Dear All Who Care,
I am writing to you today with a frustrating and heartbreaking update regarding the investigation into the death of my father, Peter Yu. As you know, he was left unmonitored for 72 hours at North York General Hospital despite a cardiac emergency.
We relied on the College of Physicians and Surgeons of Ontario (CPSO)—the public regulator—to hold the doctors accountable. Instead, they are using a legal loophole to shut our family out of the process.
Today, the CPSO investigator officially told me that she will not allow me to see the doctors' written excuses or explanations for what happened during those 72 hours. She claimed it is "not their process" to show the family this evidence before they make a decision.
What is really happening:
The CPSO is using a bureaucratic trick (known as a "Section 75" investigation) to downgrade me from a legal "complainant" to a mere "witness." By doing this, they can run the investigation behind closed doors, keep the doctors' defenses a secret, and completely strip my family of our right to appeal their final decision to an independent judge.
They are protecting the hospital and the doctors from public scrutiny.
I am fighting back. Today, I issued a formal legal demand to the CPSO leadership, and I have escalated this matter to the office of our local MPP and the Health Critic.
Please share this update on your social media (Twitter/X, Facebook, Threads, etc) so the public sees how the CPSO operates in secret.
I will not let my father’s death be swept under the rug by a system designed to protect itself. Thank you for standing with my family. I will keep you updated.
With gratitude,
Kenny Yu.
She ate lunch alone for 730 days straight. What this 16-year-old built from that pain now protects millions of kids worldwide.
Seventh grade. Natalie Hampton carried her tray through a packed cafeteria and felt it — that specific, suffocating dread of not knowing where to go.
She'd already learned what happened when you approached the wrong table. The silence. The turned backs. The whispered laughter that followed you all the way to the empty table by the wall.
The one everyone could see.
The one that said: nobody wants her.
For two full years — 730 consecutive lunches — that table was hers. Alone.
The bullying went further than whispers. She was shoved into lockers. Four physical attacks in two weeks. She came home with scratches and bruises. When she finally reported it, school administrators sent her to counseling — to find out what she was doing wrong.
The isolation grew so heavy she was hospitalized for anxiety.
Then ninth grade came. A new school. And almost overnight — everything changed. Students welcomed her. She made friends within weeks. She finally knew what safe felt like.
But she couldn't stop thinking about the kids still sitting at the wall table. Right now. Today.
She remembered what she'd needed most during all those lunches. Not a teacher. Not a pamphlet. Just one person saying: "You can sit with us."
So at 16 — with zero coding experience and "a lot of enthusiasm," as she put it — Natalie built exactly that.
She called it Sit With Us.
The idea was simple and genius: students sign up as "ambassadors," keeping their table open. Other kids privately browse available tables on their phones before ever walking into the cafeteria — and show up knowing they're already welcome.
No public rejection. No moment of judgment. Just a guaranteed seat.
Within 7 days of launching: 10,000 downloads.
Then the world found her. NPR. The Washington Post. CBS News. Messages from Morocco, Australia, the Philippines, France — kids who'd been eating alone for years, finally finding a place to belong.
Sit With Us now operates in 30 countries.
"Even if it helps one person," Natalie said quietly, "it was worth building."
She turned 730 lunches of loneliness into a lifeline for millions.
That's not just survival. That's transformation.
🔻 PROJECT GENESIS — THE CURE THEY BURIED FOR 63 YEARS.
November 12, 1961.
Three weeks before his assassination, Kennedy signed Executive Order 11063. The public version was about housing.
The classified annex — declassified by Trump, January 31, 2026 — authorized PROJECT GENESIS.
A covert program inside underground military bases to test Tesla's most dangerous claim:
That the human body can be healed — and DNA regenerated — using electromagnetic frequencies alone.
No drugs. No surgery. No Big Pharma.
⚡ WHAT THEY FOUND
Between 1962 and 1971, scientists at Fort Detrick and Dulce Base ran 4,291 classified experiments.
528 Hz — DNA strands repaired themselves within 72 hours.
7.83 Hz (Schumann Resonance) — cancer cells stopped dividing.
963 Hz — stem cell production increased by 317%.
Dr. Royal Rife proved this in 1934. He destroyed cancer using targeted frequencies. The AMA shut him down. His lab burned. Research seized.
Tesla wrote in 1899:
_"If you want to find the secrets of the universe, think in terms of energy, frequency and vibration."_
Kennedy wanted to give this to the people.
12 days later, he was dead.
🔻 WHO KILLED PROJECT GENESIS
After Dallas, Johnson transferred Genesis research to a CIA-pharmaceutical board.
— Allen Dulles (CIA Director Kennedy FIRED)
— George H.W. Bush (CIA asset)
— Pfizer, Merck, and J&J representatives
They didn't destroy the research. They weaponized it.
MKUltra used the same frequencies — not to heal, but to control. The cure for cancer repurposed to break minds.
For 60 years, Big Pharma spent $4.7 trillion keeping you sick. Every pill, every "incurable" diagnosis — a lie to keep you dependent.
They knew frequencies could heal Alzheimer's. They buried it.
They knew frequencies could reverse diabetes. They classified it.
They knew frequencies could regenerate tissue. They made it a felony.
⚡ THEN TRUMP OPENED THE VAULT
January 31, 2026.
Among 3 million pages — 1,247 pages of Project Genesis.
The frequencies. The protocols. The results.
Everything Kennedy died for.
Everything Tesla was silenced for.
Everything Rife was destroyed for.
Now public.
A 2019 Pentagon memo confirms MedBed technology — frequency-based cellular regeneration — operational in military hospitals since 2014.
Walter Reed. Bethesda. Ramstein.
Generals healed in days from injuries that cripple civilians for life.
They had the cure. Used it on themselves. Denied it to you.
🔻 THE WALL IS BREAKING
Trump's TrumpRX initiative — same frequencies, same technology — now available to patriots.
Not because they wanted to release it.
Because they can no longer hide it.
Kennedy started it. Tesla dreamed it. Trump delivered it.
⟁ Your body was designed to heal itself. They made sure you'd never know.
Empaths and highly sensitive people feel everything at a much deeper level. We don't just experience your surface-level emotions – we also notice your energy shifts, intentions, judgments, truths... and bullsh*t.
Here is my updated my patient information handout on thyroid disorders, including considerations for optimal treatment.
The Thyroid Gland: Function, Assessment, and Treatment
Thyroid Hormone Regulation
The release of thyroid hormones is regulated by the pituitary gland, a small structure located on the underside of the brain. When the brain detects insufficient thyroid hormone levels, it signals the pituitary to secrete thyroid-stimulating hormone (TSH). TSH then stimulates the thyroid gland in the neck to produce and release two main forms of thyroid hormone: thyroxine (T4) and triiodothyronine (T3).
Symptoms of Hypothyroidism
Hypothyroidism (underactive thyroid) often presents with fatigue, unexplained weight gain, cold intolerance, dry skin and hair loss, constipation, muscle/joint pain, puffy face, elevated cholesterol levels, depression, and neck swelling from goiter.
Symptoms of Hashimoto's Thyroiditis
Hashimoto's, an autoimmune cause of hypothyroidism, shares these symptoms but may include transient hyperthyroid phases (anxiety, rapid heartbeat, tremors) early on, as the immune attack releases stored hormones before gland destruction sets in.
Understanding T3 and T4
T4 is the primary hormone secreted by the thyroid gland (about 80-90% of total output) and serves as a precursor or "prohormone." It is largely inactive and must be converted to T3, the biologically active form, to exert effects on the body. The thyroid produces only 10-20% T3 directly; the majority (80%) is generated peripherally in tissues like the liver, kidneys, and muscles via deiodinase enzymes. All symptoms of hypothyroidism (underactive thyroid) stem from insufficient T3 activity, not T4 levels alone.
Factors Impairing T4 to T3 Conversion
Conversion relies on deiodinase enzymes (D1/D2), which can be inhibited, leading to low T3 despite a normal T4. Common factors which may be considered include:
Nutritional deficiencies: Selenium, zinc, or iodine** (cofactors for deiodinases).
Medications: Amiodarone, beta-blockers, corticosteroids.
Toxins: Heavy metals (e.g., mercury, lead, arsenic, cadmium).
Chronic inflammation: Linked to autoimmune diseases or infections; elevates reverse T3 (inactive form).
Sleep deprivation: Often tied to inflammation.
** While iodine is necessary for thyroid function, high iodine intake can paradoxically induce hypothyroidism through a protective mechanism called the Wolff-Chaikoff effect. Excess iodide inhibits thyroid peroxidase (TPO), an enzyme involved in the production of thyroid hormones (T4 and T3). In healthy individuals, this is usually only transient (24-48 hours), however in some patients, symptoms of underactive thyroid may last for 2-3 weeks. The risk of this occurring is increased in those with autoimmune thyroid conditions like Hashimoto’s disease.The recommended upper limit of intake for iodine is 1,100mcg, which is a little less than ½ a drop of Lugol’s 2% iodine. Doses may need to be higher in those with absorption issues, which are commonly associated with thyroid disease. Urine iodine testing is the most accurate way of assessing iodine levels. Skin patch testing is unreliable and not recommended.
Assessing Thyroid Function: The Limitations of TSH
Many clinicians rely soley on TSH as the primary screening tool for thyroid function, with a low TSH generally thought to indicate adequate thyroid hormone activity. Elevated TSH indicates the pituitary is compensating for low thyroid hormone output, signaling hypothyroidism (many people incorrectly a low TSH indicates an underactive thyroid gland).
Reference ranges for TSH (typically 0.4-4.0 mIU/L) are somewhat arbitrary and often overlap with subclinical hypothyroidism. These TSH ranges have also been used to set T3 + T4 cutoffs, limiting the clinical utility of these reference intervals.
-Problems higher up in the brain (hypothalamus) or within the pituitary can both cause low TSH, making TSH alone unable to detect these disorders.
-Impaired T4 to T3 conversion may yield normal/low TSH (as T4 can signal to the hypothalamus/pituitary that thyroid hormone levels are sufficient). Thus T4 can lower TSH even when not being adequately converted into T3.
-Treatment with thyroid hormone tends to result in increased suppression of TSH levels compared to actual thyroid hormone activity. That is, symptoms of an underactive thyroid are still common even though TSH levels may suggest sufficient thyroid activity. This suppression of TSH may be moderated through the use of sustained release T3, which results in more stable levels with reduced peak levels.
Research supports serum free T3 as the single most reliable marker of thyroid activity.
The Role of Cortisol
Cortisol influences thyroid function bidirectionally.:
Low cortisol: Common in Hashimoto's/Graves'; impairs T3 receptor binding (thyroid resistance), reducing response to therapy.
-T3 supplementation can boost ACTH leading to increased cortisol release.
-Preliminary testing via ACTH/cortisol; trial hydrocortisone if symptoms persist on T3.
-Initiating thyroid therapy may accelerate cortisol metabolism, leading to a paradoxical deficiency. Consider this if there is an increase in symptoms on initiating thyroid hormone therapy.
High cortisol: Inhibits deiodinases, impairing activation of T4 to T3 (favours production of rT3 -inactive T3).
Thyroid Hormone Supplementation
Supplementation options include:
-T4 monotherapy (such as levothyroxine): Most common; long half-life (~7 days) allows daily or weekly dosing. However, unreliable conversion to T3 can limit efficacy.
-T3 supplementation (such as liothyronine): Short half-life (~1 day) requires twice daily dosing; consideration may be given to sustained release preparations if ongoing symptoms or cardiac risk factors. T3 is ~3.5 times more potent than T4.
-Combination therapy (T4 + T3): May be synthetic or bio-identical (natural desiccated thyroid NDT from porcine glands) provide a fixed ratio (~4:1 of T4/T3). When given in synthetic form, ratios of T4/T3 tend to be closer to 15:1 which better approximates normal human levels (for example 75mcg T4 + 5mcg T3).
A key study comparing levothyroxine (synthetic T4) monotherapy, combined synthetic T4 + T3, and natural desiccated thyroid (NDT, a natural T4 + T3 extract) found largely equivalent biochemical responses across the three options. However, patient preferences varied significantly: 45% favored NDT, 32% preferred the synthetic T4 + T3 combination, and only 23% chose T4 alone.Notably, about one-third of patients who remained symptomatic on T4 monotherapy experienced significant symptom improvement when switching to either NDT or the T4 + T3 combination.This supports a practical clinical approach of starting with affordable, easy-to-dose T4 monotherapy, then trialling NDT or T4 + T3 if symptoms persist.
Target Serum Levels
Recommend adjusting to symptom relief and normal ranges of T3, not just TSH. Suggested targets:
-Free T4: 1.0–1.6 ng/dL (or total T4: 5.0–12.0 μg/dL).
-Free T3: 2.5–4.3 pg/mL (or total T3: 80–220 ng/dL).
-TSH: 0.04–2.5 mIU/L (avoid <0.04 mIU/L to minimise cardiac risks).
Adequate dosing of thyroid hormone often suppresses TSH below the standard reference interval. It is recommended to titrate doses based on symptoms and T3 levels, while ensuring TSH does not fall below 0.04 mIU/L.
Hashimoto's Disease
Hashimoto's thyroiditis is an autoimmune attack on the thyroid, leading to fluctuating or progressive dysfunction. The gland stores preformed hormones; initial attacks release them en masse, causing transient hyperthyroidism which is often experienced as episodic anxiety. Over 5-10+ years, destruction results in permanent hypothyroidism, often requiring lifelong replacement (levothyroxine is the second-most prescribed drug in the U.S.). Regeneration is unlikely once destroyed, but lifestyle interventions can slow progression and reduce replacement needs by enhancing thyroid receptor sensitivity.
Evidence supports:
-Strict gluten (and likely dairy-free diets) to reduce autoimmunity.
-Treating gut dysbiosis including bacterial and fungal overgrowth
-Eliminating seed oils/sugar for better insulin/thyroid receptor function.
-Persistent symptoms despite treatment may warrant consideration of surgical removal of the thyroid (thyroidectomy) which may reduce antibody levels and improve symptoms.
Risks and Considerations
Heart attack, stroke and blood clotting risk
There has previously been some concern regarding an increased risk of heart attack, stroke and blood clotting due to high levels of thyroid hormone. This research was based on patients with thyroid disease where their own thyroid gland secreted excessive levels of thyroid hormone. Research indicates no increased risk in patients treated with thyroid hormone therapy where the TSH remains >0.04 IU/l (which is 10 times lower than the standard reference interval). Overtreatment resulting in a TSH of <0.04 IU/l should be avoided).
Risk of atrial fibrillation, a problem with excessively rapid contraction of the heart is increased with thyroid hormone therapy. This should be considered in any patient with a history of atrial fibrillation. Furthermore, if a patient experiences any symptoms that may suggest atrial fibrillation, including a sense of palpitations (a pounding or racing heart or a sense of skipping beats), sense of excessive fatigue or breathlessness especially with exercise or chest discomfort, they should immediately seek medical attention. The risk of atrial fibrillation may be reduced by replacing immediate release T3 with sustained release T3.
Bone health - at normal levels, T3 appears to exert anabolic, or building effects on bone. At high levels however, it may become catabolic, increasing bone breakdown. It is likely that nutrition plays a key role, as bone breakdown and formation are typically tightly linked. In a setting of deficient nutrient availability, such as may be caused by a poor diet or malabsorption due to gastrointestinal pathology, bone formation may be impaired even in the presence of appropriate hormonal stimulus. It is likely that T3 will augment the state of anabolism or catabolism, whichever is dominant. Clinical assessment of bone turnover may be made with serum procollagen type 1 N-terminal propeptide (P1NP) which directly reflects bone building activity, and C-terminal telopeptide (CTX) which measures bone resorption or breakdown.
Muscle health - muscle pain and fatigue is a common symptom of an underactive thyroid gland. This is because thyroid hormone has a supportive or anabolic effect on muscle, and deficiency of thyroid hormone can result in breakdown of muscle. This can be detected by an elevated level of an enzyme typically located inside muscle cells, creatine kinase (CK), which can 'leak' into the blood when muscle cells are damaged. Accordingly, consideration should be given to assessing thyroid health if CK is detected in the blood at an elevated level.
Red blood cells / macrocytic anaemia -deficiency of thyroid hormone may impair the ability of the bone marrow to make red blood cells. This can lead to a deficiency of red blood cells, with the red blood cells often having a large size (macrocytic anaemia). Macrocytic anaemia is typically associated with low B12 or folate levels - an underactive thyroid should be considered in cases of macrocytic anaemia where B12 and folate levels are appropriate.
References
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Well done if you got this far. Any and all feedback gratefully received.
I tasted success as a young man but was never able to sustain it, because I lived by "feel" instead of by "have to".
Once I stopped making excuses and started doing things because I had to, instead of because I wanted to, everything changed.
This goes HARD.
A flawless two-minute overview of why the man-made climate change narrative is fraudulent. 🎯
"First, CO₂ is not the enemy. It's the lifeblood of this planet... Without it, life dies."
"Second... The Earth runs on cycles. Long before cars, planes, or factories, the Earth heated up and it cooled down on its own... Glaciers formed. Glaciers melted. Seas rose. And there were no humans to blame. It's nature."
"Third, the scare stories never come true. For 50 years, they've said we've only got 12 years to live. And guess what? We're still here."
"Fourth, the green energy scam... It's not science. It's a cash grab."
"Fifth, carbon taxes. You fly on a plane? Tax. You drive too far? Tax. You heat your home? Tax. They scare you with doom, then tax you for breathing."
"Finally, the biggest proof of all: If the world were really ending, if the seas were truly rising... why are banks, builders, and billionaires doubling down on the coastlines? They don't act like the world's ending. Why? Because they know it isn't."
"That's the scam. They terrify you with fear, then get rich off your compliance."
"The Earth warms and the Earth cools. It always has and always will. The only thing that's man-made here is the profit margin."