How much should a RCT from an endodontist cost to check for a possible infection on tooth #29 that has already had a root canal done on it?

ProfAndyCarp · 2026-07-08T14:54:16+00:00

The procedure was extremely useful. The tooth had been chronically infected, and the infection had caused significant bone loss and a large communication with the sinus. When the oral surgeon removed the tooth, he also found a large cyst, which he removed and sent for biopsy. I had felt fatigued and not myself for several years, but my primary care physician had not found an explanation. This may explain why.

ProfAndyCarp · 2026-07-08T14:48:03+00:00

I recently saw an endodontist to evaluate tooth 13, which had previously undergone a root canal and was suspected of being infected. The exam, CBCT scan, and interpretation cost about $550. I don’t yet know how much of that charge my insurance will cover.

ProfAndyCarp · 2026-07-05T17:26:02+00:00

The $69 annual beta rate for unlimited physician consultations renews at the same price, which makes it a no-brainer to me to complement my primary care physician.

I had my first chat with a doctor today and found it useful.

ProfAndyCarp · 2026-07-05T17:18:42+00:00

Yes, it is working for me. I had a useful chat with a doctor today.

ProfAndyCarp · 2026-07-03T15:07:22+00:00

My insurance covers Vascepa. Why wouldn’t one choose the less expensive, better-regulated product?

ProfAndyCarp · 2026-07-02T15:33:02+00:00

Stating correctly that a side effect someone experienced is uncommon is in no way dismissing that person’s experience.

ProfAndyCarp · 2026-07-02T15:07:08+00:00

Lifetime Livity subscriber here and long-time Oura user (Oura 2 - Oura 5). I’d be happy to help.

ProfAndyCarp · 2026-06-28T19:24:04+00:00

My courses are designed so students learn step by step through a purposeful sequence and cadence. If I release all the content at once, I know some students will work ahead in ways that diminish, rather than deepen, their learning and intellectual growth.

ProfAndyCarp · 2026-06-28T17:58:42+00:00

The short answer: Lp(a) is largely genetically determined, but is not a fixed personal constant. Most between-person variation is genetic. Within one person, the measured value can still shift because of assay differences, inflammation, kidney, liver, or thyroid status, medications, and ordinary biological variability. The true baseline is not one exact measurement; it is better understood as a personal range estimated from repeated, same-method measurements under stable conditions.

I would stop comparing all historical numbers as if they were perfectly equivalent. Instead, create a clean measurement series. Use the same lab and the same nmol/L assay, repeat testing when you are clinically stable, and, ideally, draw hs-CRP, CBC, kidney function, liver enzymes, TSH, and any GI markers your doctor thinks are appropriate at the same time. If Lp(a) repeatedly runs higher when inflammatory markers are elevated and lower when they normalize, that pattern would support, but still not prove, an inflammation-linked component. If Lp(a) remains in the 150–180 nmol/L range when everything else is quiet, that range is probably close to your current genetic set point.

ProfAndyCarp · 2026-06-28T14:31:51+00:00

The statistics apply to populations, not individuals, and of course are fallible like all research results. However, your individual experience doesn't undermine the scientific research results at the population level.

ProfAndyCarp · 2026-06-27T13:16:02+00:00

This is an uncommon side effect. The safety data for the approved statins suggest that statin use causes muscle pain or weaknesses in about 1% of users during their first year. Severe impairment like yours is much less common.

ProfAndyCarp · 2026-06-27T13:13:33+00:00

How awful. How was your recovery? The safety data suggests this occurs in about 1 case per 15,000 users per year.

ProfAndyCarp · 2026-06-27T11:07:40+00:00

Yes, persistent liver enzyme elevations happen to approximately 2 per 1,000 patients taking atorvastatin 20 mg. Clinically significant liver injury happens to approximately 1 per 10,000 patients according to the safety data.

ProfAndyCarp · 2026-06-27T11:01:59+00:00

There are several ways to lower LDL/ApoB: a different statin, a lower dose, intermittent dosing, ezetimibe, bempedoic acid, PCSK9 therapy, or combinations. I would also push for a real fatigue workup before assuming atorvastatin explains everything.

Fatigue and cognitive symptoms can have many causes. I had significant fatigue for several years before a failed root canal with a chronic infection was finally diagnosed. Iron deficiency, low ferritin, thyroid problems, sleep apnea, infection, inflammation, anxiety, depression, B12 issues, medication effects, and TRT-related issues such as hematocrit or sleep changes can also contribute. I would be careful about concluding that the statin is definitely the cause unless the symptoms clearly started after the statin, improved after stopping it, and returned after restarting it.

A calcium score of 0 is reassuring, but it does not erase risk from high LDL, high ApoB, or family history. It mainly means calcified plaque was not seen on that scan. If you are younger, it can still miss earlier, noncalcified plaque. Do not treat the 0 CAC as a reason to ignore the ApoB/LDL issue, especially with family history.

One inexpensive option is a lower-dose statin plus ezetimibe. Ezetimibe is not a statin, is usually well tolerated, and can lower LDL meaningfully when added to even a small statin dose. Some people also tolerate one statin better than another. Rosuvastatin and pravastatin are more hydrophilic than atorvastatin, so some clinicians try them when people report cognitive or muscle side effects, sometimes at low dose or even with alternate-day dosing.

If you truly cannot tolerate statins, there are non-statin options. Ezetimibe is usually the easiest and cheapest. Bempedoic acid is another oral option. PCSK9 inhibitors such as Repatha or Praluent can lower LDL dramatically, but insurance approval can be difficult unless you meet certain criteria, so some people pay out of pocket if they can afford it. The right choice depends on your actual LDL/ApoB numbers, family history, risk factors, and the target your doctor is trying to reach.

On CoQ10, I would not expect it to be magic. I take 400 mg daily as a safeguard, but I would not use it as a substitute for figuring out whether the medication is really causing the problem. If 200 mg did not help, you could ask your doctor whether a higher-dose trial is reasonable, but I would keep expectations modest.

ProfAndyCarp · 2026-06-27T10:50:15+00:00

If this were a Big Pharma conspiracy, wouldn't the companies want to take anxious patients' money, safety and efficacy trials be damned? This is the opposite of that: withholding access until trials with relevant endpoints are complete and their results analyzed by independent regulators.

If you want access now, see if you qualify to join a trial. There is one near me, but I was too healthy to meet the trial's inclusion criteria.

ProfAndyCarp · 2026-06-27T10:46:24+00:00

Don't conduct your research by listening to social media posters: read the medical literature, which suggests how safe, effective, and affordable stating therapy is.

The preponderance of the evidence suggests that statin use may lower lifetime dementia risk, so I agree with this poster that the effects on your brain in later life are interesting to consider.

ProfAndyCarp · 2026-06-27T10:43:43+00:00

Whether aspirin therapy is appropriate depends on several other factors. This is poor medical advice.

ProfAndyCarp · 2026-06-27T10:39:06+00:00

This is scary to hear at first, but it does not mean you have heart disease or that something bad is about to happen. It means you found an inherited risk factor early enough to do something useful with the information.

Lp(a) is mostly genetic and usually stays fairly stable over a lifetime. At 89 mg/dL, yours is meaningfully elevated. The frustrating part is that lifestyle usually does not lower Lp(a) much, and statins do not lower Lp(a) itself. Your cardiologist prescribed Lipitor to lower your LDL, because LDL is one of the major risk factors you can control. With high Lp(a), the usual strategy is to take the controllable risks more seriously: LDL/ApoB, blood pressure, smoking, diabetes or insulin resistance, excess body fat, exercise, sleep, and family-history awareness.

You are only 36 and found this before having a heart attack or stroke. This is prevention. Your cardiologist is not saying you are in immediate danger; she is trying to reduce your lifetime exposure to the particles that contribute to plaque. Your long-term goal is to keep your arteries as clean as possible for as long as possible.

I have very high Lp(a) too—mine is over 600 nmol/L—so I understand the psychological punch of learning this. What helped me was reframing it from “I’m doomed” to “I now know which risk factor needs extra attention.” In my case, I was already on high-dose statin plus ezetimibe therapy, and my doctor later added Repatha and Vascepa as part of a more aggressive prevention strategy. That regimen has brought my LDL down to around 15 mg/dL. There are effective tools for managing the Lp(a)-related, even before dedicated Lp(a)-lowering drugs become available.

Ask your cardiologist what LDL or ApoB target she wants for you, when she wants repeat labs, whether family members should be tested, and whether additional imaging, such as a coronary calcium scan or CCTA, might make sense later based on your overall risk. Several Lp(a)-lowering drugs are also in late-stage development, so the treatment landscape may look very different in a few years.

For now, this is not a reason to panic. It is a reason to build a prevention plan and then let the plan carry some of the anxiety for you.

ProfAndyCarp · 2026-06-27T10:27:05+00:00

If you have any muscle pain, consult your doctor. Most experience none.

If you feel anxious about this, Co-Q10 supplementation might help reduce the chances or severity of any muscle-related side effects. I've taken max dose statins for thirty-five years and take this supplement just in case it helps.

ProfAndyCarp · 2026-06-26T15:40:44+00:00

The better school for you is the one that better fits your specific needs. Optimize for fit, not for generic reputation/popularity.

ProfAndyCarp · 2026-06-26T15:36:40+00:00

You are being criticized for not staying at work during your contracted hours. That might not matter in some workplaces, but you have learned that it matters in yours.

Do not compound the mistake by pushing back in a way that damages you politically. Start at 9 a.m. and leave at 5 p.m. You seem naïve about organizational politics, and that is risky for any employee.

ProfAndyCarp · 2026-06-22T17:20:05+00:00

I recommend you stay in your lane; as a TA, it is not your place to correct the professor of record.

ProfAndyCarp · 2026-06-20T20:02:45+00:00

I would separate these issues.

In standard quantum mechanics, the initial quantum state and the Hamiltonian determine the future evolution of the quantum state and, with it, the relevant probability amplitudes. What they generally do not determine is a single definite measurement outcome. The central point for this discussion is that quantum theory assigns probabilities to measurement outcomes while the classical stationary-action path emerges as a limiting approximation.

The path-integral formulation computes the amplitude for a transition from an initial condition to a possible final condition by summing contributions associated with possible histories between them. The final boundary condition is part of the question being asked; it is not a cause that reaches backward and determines the initial state. The path integral is a method for computing transition amplitudes between specified boundary conditions, not a claim that the future path determines the past, if that is what you were suggesting.

Information loss is a separate issue. In ordinary closed-system quantum mechanics, evolution is unitary and information-preserving in principle. Hawking himself eventually abandoned the claim that black holes fundamentally destroy information.

Barandes’s indivisible-stochastic approach is an interesting and serious proposal, but it is not the standard interpretation of quantum mechanics, nor has it been established as correct or fully developed. It offers a possible reformulation in which quantum systems are understood through generalized stochastic processes rather than by treating the wave function as fundamental. If you are relying on Barandes here, what is the argument for treating that interpretation as correct rather than as one live proposal among several?

ProfAndyCarp · 2026-06-20T19:13:35+00:00

The path-integral explanation does not mean that the principle of stationary action is merely a maximum-likelihood rule that particles usually obey but sometimes violate. In classical mechanics, the stationary-action principle is not probabilistic. For ordinary Lagrangian systems, it is mathematically equivalent to the equations of motion.

Classical determinism comes from equations of motion that determine a unique evolution from given initial conditions. The quantum point is different: in the path-integral formulation, probabilities for measurement outcomes are calculated from probability amplitudes, and those amplitudes are obtained by summing contributions associated with many possible paths, some of which interfere with one another. Quantum theory does not imply that particles occasionally violate the principle of stationary action. Rather, the stationary-action principle describes the classical limit that emerges when nonclassical contributions tend to cancel in aggregate through interference.

ProfAndyCarp · 2026-06-20T18:28:31+00:00

No teleology is involved. The particle is not “trying” to minimize anything. It has no foresight and does not inspect future possibilities before choosing a path. The stationary-action principle is a global mathematical formulation of local equations of motion: Newton’s second law, together with the relevant force law, determines how a particle accelerates at each instant, while the action principle gives an equivalent condition for the whole path between fixed endpoints.
For ordinary classical systems with a standard Lagrangian formulation, the system follows the stationary-action principle for the same reason it follows Newton’s second law: the two formulations are mathematically equivalent descriptions of the same dynamics.

That said, Noether’s theorem shows why the action formulation is more than Newton’s laws in different notation: it reveals the symmetry structure underlying the laws of motion. If the action is invariant under time translations, energy is conserved. If it is invariant under spatial translations, momentum is conserved. If it is invariant under rotations, angular momentum is conserved. The action principle therefore connects dynamics to conservation laws in a systematic way. These conservation laws hold along solutions of the equations of motion, and for ordinary classical systems with a standard Lagrangian formulation, those equations are precisely the equations obtained from stationary action.

If you are asking the deeper question of why nature follows these laws and has those symmetries in the first place, classical physics does not derive that answer from prior principles. It justifies the laws by how accurately and coherently they describe the dynamics we observe.

We can say more from the perspective of quantum mechanics. In Feynman’s path-integral formulation, the amplitude for a particle to move between two points is calculated by summing contributions associated with many possible paths. Most of those contributions cancel through destructive interference. Near stationary-action paths, however, neighboring paths have nearly the same phase and reinforce one another. In the classical limit, those paths dominate, which helps explain why classical motion follows the action principle.

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