Cardiovascular Health

[John_Hemming]

I asked o3 for a longer transcript

Below is a “tidied-up” transcript—the video is still presented chronologically, but I’ve:

• removed repeated greetings, filler words (“um,” “you know,” etc.), long pauses, and on-screen music cues
• merged sentences for flow and fixed obvious grammar/punctuation errors
• kept timestamps at key transition points so you can still navigate back to the original video if needed
• lightly paraphrased a few phrases for clarity (technical terms are unchanged)

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0:00 – 1:30 Welcome & Set-up

Good morning, afternoon, or evening—depending on where you are.
We’re starting an hour later than planned because I had to finish a Medicare-project meeting and had some last-minute studio glitches.
Today’s topic: how to measure cardiovascular inflammation, the real driver behind heart attacks and strokes. Most doctors still focus only on LDL cholesterol.

1:30 – 4:00 Why Cholesterol Isn’t the Whole Story

Yes, plaque contains a lot of cholesterol, but cholesterol isn’t the problem until you irritate the arterial intima (the single-cell lining of every artery). When that lining is “burned,” LDL sneaks through and starts an immune cascade.

4:00 – 6:30 Doctors Miss Pre-Diabetes & Insulin Resistance

Primary-care physicians routinely overlook insulin resistance, even though it causes most heart attacks, strokes, blindness, and kidney failure. That’s why I created webinars, online courses, and the book “Prevention Myths.”

6:30 – 9:30 Misconceptions & The Inflammatory Spiral

Myth: “A stress test will tell me if I’m going to have a heart attack.”
Reality: Stress tests detect ≥50 % arterial blockage, not soft plaque.
When the intima is damaged, oxidised LDL attracts monocytes → macrophages → foam cells. Cytokines thin the fibrous cap; rupture + clot = heart attack or stroke.

9:30 – 12:30 Markers Rise in Sequence

A typical progression: Oxidised LDL → high-sensitivity CRP → Myeloperoxidase (MPO) → LP-PLA₂ → high-sensitivity Troponin T.

12:30 – 18:55 The Five Tests I Order Most

1. Oxidised LDL – difficult to obtain but useful if available.
2. hs-CRP – good screening tool, but many false positives (e.g., after a flu shot).
3. Micro-albumin/creatinine ratio – best window on intimal “leakiness.”
4. LP-PLA₂ (Plaque-2) – enzyme released by activated macrophages.
5. MPO – enzyme from neutrophils; highly specific for arterial inflammation.
   (IL-6 is informative but we don’t order it routinely.)

18:55 – 25:30 Pathology Deep Dive

• Transcytosis lets oxidised LDL pass through intimal cells.
• Macrophages engulf LDL, become foam cells, and secrete more inflammatory enzymes (LP-PLA₂, MPO).
• The process continues silently for years until the fibrous cap cracks.

25:30 – 33:30 hs-CRP Caveats & The Power of Albuminuria

Two-thirds of healthy people will spike hs-CRP 48 h after a flu shot.
Albumin in urine, though, is a direct proxy for endothelial damage: if your kidney filters (also lined by intima) leak protein, your arteries probably leak LDL.

33:30 – 40:00 Oxidation, Homocysteine & Methylation

Oxidation = inflammation. We counter it biologically by methylation; poor methylators accumulate homocysteine. A methylated B-complex (e.g., 5-MTHF) helps.

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40:00 – 1:18:20 Audience Q & A (Highlights Only)

Timestamp	Question	Short Answer
44:30	Optimal MPO & LP-PLA₂ cut-offs?	MPO < 400 pmol/L; LP-PLA₂ < 120–140 ng/mL (check your lab’s range).
45:10	Do I need fasting insulin if I’m already diabetic?	Yes—still shows how hard your pancreas is working.
46:50	Does chronic pain raise inflammation?	Indirectly, via cortisol spikes → higher blood sugar → insulin resistance.
48:30	Factor V Leiden screening?	Monitor inflammation too; clotting and plaque risk add together.
52:00	Stress test vs CIMT vs CT angiogram?	CIMT is my go-to because it shows soft plaque and gives an “arterial age.”
54:40	Vitamin K2 while on Eliquis?	K2 is not the same as K1; generally safe, but confirm with your doctor.
58:00	Intermittent fasting and autophagy?	Solid evidence that skipping breakfast/time-restricted eating lowers inflammation.
1:03:00	Baby aspirin—still worth it?	In insulin-resistant patients, I still favor 81 mg despite recent headlines.
1:06:00	Femoral-IMT in addition to carotid?	Adds value only if carotid CIMT is pristine; <2 % reveal hidden plaque elsewhere.

(Numerous other chat comments on vaccines, ivermectin, intro music, etc., have been omitted for brevity.)

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1:18:20 Wrap-up

Thanks for your patience with the late start. We’ll keep balancing Medicare-clinic work with these weekly live streams. See you next time.

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Note: Technical terms (intima, LP-PLA₂, MPO, etc.) are retained exactly as spoken. If you need a plainer-English glossary or want the entire verbatim chat section, just let me know!

[John_Hemming]

This still does not answer the question so I have tried to find the relevant bit of the actual transcript

tests as well micro albumin creatinine ratio that’s really one of the most important
Microalbumin creatinine ratio
16:32
tests it measures the amount of albumin or protein in the urine
16:38
now we make a lot of our bodies make a lot of albumin in fact it’s by far the the most common protein in
16:45
our body we’re not going to lose so much albumin that we’re worried about losing albumin
16:50
the reason we’re interested in microalbumin creatinine ratio is we understand
16:57
how much we’re leaking protein why do we worry about that it’s a thing called the glomerulus a
17:05
glomerulus again it’s another big word all it is is a filter in fact each of your kidneys has about
17:12
1 million filters now why are we worried about that filter
17:19
well let’s go back and connect another dot that filter has most filters have a structure that
17:25
supports a membrane right and then the fluid passes through the membrane
17:30
that’s exactly what happens with the glomerulus or the the million filters in each of our
17:36
kidneys there’s a structure that supports it and then there’s a membrane
17:42
that membrane happens to be the intima the membrane that lines the artery wall
17:48
the membrane that we were talking about just a minute ago that can get damaged during an
17:55
inflammatory process so here’s what we’re looking at if we can measure the amount of damage
18:03
to that membrane by looking at microscopic amounts
18:08
of protein loss through the kidney then we can start getting an estimate of
18:14
how much damage you have to the intimate layer of your arteries
18:22
so if we know that that’s going on then we know that if that intima is leaking protein
18:30
it’s likely leaking ldl if it’s leaking ldl then everywhere you have an artery
18:35
you’ve got an intima that’s leaking ldl or that quote bad what most people
18:42
call bad cholesterol through that lining and getting stuck into the artery wall
18:48
so as you see that’s a very direct indicator of the root cause process itself
Plaque 2 LPPLA2
18:56

That does not seem to explain why the ratio of albumin to creatinine (which is subject to a wide range of influences) links to inflammation or even which way it should be to indicate inflammation.

[World_Traveler]

John it had a video transcript at the bottom after pressing more. It would have taken you directly to the subject matter. All this posted transcript not necessary.

[John_Hemming]

That still does not explain why the ratio of albumin to creatinine in urine is considered to be a proxy for inflammation. I don’t see what the mechanism is.

I know that albumin in serum is vulnerable to lots of short term changes like fasting and creatinine in serum can be increased by exercise. I would expect that creatinine in urine would follow that and similarly with albumin hence the ratio could vary by a lot on factors not relating to the permeability of the intima in the kidney.

[World_Traveler]

The intima in kidneys is exactly identical to intima in arteries through out the body including heart, brain, etc. The degree of inflammation in kidneys will be the same in all the arteries through out the body

[John_Hemming]

What do you mean by “inflammation”?

[John_Hemming]

This is a good paper which explains why the intima in the kidney is different to more generally (although not only the kidney).

Fenestrated Endothelial Cells across Organs: Insights into Kidney Function...

This explains what fenestrated means

Fenestrated Capillaries: Types, Function and Anatomy

[Neo]

@KiwiGuy

You get more radiation when you take an international flight

That does NOT seem to be correct - see below. What do you base it on?

I’ll research this more before the next time I consider doing any non MRI, ultrasound or Dexa imaging.

But while CT imaging can be very valuable, it does seem like it should be traded against the risks of it: see for instance

Study reveals CT scan overuse could account for 1 in 20 new US cancers

Study reveals CT scan overuse could account for 1 in 20 new US cancers

A new study published in JAMA Internal Medicine reveals that the radiation dose currently used in routine computed tomography (CT) examinations in the United States is projected, using modeling, to eventually account for 5% of all new cancer diagnoses annually. The study estimates a range of 80,000 to 127,000 projected cancers based on sensitivity analyses, with a central estimate of approximately 103,000 future lifetime cancers from CT scans performed in 2023, and provides 90% uncertainty limits for these projections.

Paper: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2832778

People can research themselves but @KiwiGuy ‘s statement may not bit be correct:

Two different AI models gave a similar answer on comparing the radiation to air flight:

Unpacked as

[relaxedmeatball]

@John_Hemming

I think that is the case with atherosclerosis. That does not mean that lipids are irrelevant, but it does mean they are not the only factor.

Sorry to be picky here, but atherosclerosis is literally defined by the formation of lesions in the arterial wall. You can’t have those lesions without lipids. You can have inflammation, poor blood flow, aneurysms, or other vascular problems, yes, but you can’t have atherosclerosis without lipid accumulation. So maybe not the only factor, but certainly the most important.

I do agree that lipids don’t magically accumulate by themselves, and some sort of insult to the arterial endothelial layer is necessary. However, I don’t think it’s realistic that people will be able to live without that happening. There’s evidence that even just the simple shear forces of the blood flow itself is injurious. There are examples of foetuses with arterial plaque. So the lipids are by far the most influential thing, and they’re easily modifiable. I would say that one only needs to worry about EC senescence, differentiation etc once their ApoB is below like 40mg/dl. Otherwise you’re missing the wood for the trees.

In some way, this represents a microcosm of the entire problem in the field. Heart attacks and strokes are still the biggest killers in the world, completely unnecessarily, when we already have a bunch of different ways to prevent the majority of them. But you still have people doing shots of coconut oil and other crazy stuff due to simple misinformation.

[KiwiGuy]

Appreciate the links — but let’s not get carried away.

My CTA was 1.31 mSv — that’s roughly 9–13 long-haul flights worth of radiation. Not trivial, but not exactly playing with uranium either. If that level of exposure were genuinely dangerous, we’d see sky-high cancer rates in pilots, flight attendants, and astronauts — people who get this kind of dose every few weeks as part of their job. But we don’t. Airline industry studies consistently show no meaningful increase in solid tumor cancer rates, even among long-haul crew with decades of exposure.

Now, the JAMA paper claims 103,000 future cancers from CT scans performed in 2023. That’s not based on observed data — it’s a hypothetical projection, based on the linear no-threshold (LNT) model, which assumes that any radiation exposure increases cancer risk, linearly and cumulatively. That model is widely debated and likely overstates low-dose risk, especially with modern imaging protocols.

Just to put that claim in perspective:

• Smoking kills ~160,000 Americans from cancer every single year — real data.
• JAMA suggests CT scans from one year might eventually cause 103,000 cancers — modeled guesswork, and not all would be fatal.

So essentially they’re implying that one year of CT scans is nearly as carcinogenic as all smoking in the U.S. in the same year. That’s… bold.

CT overuse should absolutely be questioned. But a 1.3 mSv cardiac CTA, done for the right reason on a modern scanner, is incredibly low-risk. The idea that this sits anywhere near smoking in terms of cancer risk is pure extrapolative fiction — and wildly out of step with what we see in high-exposure professions like aviation.

[John_Hemming]

So we don’t disagree in a broader sense. I think it is worth controlling lipids. Statins have their role in this. Personally I keep an eye on LDL-C, ApoB and Lp(a).

[LukeMV]

How ironic that I am reading this right now while on an international flight WiFi

[desertshores]

I worked at the Nevada Test Site for 15 years in my younger days. I worked in the “forward area”. This was during the era of underground testing, but occasionally the tests vented (leaked radiation), so on a couple of occasions, I received more than my fair share of exposure to ionizing radiation, specifically radioactive xenon and iodine.

Although there weren’t many studies about low-dose exposure to ionizing radiation, I did visit Oak Ridge National Laboratories. While there I talked to health physicists who were studying the survivors of Nagasaki and Hiroshima. They were surprised that the amount of leukemia and other effects of high radiation exposure was lower than expected.

I am 84 and still living to tell the tale.

If you have watched any of the videos about the aftereffects of wildlife in the high-radiation areas around Chernobyl, it appears that plant life and wildlife, including feral cats, are thriving in the absence of people, many years after the initial incident.

“Some early animal studies, and even some more recent ones (e.g., on certain strains of mice or beagle dogs exposed to very low, continuous gamma irradiation), have reported extended mean lifespans or reduced disease incidence in the low-dose groups compared to unexposed controls.”

In any case, here are a couple of articles that support the idea that a bit of radiation isn’t particularly harmful. Albeit current health physicists will probably tell you all ionizing radiation is harmful.

The theory on which low radiation exposure being beneficial is:

“Hormesis is the concept that biologic systems can respond in a positive way, or be stimulated by, physical or biologic exposure to low doses of an agent that is toxic at higher doses (1). Additionally, hormesis is defined as “any physiological effect that occurs at low doses which cannot be anticipated by extrapolating from toxic effects noted at high doses” (2). Therefore, radiation hormesis is the theory that biologic systems can respond positively to exposure to low doses of ionizing radiation.”

Low-dose ionizing radiation as a hormetin: experimental observations and...

Radiation Hormesis: Historical and Current Perspectives

Hormesis from Low-Dose Radiation

[John_Hemming]

I am not myself persuaded that a little bit of DNA damage is a good thing.

Here is a tidy transcript, summary, and critique of the video “Hormesis from Low-Dose Radiation” (YouTube link).

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Tidy Transcript

Title: Hormesis from Low-Dose Radiation

Hormesis was first shown to extend life over a century ago when low doses of radiation increased the lifespan of beetles. Scientists originally intended to use x-rays to sterilize grain pests, but instead, low doses made the beetles live longer.

This effect was later replicated using gamma rays and in over a dozen other insect species—houseflies, crickets, wasps, mosquitoes—showing consistent lifespan extensions of 20–60%.

What’s going on?

Hormesis is thought to be an adaptive response to low-level stress. The body perceives a mild insult, triggering a compensatory overcorrection that more than offsets the initial damage—resulting in a net benefit.

In radiation’s case, high doses damage DNA and kill cells. But DNA repair machinery is metabolically expensive to run full-time. Low-dose radiation may signal a DNA-damaging environment, prompting the body to ramp up its repair systems. This increased DNA protection might explain the longer lifespan observed—what doesn’t kill you makes you stronger.

Hormesis might not be limited to insects. One study claimed that survivors of the Hiroshima and Nagasaki bombings who were exposed to low-dose radiation had lower cancer mortality and longer lives compared to unexposed people. In contrast, those closer to the blast suffered higher cancer rates and shorter lives.

Some of the longevity benefit might be due to superior medical care provided under the Law Concerning Relief to Atomic Bomb Survivors, but hormesis may also play a role.

Marie Curie, who discovered radioactivity and later died of radiation-induced bone marrow failure, is quoted: “Nothing in life is to be feared; it is only to be understood.” Her remains were buried in a lead-lined coffin.

Why would animals evolve to withstand radiation?

Because the Earth is constantly bombarded by cosmic rays—our bodies receive ~20,000 hits per second. What happens if we remove that exposure?

Experiments show that single-celled organisms like Paramecia grow poorly in lead-shielded boxes, and the thicker the shielding, the more their growth is inhibited. Human cells under these conditions show increased DNA damage and mutations.

This suggests that natural background radiation might have a beneficial hormetic effect by keeping our stress-response systems engaged.

Even a foot of lead only blocks about one-third of cosmic rays. To reduce exposure more drastically, researchers went over a mile underground into SNOLAB (Sudbury Neutrino Observatory) in Canada.

Unexpectedly, fish raised underground grew larger and heavier than surface fish. Researchers speculated that radon gas trapped in the mine may have offset the lack of cosmic rays—so the results remain inconclusive.

Conclusion: We don’t yet know enough about low-dose radiation to exploit hormetic effects safely. Fortunately, there are safer ways to leverage hormesis for health and longevity.

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Summary

• Hormesis is a biological phenomenon where low-dose stressors (like radiation) trigger adaptive, overcompensating protective responses.
• First shown in beetles in the early 20th century, radiation hormesis increased lifespan across multiple insect species.
• The suggested mechanism is DNA repair upregulation in response to mild DNA damage.
• Some data from atomic bomb survivors indicate that individuals exposed to lower radiation doses had lower cancer risk and longer lifespans, possibly due to hormesis—but confounding factors like enhanced medical care complicate interpretation.
• Natural background radiation may play a low-level regulatory role in cell growth and DNA stability. Shielding organisms from it leads to more, not fewer, mutations.
• In one deep-underground study, fish grew larger, possibly due to altered radiation environment, but radon exposure complicates conclusions.
• Caution is urged: radiation hormesis may exist, but its safe exploitation in humans is not yet justified.
• Safer hormetic strategies include exercise, intermittent fasting, and phytochemicals.

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Critique

Strengths

1. Clear, logical structure: Moves from insect studies → mechanistic theory → human epidemiology → background radiation → lab experiments → conclusion.
2. Balanced skepticism: Emphasizes the uncertainty surrounding the safety and generalizability of radiation hormesis.
3. Wide-ranging examples: Covers both controlled lab observations and historical human data, broadening relevance.
4. Scientific humility: The final takeaway urges caution, discouraging premature therapeutic use of radiation hormesis.

Weaknesses

1. Overinterpretation of A-bomb survivor data:

   • The claim that low-dose-exposed survivors lived longer is controversial.
   • Many studies (e.g., Preston et al., Radiation Research, 2003) emphasize increased cancer risk even at low doses.
   • The observed benefit may be survivorship bias or due to better medical care, not hormesis.

2. Inconclusive mechanistic evidence:

   • DNA repair activation is plausible but still speculative in long-term lifespan enhancement.
   • Animal data is solid for insects, but poorly replicated in mammals, particularly humans.

3. Fish study lacks rigor:

   • Confounding by radon undermines any claim about suppressed cosmic rays.
   • Growth rate changes in fish are not equivalent to increased healthspan or lifespan.

4. Potential for misapplication:

   • The video could unintentionally encourage pseudoscientific practices involving radiation exposure.
   • Needs stronger disclaimers about dose-dependent toxicity.

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Conclusion

While radiation hormesis is a scientifically interesting phenomenon with some experimental support, especially in simple organisms, it is not currently a safe or validated approach for human longevity. The video provides a thoughtful exploration but must be interpreted cautiously due to:

• methodological limitations in human data,
• unresolved mechanisms, and
• the inherently toxic potential of ionizing radiation.

Practical takeaway: Stick to well-studied forms of hormesis—like exercise, thermal stress, and dietary restriction—to promote health and longevity safely.

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Would you like a list of peer-reviewed studies on radiation hormesis or background radiation effects on DNA stability?

[Neo]

Fascinating

I think I’ll still be on the conservative side until much more info comes out

But very interesting hypothesis

[CronosTempi]

Statins as Antithrombotic Drugs

https://www.ahajournals.org/doi/10.1161/circulationaha.112.145334

“In this review, we present experimental data in support of the ability of statins to interfere directly with the clotting system and platelet activation, as well as the clinical settings that suggest that statins exert beneficial effects related to their antithrombotic properties.”

Effect of statins on platelet function in patients with hyperlipidemia

https://www.researchgate.net/publication/256764786_Effect_of_statins_on_platelet_function_in_patients_with_hyperlipidemia

“It is generally assumed that cholesterol reduction by statins is the predominant therapeutic result underlying their beneficial effects in cardiovascular disease. However, the action of statins may be partially independent of their effects on plasma cholesterol levels, as they combine lipid lowering with positive effects on hemorheological conditions and endothelial function. We evaluated the impact of statin treatment on platelet adhesion to fibrinogen (spontaneous and ADP-activated), along with ADP, collagen or ristocetin-induced aggregation in type II hyperlipidemic patients. The study group included 70 persons: 50 patients affected by type II hyperlipidemia without concomitant diseases and 20 healthy volunteers. The effects of 8-week statin treatment (atorvastatin 10 mg/day, simvastatin 20 mg/day, or pravastatin 20 mg/day) on platelet activation were evaluated. Regardless of the type of statin, a significant decrease in ADP-induced platelet aggregation was observed: for atorvastatin 50.6 ±12.8% vs. 41.1 ±15.8% (p < 0.05), for simvastatin 57.2 ±18.0% vs. 44.7 ±22.1% (p = 0.05), and for pravastatin 55.8 ±19.5% vs. 38.8 ±23.3% (p < 0.05). There was no significant effect of statins on collagen or ristocetin-induced platelet aggregation and adhesion. Therapy with statins beneficially modifies ADP-induced platelet aggregation in patients with hyperlipidemia and does not affect spontaneous or ADP-induced platelet adhesion to fibrinogen and platelet aggregation induced by collagen or ristocetin.”

The Effects of Statins, Ezetimibe, PCSK9-Inhibitors, Inclisiran, and Icosapent Ethyl on Platelet Function

https://www.mdpi.com/1422-0067/24/14/11739

Effect of Statins on Platelet Activation and Function: From Molecular Pathways to Clinical Effects

https://onlinelibrary.wiley.com/doi/10.1155/2021/6661847

Antiplatelet Actions of Statins and Fibrates Are Mediated by PPARs

https://www.ahajournals.org/doi/10.1161/atvbaha.108.183160

Independent association of Lp(a) with platelet reactivity in subjects without statins or antiplatelet agents

https://www.nature.com/articles/s41598-022-21121-7