Category: Health Tips

(From a post on Facebook.)

Here’s what I’ve learned after more ticks than I care to count.

First, whatever your uncle told you, forget it. No matches. No nail polish. No Vaseline. No soap on a cotton ball. All of those do the same terrible thing, they stress the tick out, and a stressed tick empties its gut back into the bite before letting go. Which, if you think about what that actually means for a second, is literally how Lyme and the rest get transmitted so you’re not speeding up its exit. You’re making it throw up into you.

Fine-tipped tweezers. Grip right where the mouthparts enter the skin, not the body, the head. Pull straight up, steady, no twisting, no jerking. It’ll feel like it’s resisting because it is, the mouthparts are barbed. Just keep the pressure on and it lets go in a few seconds. If a piece breaks off in the skin, leave it alone. Your body pushes splinters out. Digging around with a needle does more damage then the fragment ever would.

Clean it with alcohol or soap. Wash your hands.

Now here’s the part most people skip: don’t flush the tick.

Tape it to an index card. Clear packing tape right over the body, write the date and where on your body it was, and stick the card in a drawer. If you come down with anything weird in the next 30 days, rash, fever, joint pain, that flu-that-isn’t-flu feeling, that tick goes with you to the doctor. Some labs will test the tick itself, which is faster and often more reliable than waiting for antibodies to show up in your own blood. A dated tick taped to a card is one of the most useful things you can hand a doctor who’s trying to figure out what’s wrong with you.

The other thing worth saying out loud: if the tick was engorged when you pulled it, and you can’t swear it was off your body within 24 hours, call your doctor that same day. Don’t wait for a rash. Fewer than three out of four Lyme cases even produce the classic bullseye. A single preventive dose of doxycycline within 72 hours of a deer tick bite cuts the Lyme odds way down, and most docs in tick country will write that prescription without giving you a hard time, especially if you walk in with the tick taped to a card and a clear timeline.

In 1974, a research team at the National Institutes of Health published a quiet observation that should have rewritten clinical gastroenterology. The cells lining the human small intestine — called enterocytes — are among the most metabolically active cells in the entire body. They turn over completely every three to five days. They regenerate constantly, faster than any other tissue except bone marrow. And they have one unusual property no other cell type shares: their primary metabolic fuel is not glucose. It is the amino acid L-glutamine.

This was confirmed in animal studies, then human surgical patients, then bone marrow transplant recipients whose gut barriers had been destroyed by chemotherapy. Every time, the same finding: when L-glutamine was supplemented, gut barrier integrity restored measurably. When it was withheld, the gut lining thinned and leaked.

For five decades, this research has remained quietly accumulating in surgical, oncological, and critical care literature. Yet mainstream gastroenterology continued to dismiss “leaky gut” — the popular term for intestinal hyperpermeability — as a pseudoscience marketing concept. Functional medicine practitioners who acknowledged the science were dismissed as unscientific. The pharmaceutical industry built no drugs around the L-glutamine pathway because the molecule is endogenous and unpatentable.

Meanwhile, the same intestinal permeability that mainstream medicine refused to name began to be reluctantly acknowledged under the more clinical label “increased intestinal permeability” and its connection documented to autoimmune disease, food sensitivity, chronic inflammation, brain fog, joint pain, skin disorders, and even depression through the gut-brain axis.

L-glutamine acts on three independent pathways simultaneously. It is the direct fuel source for enterocyte ATP production — the cellular energy required for active tight junction protein synthesis. It is a substrate for glutathione production — the body’s primary antioxidant defense that protects intestinal cells from oxidative damage. And it directly upregulates the expression of claudin and occludin proteins — the structural proteins that physically clamp adjacent enterocytes together to form the tight junction barrier.

Without sufficient L-glutamine, all three pathways collapse together. The intestinal lining cannot generate the energy to maintain itself, cannot defend against oxidative damage, and cannot synthesize the structural proteins of the barrier. The gut leaks. Endotoxins enter the bloodstream. Systemic inflammation rises.

Hospital pharmacies stock IV L-glutamine for burn patients, surgical recovery patients, and chemotherapy-induced gut damage. Functional medicine clinics use oral L-glutamine for autoimmune protocols, food sensitivity reversal, and post-antibiotic recovery. The data is identical. The institutional acceptance is not.

Rebuild the gut wall:

– The 5g / Twice Daily Floor: Therapeutic oral L-glutamine starts at 5 grams twice daily — taken on an empty stomach in 8 oz of water. Lower doses produce maintenance effect; serious gut barrier repair requires the higher window. Some clinical protocols extend to 10 g twice daily for acute autoimmune flare-ups.

– The Empty Stomach Rule: L-glutamine competes with other amino acids for intestinal absorption. Take it 30 minutes before meals or 2 hours after, with nothing but water. Mixing with protein meals dilutes the targeted delivery to enterocytes.

– The Zinc Carnosine + Slippery Elm Stack: The fastest gut barrier repair protocol combines 5 g L-glutamine + 75 mg zinc carnosine + 1 teaspoon slippery elm bark powder, taken twice daily for 8-12 weeks. This is the protocol used in integrative gastroenterology clinics in Sydney and Vienna. It outperforms PPI medications for symptom relief and addresses the underlying barrier defect rather than suppressing acid.

Journal of Parenteral and Enteral Nutrition. “Glutamine metabolism and the gastrointestinal tract”.

Annals of Surgery. “Glutamine supplementation in critically ill patients: clinical trials and outcomes”.

Across medieval Europe, from the British Isles to the Carpathian mountains, village bone-setters used a single plant to repair fractured limbs and crushed skulls. They called it “knitbone,” “boneset,” or “bruisewort.” In Latin its name was Symphytum officinale — comfrey. Greek physician Dioscorides documented it in the first century AD. Roman legion field medics carried it in dried form to set the broken bones of soldiers in distant campaigns. For nearly two thousand years, every culture in Europe agreed: comfrey didn’t just speed up bone healing — it visibly forced fractured bones to fuse.

In 1962, agricultural chemists isolated the active compound and named it allantoin. They discovered something that should have rewritten orthopedic medicine: allantoin is one of the most potent natural cell-proliferative agents ever identified.

When a human bone fractures, a structure called the periosteum (the bone’s outer skin) is responsible for triggering the healing cascade. Dormant osteoblast cells embedded in this layer must wake up, divide, and start secreting a calcium-phosphate scaffold across the gap. This scaffold is called the bone callus. Without a strong callus, the bone never fuses properly — and the orthopedic surgeon is forced to install titanium plates and screws.

Allantoin acts as a direct mitogen on osteoblasts. When applied topically over a fracture or ingested as a tea (controversial, see below), the molecule diffuses into the periosteum and tells osteoblast cells to begin dividing immediately. Studies measured a 30 to 50 percent acceleration in callus formation in comfrey-treated fractures compared to controls. Pediatric orthopedic clinics in Germany still recognize comfrey ointment as an evidence-based adjunct after pediatric fractures.

So why did comfrey nearly disappear from American pharmacies? Because in the 1970s, internal use of comfrey root in massive long-term doses was linked to liver damage from pyrrolizidine alkaloids. Regulators panicked and recommended a near-total ban, even though those alkaloids exist in trace amounts in the leaves and are virtually absent in topical preparations. The bone-setting tradition collapsed in a single decade.

Activate the periosteum:

– Topical Only, Not Internal: Apply comfrey as a poultice, salve, or pharmaceutical-grade ointment directly over the skin near the fracture site. Do not consume comfrey root tea — this is the part where the alkaloid risk concentrates. Leaves are safer, but topical use eliminates the concern entirely.

– The 10-Day Window: Comfrey accelerates the early phase of bone healing — the callus-formation phase that happens during days 4 through 21 after fracture. Apply twice daily during this window for measurable acceleration.

– The Mandatory Co-Factor: Allantoin builds the scaffold, but the scaffold must be filled with calcium phosphate. Supplement with 5,000 IU vitamin D3 plus 200 mcg K2-MK7 daily during recovery to ensure your osteoblasts have the raw mineral substrate to lay down on the comfrey-accelerated matrix.

Sources:

Phytotherapy Research. “Efficacy of a Symphytum officinale extract in the treatment of upper or lower back pain”.

Journal of Wound Care. “Comfrey extract topical application in fracture and contusion healing.”

What determines human strength? Is it training, environment, genetics — or a combination of all three? In this video, we explore the controversial scientific discussions surrounding strength genetics across different human populations and what researchers have discovered about muscle composition, endurance, athletic performance, and evolutionary adaptation.

View Video: https://www.youtube.com/watch?v=tRH4rdDFBGA

Misdiagnosed and drugged, the true story of Leonard Lawrence

Story by CCHR United Kingdom

Leonard Lawrence was a fully fit and experienced commercial/airline pilot. He had been working for British Aerospace since 1989 when he experienced and recorded his first ’fume event’ – the presence in a plane’s onboard air system of toxins. In the most serious cases, these toxins contain organophosphates identical to those responsible for deaths and brain damage among agricultural workers. Research was conducted on behalf of the United States Air Force and early warnings were given in 1955 of the neurological dangers of aircraft cabin bleed air.

On the 29th of November 1991, just as his aircraft reached take-off speed, the flight deck filled with hot acrid fumes that were so dense it was impossible to see the instruments and controls and impossible to breathe.

Both Len and his captain were blinded by the fumes as, their eyes and skin burning, their aircraft began to ascend at over 160 mph. Only willpower and long experience enabled the captain to feel his way among the array of instruments for the ’dump valve’ control, which would evacuate the contaminated air from the aircraft engines.

The incident was over in about fifteen seconds, and both pilots soon regained their eyesight, enabling them to commence emergency mayday procedures with Air Traffic Control and safely achieve an emergency forced landing.

This was by no means an isolated experience, as evidenced by the fact that British Aerospace and others later entered into a secret settlement agreement regarding aircraft fumes. In the course of an Australian senate inquiry in 1999, a spokesman for British Aerospace admitted: ’There is absolutely no doubt in our minds that there is a general health issue here. The number of people who have symptoms indicates that there is a general issue. With the weight of human evidence and suffering, which is quite clear, there must be something there.’

Len himself experienced a series of these events, the last in 2004, when he was co-pilot to a recently-retired Civil Aviation Authority flight operation inspector.

Len recalls that he and the captain were aware of an oily smell. What followed was and remains a blank. The plane had descended to five hundred feet above Amsterdam – not aligned to any runway – before they pull out of the descent and return to the correct flight path.

Both men were still suffering from mental confusion, and this time it didn’t go away.

The next day they were flying together again when they received an instruction from Swiss Air Traffic Control to re-route their London bound flight. ’Both the captain and Len were unable to process the information being given,’ says Len. ’That was my last ever flight before I resigned. I could not, and indeed still cannot, think clearly enough to fly.’

Having helped to avert a number of potential disasters caused by the ongoing mechanical fault and the airlines’ failure to fit air quality sensors to their aircraft, Len selflessly retired when he felt he was no longer safe to fly. It might be thought that his employers owed him some respect and appropriate treatment for the damage he had sustained in their employ.

Instead, Len was sent to a psychiatrist, who ignored both the symptoms and the chain of causation, declaring Len to be ’mentally ill’ and in need of pharmaceutical drugs.

There was no mystery about the real causes of Len’s problems. As the Australian Senate enquiry had been told five years previously, ’The source of the odours has been identified as primarily Mobil Jet Oil II leaking past oil seals in the engines and or APU unit (Auxiliary Power Unit) into the air conditioning system.’

In the case of organophosphate poisoning, the psychiatrist’s action was not merely one of standard incompetence and drug pushing. It is recognised that pharmaceutical drugs are inclined to react with the existing toxins to cause cell damage and develop even more poisonous compounds, so are the last thing that should be prescribed.

As a ’mental case’, Len was held by the Official Solicitor to the Senior Courts and medicated with psychiatric medication until he lost mental capacity. Multiple Court of Protection, Medical Certicare’s, were issued to protect Len, but these multiple Court of Protection, Medical Certificates were never disclosed to the Court of Protection by the Official Solicitor and others.

Len was held for more than a year, during which time, to add insult to injury, his assets, savings and home were disposed of illegally by barristers and solicitors without the knowledge of the Court of Protection.

Having lost his home and his marriage the British Airline Pilots’ Association came to his rescue, by-passing the Official Solicitor and referred Len to the Civil Aviation Authority’s psychiatric advisor, Professor Gordon Turnbull FRCP, FRCPsych, RAF (Rtd) who immediately took Len off the drugs and arranged for him to receive long overdue specialist treatment for organophosphate poisoning.

Len Lawrence is clearly a survivor. He has lived through industrial poisonings, multiple losses, corporate and official obstruction and efforts by psychiatrists to suppress and silence him. Not only is he still with us, but he continues to fight for the exposure of cover ups and crooked deals that affect us all.

Black seed oil from Nigella.

Watch video: https://www.facebook.com/share/r/1AbTDxMbdh/

A University of Kentucky epidemiologist convinced 678 Catholic nuns to donate their brains and their entire life records to science, and the autopsies he performed quietly rewrote everything modern medicine thought it knew about Alzheimer’s disease.

The findings have been published in JAMA and the New England Journal of Medicine.

Almost nobody outside the field of neurology has heard of them.

His name was David Snowdon.

He was a young epidemiologist at the University of Minnesota in 1986 when he had what most of his colleagues considered a crazy idea. He wanted to study Alzheimer’s disease the way it had never been studied before. Not through brain scans of confused 80-year-olds in a hospital. Not through self-reported family histories. He wanted to find a group of people whose entire lives were on paper, from their twenties to their deathbeds, and then look inside their brains after they died and see what the autopsies actually showed.

He chose 678 Catholic sisters from the School Sisters of Notre Dame congregation.

The choice was not random. Nuns lived almost identical lifestyles. Same diet. Same housing. Same daily schedule. Same medical care. No smoking. No drinking. No pregnancies confounding the hormonal data. They were, statistically speaking, the cleanest research population on Earth. And they had something no other study population had ever offered.

Their entire lives were already documented. Every nun in the order had written a one-to-two-page autobiography in her early twenties, before taking her final vows. The essays had been sitting in convent archives for 60 years, untouched, waiting to be discovered.

Then Snowdon did the part most researchers would never have agreed to. He asked the nuns, in person, one at a time, if they would donate their brains to science after they died.

They said yes. All of them.

The study ran for over 25 years. Annual cognitive tests. Annual physical exams. Detailed medical records. And at the moment of death, every single brain was carefully removed and analyzed under a microscope.

The findings broke modern neuroscience.

The first thing the autopsies showed was that many of the nuns had brains riddled with the classic plaques and tangles of full-blown Alzheimer’s disease. Severe damage. The kind of damage that, in any other patient, would have produced complete dementia.

But while they were alive, these particular nuns had shown no symptoms at all. They had stayed sharp until the day they died. They had taught classes. They had run errands. They had recognized everyone. Their brains were destroyed. Their minds were intact.

Something was protecting them that nobody had ever measured before.

Snowdon called it cognitive reserve. The brain, he argued, can absorb extraordinary amounts of damage without showing symptoms, as long as it has been built thick enough beforehand. The nuns who stayed sharp had brains that had been so well-developed over a lifetime of learning, teaching, reading, and thinking that they could afford to lose huge sections of tissue and still keep functioning.

Then he found the second thing. The one that made the study famous.

He pulled the autobiographies out of the archives. The essays written by the same nuns 60 years earlier, when they were 22 years old.

He measured a single linguistic feature called idea density. How many distinct ideas a writer packed into each ten words of prose. Not vocabulary. Not grammar. Not style. Just the raw informational compression of a young mind.

The result was so clean it should be illegal to ignore.

The nuns who had the lowest idea density at age 22 were 59 times more likely to develop Alzheimer’s by age 85 than the nuns who had the highest idea density. Snowdon could predict with roughly 80 to 90 percent accuracy who would develop dementia 60 years before it happened, from a single essay written before the woman had even taken her vows.

The detail that should disturb every adult reading this is what happened when the researchers controlled for the obvious objections.

When they controlled for education, the effect held.

When they controlled for occupation, the effect held.

When they controlled for the age at which the nun entered the convent, the effect held.

The cognitive complexity of the 22-year-old mind, measured in a single autobiographical paragraph, was a stronger predictor of Alzheimer’s six decades later than any other variable Snowdon could find.

Then he ran the second analysis. The one that almost nobody quotes.

He measured the emotional tone of the same autobiographies. The frequency of positive words like joy, gratitude, hope, love, contentment. The nuns who wrote about their lives in positive emotional terms at age 22 lived an average of 10.7 years longer than the nuns who wrote in neutral or negative terms.

Same convent. Same diet. Same medical care. Same prayer schedule.

The lifespan was being shaped by something invisible. Something that had been written down before the nun had any way of knowing it would matter.

The paper landed in JAMA in 1996. It has been cited thousands of times since. Almost no one outside academic neurology has heard of it.

The reason most people resist this finding is that it sounds like a sentence handed down before adulthood even began. If the architecture of your old-age brain is being built by what you do with your mind in your twenties, and your emotional resilience is being calibrated by the words you use about your own life, then your eighties are being shaped right now by patterns you cannot even feel yourself making.

Snowdon argued the opposite. He said the data showed cognitive reserve could be built throughout life. The nuns who continued to learn languages, teach courses, read difficult books, and engage in complex conversations in their 60s and 70s also showed slower decline. The brain does not stop responding to mental work just because you got older. It only stops responding when you stop asking anything of it.

The most uncomfortable part of the research is the contrast Snowdon repeatedly emphasized.

Two nuns could have identical brain damage on autopsy. Identical plaques. Identical tangles. Identical genetics. One would have lived her last years confused, frightened, and lost. The other would have lived her last years lucid, joyful, and intact. The only meaningful difference between them was the depth of the cognitive and emotional architecture each had built across the decades before the damage arrived.

The brain you will have at 85 is being constructed right now by the books you choose not to read, the conversations you choose not to have, and the words you choose to use about your own life.

The dementia that arrives at 80 is not a verdict. It is the bill for a structure you either built or did not build between 22 and 60.

Almost nobody walks through the window because almost nobody knows it is open.

You can be the one who does.

https://x.com/sukh_saroy/status/2058493903637266440?s=20