Omega-3 Foods-[KEY]

~Content Source –

While both omega-3 and omega-6 fatty acids are important to health, the balance of these two types of EFAs in our diet is extremely important. Most experts believe the ratio of omega-6 to omega-3 fatty acids in a healthy diet should be 4-to-1 or lower.

Unfortunately, the typical American diet, characterized by significant amounts of meat and processed foods, tends to contain 10 to 30 times more omega-6 than omega-3 fatty acids. This imbalance of omega-6 (“bad”) fatty acids to omega-3 (“good”) fatty acids appears to be a contributing cause of a number of serious health problems, including heart disease, cancer, asthma, arthritis and depression.

One of the BEST STEPS YOU CAN TAKE to improve your diet is to eat more foods that are rich in omega-3 fatty acids and fewer that are high in omega-6 fatty acids.


Although your body needs both in order to function and thrive, most people take in much more omega-6 fatty acids than omega-3s.

The typical Western diet is estimated to contain as much as 20 times more omega-6s than omega-3s due to high amounts of refined vegetable oils and processed foods. Source: An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity

For reference, the ratio of omega-6s to omega-3s in a traditional hunter-gatherer diet is closer to 1:1.

Further Reading

Source: The importance of a balanced ω-6 to ω-3 ratio in the prevention and management of obesity

Diets high in omega-3 fats have been linked with lower incidences of diabetes, heart disease, dementia and obesity, while diets high in omega-6 fats have been shown to increase the risk of these diseases.

Source: A fish a day, keeps the cardiologist away! – A review of the effect of omega-3 fatty acids in the cardiovascular system

Source – An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity

Source: Dietary omega-3 fatty acids and fish consumption and risk of type 2 diabetes.

Source: The omega-6/omega-3 ratio and dementia or cognitive decline: a systematic review on human studies and biological evidence.

But Why? 2019.08.09

I see statements like the following.

It(Copper) helps maintain a healthy metabolism, promotes strong and healthy bones and ensures your nervous system works properly.

Am I the only one to stop and ask why? Or how this statement can be made without qualification?

These are simply observations of what a body with sufficient levels of copper does.

  1. Maintains a healthy metabolism.
  2. Promotes strong healthy bones.
  3. Ensures peak nervous system performance.

But why?

Because your body uses copper to fight disease in its tissues. If you are deficient in copper it may be because of an underlying issue of disease not yet visible to your senses or immune system.

If your body is chronically battling disease, over time the bodies soft tissues will become filled with calcifications or tumors where disease lost and your immune system entombed it in minerals(calcium). A healthy body has strong bones because it is not constantly having to rob calcium from the bones to entomb diseased tissue.

Peak nervous system performance is realized though the anti-bacterial effects sufficient systemic copper. Certain human pathogens are known to travel along the nervous system pathways causing damage to the nervous system. Even sometimes resulting in disorders of the tissues in the brain resulting in inflammation and calcifications.

And all that thought process from the first few lines of this article.

Strongyloides and its Stranglehold. A Tale of a Tail of a Fleeing Serpent.


Classification: Taxonomic ranks under review (cf. Encyclopedic Reference of Parasitology, 2001, Springer-Verlag)

Metazoa (Animalia) (multicellular eukaryotes, animals)
Nemathelminthes (nematodes)
Secernentea (Phasmidea) (with chemoreceptors known as phasmids)
Rhabditida (early-stage larvae with rhabditiform pharynx)
Rhabdiasoidea (threadworms, parthenogenetic females embedded in mucosa)

Family: Strongyloididae

These slender cylindrical worms have a long oesophagus and uterus intertwined, giving the appearance of a twisted thread, hence their common name of ‘thread-worms’. They are unique amongst nematodes, being capable of both parasitic and free-living reproductive cycles. Only parthenogenetic female worms are parasitic, living in the small intestinal mucosa of various mammals, birds, reptiles and amphibians. Transmission involves a geo-helminth phase, where rhabditiform larvae in the soil form infective filariform larvae which penetrate the skin of their hosts. Sometimes, however, larvae develop into male and female worms which undergo one or more free-living cycles in the soil before producing infective larvae again.Strongyloides stercoralis [this species causes enteritis, Cochin diarrhoea, larval currens in humans]Parasite morphology: The parasite has an unusual developmental cycle involving the formation of eggs, free-living and parasitic larvae, free-living male and female adult worms, as well as parasitic parthenogenetic female worms. Eggs appear as small oval thin-shelled bodies, measuring 50-58µm in length by 30-34µm in width, and are partially embryonated at the 2-8 cell stage of development. Free-living larvae (L1 and L2) measure up to 350µm in length and have a rhabditiform pharynx (with a muscular oesophagus for feeding on particulate material). Infective third-stage larvae (L3) measure up to 600µm in length and have a filariform pharynx (with a long fine oesophagus for sucking fluids after penetrating host tissues). These larvae do not feed in the soil and are ensheathed with a closed mouth and a pointed notched tail. Parasitic worms are all parthenogenetic females, measuring from 2-3mm in length and characterized by the presence of an extremely long filariform pharynx (one third of body length) and a blunt pointed tail. Free-living male and female worms have a rhabditiform pharynx and are smaller in size, measuring up to 1mm in length. Males have two simple spicules and a gubernaculum, and a pointed tail curved ventrally. Females are stout with the vulva located around the middle of the body.

Host range: Thread-worm infections occur in a range of mammalian species throughout the world, particularly in tropical and temperate regions with warmer climates favouring the survival of parasite developmental stages in soil. Different species vary in their host-specificity, the species S. stercoralis being found in humans and companion animals, and thus should be considered zoonotic.

StrongyloidesspeciesHostsLocationClinical signsGeographic distribution

S. stercoralis – humans, primates, dogs, cats. Small intestine, bloody diarrhoea.Worldwide, esp. warmer regions in South America and southeast Asia

S. fuelleborni – apes, humans. small intestine, bloody diarrhoea. Africa, Asia

S. ransomi – pigs, small intestine, bloody diarrhoea. worldwide

S. planicepscatssmall intestinenon-pathogenicworldwide

S. cati (felis)catssmall intestinenon-pathogenicworldwide

S. tumefacienscatslarge intestinesmucosal tumoursworldwide

S. papillosussheep, cattlesmall intestinediarrhoea, anorexiaworldwide

S. westerihorses, donkeys, zebra, pigssmall intestinediarrhoeaworldwide

Site of infection: Parasitic female worms become embedded in the small intestinal mucosa, forming tunnels in the epithelium at the bases of villi in the small intestines. Eggs and first-stage larvae are passed with host faeces. Infective third-stage larvae penetrate the skin and undergo pulmonary migration before forming parthenogenetic females in the intestines.

Pathogenesis: Light thread-worm infections remain asymptomatic, even though they may persist for years due to auto-infection or re-infection. Heavier infections, however, can cause several forms of disease in humans; including dermal, pulmonary, enteric and disseminated disease. Migrating larvae can race through the skin (up to 10 mm per hour) causing larval currens, characterized by urticaria, pruritis, eosinophilia, dermatitis, and inflammation. Pulmonary migration may cause a mild transient pneumonia, with coughing, wheezing, shortness of breath, and transient pulmonary infiltrates (Loeffler’s syndrome). Lesions caused by adult worms generally consist of catarrhal inflammation, although severe infections may result in necrosis and sloughing of the mucosa, haemorrhage, epigastric pain (may mimic peptic ulcer or Crohn’s disease), vomiting, abdominal distention, diarrhoea with voluminous stools and a malabsortion syndrome with dehydration and electrolyte disturbance, peripheral eosinophilia, and possibly reactive arthritis. Hyper-infections can develop when individuals are stressed or immuno-compromised resulting in the production of large numbers of filariform larvae which can penetrate the bowel and disseminate, causing colitis, polymicrobial sepsis, pneumonitis or neurological manifestations, such as meningitis and cerebral or cerebellar abscesses.

Mode of transmission: Even though thread-worms may form parasitic or free-living adults, they all have direct life-cycles involving a geo-helminth phase where infective larvae in soil penetrate the skin of their hosts. Parasitic parthenogenetic females produce partially embryonated eggs (several dozen per day) which hatch prior to excretion with host faeces. The emergent rhabditiform larvae (L1) feed on bacteria and organic debris, moult to second-stage larvae (L2) which feed and then develop either as parasitic or free-living stages. Homogonic strains develop directly into infective third-stage filariform larvae (L3) which can live in moist soil for several weeks. Heterogonic strains moult twice to form a generation of free-living males and females which feed on bacteria with a rhabditiform pharynx before producing unembryonated eggs which grow and moult twice to form infective filariform larvae. All filariform larvae penetrate the skin (or oral mucosa) of their hosts where they enter the circulation. Most larvae are carried to the lungs where they undergo pulmonary migration by penetrating alveoli and moving up the trachea to be swallowed (other routes of larval migration have been shown in experimental animal models). Parthenogenetic female worms parasitize the small intestines and only live for a few months, yet infections can continue indefinitely because hosts undergo self-infection (auto-infection). This occurs when eggs hatch in the intestines and develop into infective larvae which directly penetrate the lower gut or peri-anal region, thus leading to a new cycle of infection. 

Differential diagnosis: Infections are diagnosed by the detection of larvae in faecal samples, as most eggs hatch internally within the host releasing rhabditiform larvae. Filariform larvae may occasionally be detected, especially during hyper-infection, and they can be identified by their notched tails. Although eggs are rarely detected in faeces, they are similar in size, shape and appearance to hook-worm eggs. Faecal culture can increase the sensitivity of microscopic diagnosis, by either concentrating larvae (Harada Mori technique) or amplifying populations through a generation of free-living males and females. Larval cultures also differentiate between thread-worm (Strongyloides) and hook-worm (Ancylostoma and Necator) infections, an important undertaking as treatment options differ (thread-worm larvae have a smaller buccal cavity and a larger genital primordium). Non-nutrient agar plate cultures of faeces have also been used to detect motile larvae. Several immunoserological tests have also been developed to detect host antibodies against thread-worm antigens, but they have difficulty in distinguishing between past and active infections.

Treatment and control: Several anthelmintics are reasonably effective against threadworm infections, but none are entirely satisfactory. Thiabendazole has been widely used but it has unpleasant side-effects, including nausea, vomiting, dizziness, malaise and smelly urine. Albendazole and levamisole have also shown some activity, but infections are not responsive to mebendazole or pyrantel. Treatment should be repeated after a week because of difficulty in confirming cure. Immuno-suppressive treatments should be avoided as they can result in rampant auto-infection. Preventive measures include the wearing of solid shoes in endemic areas, thoroughly washing salad vegetables, prohibiting the use of nightsoil to fertilize gardens, the sanitary disposal of faeces, the provision of latrines in poor areas, and public education campaigns.

Further Reading: Enjoy!!! – SCIENCE.GOV –

Worming in Harmony with Lunar Cycles – Worming, Herbs and Lunar Cycles

The practice of worming horses and farm animals in accordance with the lunar cycles is an old tradition that can offer a surprising degree of success

Did you know you can effectively control parasites with magnetism and the moon? Trust us, it’s not lunacy!

Giddy Up!!!


Friedrich Küchenmeister

From Wikipedia, the free encyclopedia

Gottlieb Heinrich Friedrich Küchenmeister[1] (January 22, 1821, Buchheim (now Bad Lausick) – April 13, 1890 Dresden) was a German physician.


Küchenmeister studied medicine in Leipzig and Prague, and in 1846 became a general practitioner in Zittau. In 1847 he married, and in 1856 he moved to Dresden. He conducted research on tapeworms, trichinosis, and other parasites and wrote about it several works. He was also publisher of the Allgemeine Zeitschrift für Epidemiologie(General Journal of Epidemiology). In 1852, his theory that bladder-worms are juvenile tapeworms gained the attention of the medical profession.[2][3] In the later 1850s, he carried out an experiment demonstrating this by feeding pork containing cysticerci of Taenia solium to prisoners awaiting execution, and after they had been executed, he recovered the developing and adult tapeworms in their intestines.[4][5][6] By the middle of the 19th century, it was established that cysticercosis was caused by the ingestion of the eggs of T. solium.[7]

Küchenmeister was an advocate of cremation, as he saw the risk of soil contamination in the putrefaction and decomposition products that occur after burial.[8] In Dresden, he founded the group The Urn: Association for Facultative Cremation. In 1876, he took part in the first European Congress of the Friends of Cremation, also in Dresden.[9]

Unusual variants of mycosis fungoides

~Content Source

Conventional presentations of mycosis fungoides may be diagnostically challenging, particularly in light of the controversial boundaries defining the disease. Variant presentations of this cutaneous T-cell lymphoma add a further layer of complexity, requiring a sophisticated and informed perspective when evaluating lymphoid infiltrates in the skin. Herein we discuss well-defined (WHO-EORTC) variants pagetoid reticulosis, granulomatous slack skin and folliculotropic mycosis fungoides as well as less well-defined morphologic/architectural variants, and divergent immunohistochemical presentations of this typically indolent T-cell lymphoproliferative disease.

~Read More at the Fungal Underground


Thujone/Wormwood – Dr.Axe

Dirofilariasis FAQs

Mabendazole-Antacid – Warts, Tumors and Worms; OH MY.

Human and Animal Dirofilariasis: the Emergence of a Zoonotic Mosaic

Metformin—used worldwide to reduce hyperglycemia and hyperinsulinemia in diabetics—is one such medication that mimics caloric restriction across animal phyla and prolongs life in rodents and nematodes. <–THIS FRIGHTENS ME TO NO END!!!

Heartburn drug cure.

Q: We gave our 6-year-old daughter a heartburn medicine, cimetidine, for her warts. It’s amazing! She had up to 40 warts, and they were starting to spread to her wrist and other hand. Finally, we gave her cimetidine daily for eight weeks, and they just disappeared.

A: The cimetidine (Tagamet) “cure” for warts was first written about in the early 1990s. This was an unusual use; Tagamet was a popular prescription drug for ulcers at that time.

Since then, studies have tested such acid-suppressing drugs against warts. Although some research subjects had a good response like your daughter, most of the well-controlled trials showed no benefit over placebo (Annals of Pharmacotherapy, July/August 2007).

See More~ Prilosec or Nexium and Cancer?

What If’s-2018-03-31

What if…Something as simple as Prilosec or Nexium could aid in disrupting the lifecycle of cancer? Imagine that. An over the counter antacid used in an off-label manner leading to countless spontaneous remissions of various types of cancers.

I think I have connected those dots and I’m not the only one. Yay…

Utilization of omeprazole to augment subtherapeutic voriconazole concentrations for treatment of Aspergillus infections.

Mycosis fungoides responding to systemic itraconazole.

Repositioning of proton pump inhibitors in cancer therapy.

ASPERGILLUS TREATMENT: Black Mold-Utilization of omeprazole to augment subtherapeutic voriconazole concentrations for treatment of Aspergillus infections.

What If’s-2018-03-01

Happy March 2019-

What if…Bio-scenario_001-Life begins at conception and ends once decomposition ends.

What if…Cancer is a part of that biological process, a molecular bio-remediation tool used that has remote switching by the hosts immune system but no off switch. These cancers are proteins who’s DNA can be disrupted and modified.

The reason there is no off switch is because there is no need for one. These are the clean up crew that is activated upon chemical signaling caused by host death. Why would a Consumer, designed to do just that need an off switch? These cells that the cancer consume already had that function built in called apoptosis.

On occasion a host is resuscitated after the host death message is sent. The problem now being that the host is alive again but with cancer crew having already been activated.

These cancer cells once activated are set to consume the host and will continue to do so until disrupted and eradicated or until all host tissue has been consumed.

On their own each of these cells, even at post invasion levels can be overcome by the hosts immune system if it is functioning at a minimum of 90% capacity. If host immunity is below 80% full scale colonization can begin.

More to come…

…What triggers initial colonization of what will eventually become identified as a problematic cancer in the future. A tumor?

…Mary, Jesus, spot & blemish?

…3rd Trimester, Goal Posts and immune system autonomy between mother and child.

…how far back can we go with cleansing diets and digestive enzymes on full tilt?

Looking again…At the skin as an atmosphere for our body. The subcutaneous layer of our skin being equivalent to soil on Earth. Where do we make changes to our outermost layer of skin?