Category: General Interest

(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.”