was unique for mediating lactate uptake,” said Professor Olivier Feron of the UCL Unit of Pharmacology & Therapeutics.

Blocking MCT1 did not kill the oxygenated cells, but it nudged their metabolism toward inefficiently burning glucose. Because the glucose was used more abundantly by the better-oxygenated cells, they used up most of the glucose before it could reach the hypoxic cells, which starved while waiting in vain for glucose to arrive.

“This finding is really exciting,” Dewhirst said. “The idea of starving hypoxic cells to death is completely novel.”

Even though hypoxic tumor cells have been identified as a cause of treatment resistance for decades, there has not been a reliable method to kill them. “They are the population of cells that can cause tumor relapse,” said Professor Feron.

A significant advantage of the new strategy is that a new drug does not need to reach hypoxic cells far from blood vessels and it does not need to enter into cells at all – it merely needs to block the transporter molecule that moves the lactose, which is outside of the cells. “This finding will be really important for drug development,” said Sonveaux.

The researchers also showed in mice that radiation therapy along with MCT1 inhibition was effective for killing the remaining tumor cells, those nearest the blood vessels. This proved to be a substantial antitumor approach.

The study was funded by grants from the National Institutes of Health; the Belgian American Educational Foundation (BAEF); from governmental foundations, F.R.S.-FNRS, Communauté française de Belgique and Région wallonne; and the J. Maisin and St. Luc Foundations in Belgium.

Other authors included, from Duke University Medical Center: Thies Schroeder, Melanie C. Wergin, Zahid N. Rabbani, and Kelly M. Kennedy from the Department of Radiation Oncology; Michael J. Kelley, from the Division of Hematology and Medical Oncology; and Miriam L. Wahl from the Department of Pathology. And from the Université catholique de Louvain (UCL), in Brussels, Belgium: Frédérique Végran, Julien Verrax, and Christophe J. De Saedeleer from the Unit of Pharmacology & Therapeutics; and Caroline Diepart, Bénédicte F. Jordan, and Bernard Gallez of the Unit of Biomedical Magnetic Resonance.

Story Source:

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

Alpha Hydroxy Acid and Skin Cancer

Content Source ~ Oncology Training International

Alpha Hydroxy Acid (AHA) is derived from fruit and milk sugars, and it is commonly used to improve sun damaged skin and reduce wrinkles and age spots. AHA is also known under the following names: glycolic acid, lactic acid, citric acid, α-hydroxyoctanoic acid, and α-hydroxydecanoic acid.


The safety of AHA’s was assessed by the Food and Drug Administration (FDA) in the USA who sponsored two studies on this chemical. The studies showed an association between AHA use by:

  • an increase in both the number of sunburn cells on the skin, and
  • UV induced redness

Studies by the cosmetics industry show that AHA increases skin sensitivity to UV radiation. The sensitivity is reversible, and skin regains its original sensitivity approximately a week after use of AHA is stopped. Of course, serious burns occurring on the skin increase the risk for skin cancers in the future.


The Cosmetic Ingredient Review (CIR) expert panel concluded that glycolic and lactic acid are safe for use in cosmetic products at concentrations of 10 percent, “when formulated to avoid increasing sun sensitivity or when directions for use include the daily use of sun protection.” ~ source

asper-linkage-2018.07.15

Tree line ~ wikipedia

Vortex Trees ~ Krummholz

Libidibia coriaria ~ Divi-divi

Oohmycete ~ Wikipedia

Diseases caused by fungal infections ~

The Normal Bacterial Flora of Humans ~ Page 1 of 5


Unusual Fungal and Pseudo-fungal Infections of Humans ~

Root Nodules ~

Effect of addition of citric acid and casein phosphopeptide-amorphous calcium phosphate to a sugar-free chewing gum on enamel remineralization in situ. ~

McMurdo Dry Valleys ~ For Geographical detail.

Love this Tree Line Illustration

By Alexander Keith Johnston(Life time: 28 December 1804 – 9 July 1871) - Original publication: The Physical Atlas of Natural Phenomena: Reduced from the Edition in Imperial Folio for the Use of Colleges, Academies and Families, author Alexander Keith Johnston, publisher W. Blackwood, 1850Immediate source: digitized 2013 for Google Books, original held by University of California https://books.google.com/books?id=UB0-AQAAMAAJ&dq=Alexander+Keith+Johnston+The+physical+atlas&source=gbs_navlinks_s&redir_esc=y, PD-US, https://en.wikipedia.org/w/index.php?curid=56170657

 

 


The tree line is the edge of the habitat at which trees are capable of growing. It is found at high elevations and high latitudes. Beyond the tree line, trees cannot tolerate the environmental conditions (usually cold temperatures or associated lack of available moisture). The tree line is sometimes distinguished from a lower timberline or forest line, which is the line where trees form a forest with a closed canopy.

At the tree line, tree growth is often sparse, stunted, and deformed by wind and cold krummholz(German for “crooked wood”).

The tree line often appears well-defined, but it can be a more gradual transition. Trees grow shorter and often at lower densities as they approach tree line, above which they cease to exist.

Source ~